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National Research Council (US) Subcommittee on Laboratory Animal Nutrition. Nutrient Requirements of Laboratory Animals: Fourth Revised Edition, 1995. Washington (DC): National Academies Press (US); 1995.

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Nutrient Requirements of Laboratory Animals: Fourth Revised Edition, 1995.

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4Nutrient Requirements of the Guinea Pig

The domestic guinea pig (Cavia porcellus) has been bred in captivity for at least 400 years and probably originated in Peru, Argentina, or Brazil (Weir, 1974). Many laboratory guinea pigs were bred from a strain established by Dunkin and Hartley in 1926 (Dunkin et al., 1930). [See National Institutes of Health (1982) for other strains.] Unless otherwise indicated, the strain referred to in this chapter is the outbred Hartley.

In its natural habitat this herbivorous animal consumes large quantities of vegetation (Navia and Hunt, 1976). The molar teeth are especially suited to grinding and, like other species of rodents, the guinea pig has open-rooted incisors that grow continuously throughout its life. Like the rat, mouse, and rabbit, the guinea pig is simple-stomached; but in contrast to these species, the entire stomach of the guinea pig is lined with glandular epithelium (Breazile and Brown, 1976; Navia and Hunt, 1976). The intestine allows the development of predominantly gram-positive bacterial flora, which may contribute to the nutritional requirements of the host perhaps through direct absorption of bacterial metabolites or digestion and absorption of intestinal bacteria and other materials following coprophagy. The guinea pig has a large semicircular cecum with numerous lateral pouches. This organ resembles that of the rabbit and possibly has similar digestive functions—e.g., synthesis of B vitamins and indispensable amino acids by microorganisms and recycling of intestinal contents by coprophagy (Hunt and Harrington, 1974). Few serious attempts have been made to determine the contribution of coprophagy to the nutrition of the guinea pig.

Behavioral And Nutritional Characteristics

In the laboratory, the guinea pig's diet is much higher in energy density and lower in fiber content than the diet of green vegetation and fruits it consumes in the wild. The guinea pig consumes many small meals throughout the day, is fastidious in choice of foods, and may resist abrupt changes in composition or form of the diet. Animals fed pelleted natural-ingredient diets often do not readily accept a powdered purified diet unless introduced gradually. Pelleting the powdery diet (Ostwald et al., 1971), moistening the food with water (O'Dell and Regan, 1963; Singh et al., 1968), and using gel diets (Navia and Lopez, 1973; Apgar and Everett, 1991b) have been successful in promoting diet acceptance. These behavioral characteristics and special nutritional requirements need to be considered when designing nutritional or metabolic studies.

Water intake is variable and food intake is largely influenced by the form and composition of the diet and the age of the animal. Liu (1988) reported a mean water intake of 21.7 mL/100 g BW/day and mean consumption of a natural-ingredient diet 3.0 Mcal/kg (12.6 MJ/kg) to be 6.9 g/100 g BW/day in 6-week-old male guinea pigs (312 ± 13 g) that were individually housed on sawdust. Water and food consumption was 7.5 mL/100 g BW/day and 4 g/100 g BW/day, respectively, in male guinea pigs weighing 698 ± 19 g and fed a nonpurified diet containing 20 percent crude protein (Tsao and Young, 1989). Adult male guinea pigs weighing 725 to 750 g consumed daily 32 g of a purified diet containing crystalline amino acids (equivalent to 160 g protein/kg diet) as the sole nitrogen source (Schiller, 1977).

The guinea pig is best known, from a nutritional standpoint, by its requirement for dietary vitamin C. This feature has made the guinea pig particularly useful in studies of collagen biosynthesis, wound healing, and bone growth. The young guinea pig seems to have a relatively high dietary requirement for arginine, folic acid, and selected minerals, although this may not prove to be true as more information on specific nutrient requirements becomes available. These characteristics and others mentioned above are discussed in greater detail in The Biology of the Guinea Pig (Wagner and Manning, 1976).

Germ-free guinea pigs have been used in the study of specific disease states. Diets for germ-free and specific-pathogen-free guinea pigs have been discussed by Wagner and Foster (1976).

Growth And Reproduction

The guinea pig has a mean gestation period of 68 ± 2 SE days (range 59 to 72 days) (Labhsetwar and Diamond, 1970), which may contribute to its advanced development at birth. Dams usually bear 3 to 4 (range 1 to 8) offspring weighing an average of 85 to 100 g each (Ediger, 1976; Sisk, 1976; Apgar and Everett, 1991a). Guinea pigs born weighing less than 50 g have a low probability of survival (Ediger, 1976). Newborn animals can consume semisolid and solid food immediately, although weaning occurs at about 21 days of age when body weight is approximately 250 g (Ediger, 1976). Guinea pigs normally gain as much as 5 to 7 g/day during the rapid growth period when allowed to eat commercial natural-ingredient or purified diets ad libitum (Shelton, 1971; Navia and Lopez, 1973; Jeffery and Typpo, 1982; Liu, 1988; Typpo et al., 1990b). These gains occur routinely and are greater than those obtained with some of the diets used earlier (4 g/day; Woolley and Sprince, 1945). Growth slows after 2 months and maturity is reached at about 5 months. Weight gain can continue until 12 to 15 months of age and levels off at 700 to 850 g for females and 950 to 1,200 g for males (Ediger, 1976). Mating is most often successful when females are 450 to 600 g (2.5 to 3 months old; Ediger, 1976).

Estimation Of Nutrient Requirements

Estimates of the energy and nutrient requirements for growth of the guinea pig are presented in this chapter. Considerable variation in requirements can occur as a consequence of several factors—the same as those affecting the nutrient requirements of the rat or mouse: developmental stage, reproductive activity, and age; gender; strain. The nutrient requirements listed in this chapter represent mean values that are thought to be representative but not necessarily sufficient in all circumstances. Further research to quantify nutrient requirements and to identify sources of variation in nutrient requirements of the guinea pig is needed.

Recommendations in this chapter for nutrient concentrations have not been increased to allow a margin of safety for variations in dietary ingredients or for differences among guinea pigs. The data on which requirements are based were reported from several different laboratories using different colony management practices. They are adequate for guinea pigs in most laboratory conditions, but particular laboratory protocols, such as maintenance of germ-free colonies or testing of experimental drugs (see Chapter 1), may alter the requirements for one or more nutrients. The data are not sufficient to differentiate between adult maintenance requirements and growth, pregnancy, or lactation requirements; hence, estimates are provided for growth only (Table 4-1). When data were insufficient to determine requirements, adequate concentrations were determined on the basis of feeding studies that produced adequate growth or on well-established concentrations that produce adequate growth in the laboratory rat. If cited papers provided nutrient intake per day but did not specify dietary concentrations, the values have been converted to dietary content by assuming a dietary intake of 20 to 25 g/guinea pig/day for growth.

TABLE 4-1. Estimated Nutrient Requirements for Growth for Guinea Pigs.


Estimated Nutrient Requirements for Growth for Guinea Pigs.

Examples Of Diets For Guinea Pigs

The composition of an open-formula diet used successfully for growth, reproduction, and longevity is shown in Table 4-2. This natural-ingredient diet is the formulation developed by the National Institutes of Health for production and research colonies of conventional guinea pigs.

TABLE 4-2. Example of a Natural-Ingredient Diet Used for Guinea Pig Breeding Colonies at the National Institutes of Health.


Example of a Natural-Ingredient Diet Used for Guinea Pig Breeding Colonies at the National Institutes of Health.

Several purified diets have been used that successfully support growth in guinea pigs, although it is not always clear why. Of historical importance is the purified diet developed by Reid and Briggs (1953) for the growing guinea pig; it is still used in original or modified (Typpo et al., 1985) forms. The Typpo et al. (1985) diet and three other examples of purified diets that support satisfactory growth (Navai and Lopez, 1973; O'Dell et al., 1989) and reproduction (Apgar and Everett, 1991a,b) are given in Table 4-3. Two of these are agar gel diets—one satisfactory for growth (Navia and Lopez, 1973) and the other for gestation (Apgar and Everett, 1991a,b). Proteins other than casein—such as soybean, egg white (O'Dell et al., 1989), and lactalbumin (Hsieh and Navia, 1980)—have been used, and the lipid source and amount vary, suggesting that the guinea pig does well on a wide range of lipid intakes (Navia and Hunt, 1976). Fiber sources vary from wood pulp to cellophane. Jeffery and Typpo (1982) developed a purified diet in which crystalline amino acids replaced protein. This diet has been used successfully for growth (Typpo et al., 1990a) and maintenance (Schiller, 1977) of adult guinea pigs. A summary of recommended nutrient allowances for growing guinea pigs is presented in Table 4-1. Requirements for specific nutrients for reproduction and longevity are unknown.

TABLE 4-3. Examples of Four Satisfactory Purified Diets for Guinea Pigs.


Examples of Four Satisfactory Purified Diets for Guinea Pigs.


Research has not been conducted with the specific objective of determining the actual energy requirement of the guinea pig; applying energy values of feedstuffs designed for rats or mice to the guinea pig may not be appropriate, as it is likely that the guinea pig can utilize fibrous feedstuffs more efficiently than mice and rats. Hirsh (1973) diluted a diet to 50 percent with finely ground cellulose (a calculated reduction in calories of 40 percent) and reported that the guinea pig did not increase food intake but did, after some initial loss, maintain body weight. Henning and Hird (1970) found that the cecum of the guinea pig contained concentrations of short-chain fatty acids similar to those in the bovine rumen. In fact, the guinea pig is a hindgut fermentor, and its cecum—the primary site of fermentation—has a fermentive capacity similar to that of the colon and rectum of horses (Parra, 1978). The cecal fermentive capacity of the guinea pig is 2.5 times the colonic fermentive capacity of the rat. The ability of the guinea pig to derive energy from fibrous materials must be considered when developing experimental strategies to quantify the energy requirement of this animal.

A variety of commercial diets designed to meet the nutrient requirements of the guinea pig have been used (Argenzio et al., 1988; Tsao and Leung, 1988; Berger et al., 1989; Fernandez et al., 1990) for a variety of experimental purposes. A commercial natural-ingredient rabbit diet has also been fed to guinea pigs, apparently with satisfactory results (Johnston, 1989; Johnston and Huang, 1991). A variety of purified diets also have been described. In general, these diets have a cornstarch/sucrose mixture as the primary energy source; protein sources include soybean protein, casein, and egg white solids (Miller et al., 1990; Apgar and Everett, 1991b; Fernandez and McNamara, 1991; Simboli-Campbell and Jones, 1991). Unfortunately, food consumption was not reported; thus, estimation of energy requirements is impossible. However, the fact that the guinea pigs appeared to function in a normal physiological manner indicates that the diets contained the necessary energy density.

The energy densities of the diets discussed above have been estimated in terms of metabolizable energy (ME) using the physiological fuel value system and on an ''as is" basis. In estimating the ME values of the diets, fiber was not included. As it is most likely that the guinea pig can convert fiber to useful energy, the estimated ME values are conservative. In all diets considered, fiber made up no more than 16 percent of the total weight of the diet. The commercial diets contained from 2.8 to 3.2 Mcal/kg diet (11.9 to 13.4 MJ/kg diet), not considering the fiber. From the data of Berger et al. (1989) and Argenzio et al. (1988) it can be estimated that the maintenance energy requirement of the 400- to 600-g guinea pig can be met by approximately 136 Kcal ME/BWkg0.75 (570 kJ), where BWkg0.75 represents metabolic body weight in kilograms. The purified diets contained from 3.1 to 3.5 Mcal ME/kg diet (13.2 to 14.6 MJ ME/kg diet), again not considering the dietary fiber. A crystalline amino acid diet containing 50 g of corn oil and 150 g of fiber per kg of diet contained 3.4 Mcal ME/kg (14.2 MJ ME/kg)(not considering the fiber) and resulted in a growth rate of 7 g/day when fed to 3- to 6-week-old male guinea pigs (Typpo et al., 1990a,b). At present natural-ingredient and purified diets should contain a minimum of 3.0 Mcal ME/kg (12.5 MJ ME/kg) and approximately 15 percent fiber. Further data are necessary to precisely evaluate the ability of the guinea pig to utilize dietary fiber and thus provide more precise energy requirements.


An optimal concentration of dietary lipid has not been established for the guinea pig. Reid et al. (1964) fed 2- to 5-day-old male guinea pigs (Hartley strain) purified diets containing 0, 10, 30, 75, 150, and 250 g corn oil/kg diet for 6 weeks. They found an increase in weight gained in groups fed 0 and 10 g corn oil/kg diet, a plateau in weight for those fed 10 to 150 g corn oil/kg diet, and a slight decrease in weight of those fed 250 g corn oil/kg diet. The effects of dietary fat concentration on optimal reproduction, lactation, or longevity have not been determined.

Essential Fatty Acids (EFA)

n-6 Fatty Acids

Reid et al. (1964) conducted several studies to assess the requirement for n-6 fatty acids. In one experiment, they measured the appearance of dermatitis (a sign of EFA deficiency) in young male guinea pigs. These animals were fed diets containing 0, 0.17, 0.33, 0.67, 1.33, or 4.0 g methyl linoleate and 10 g corn oil/kg. The diets were found to actually contain 0.15, 0.20, 0.24, 0.34, 0.54, 1.31, and 1.89 percent, respectively, of the calories as linoleic acid after accounting for the linoleic acid supplied by the cornstarch. Dermatitis occurred until the concentration of linoleic acid in the dietary treatment reached 1.31 percent of calories; thus, the amount of linoleic acid needed to prevent dermatitis falls between 0.54 and 1.31 percent of total calories. Guinea pigs grew normally when the concentration was only 0.24 percent. Thus, a higher concentration of linoleic acid is required to prevent dermatitis than is needed for normal growth.

Reid et al. (1964) also measured the requirement for linoleic acid by measuring the triene:tetraene ratio [20:3(n-9) to 20:4(n-6)] in erythrocytes in response to increasing concentrations of dietary linoleic acid, a method developed previously by Holman (1960) for rats. The requirement for linoleic acid was estimated as the percentage of the total calories of linoleic acid at the breakpoint of this dose-response curve. The actual dietary treatments provided 0.15, 0.46, 0.88, 1.04, 1.25, and 1.42 percent linoleic acid (supplied by safflower oil). Based on this method, the linoleic acid requirement for guinea pigs was determined to be between 0.88 and 1.04 percent of total calories.

n-3 Fatty Acids

As in other mammals, in the guinea pig n-3 fatty acids concentrate in certain tissues, including brain and testes (Tinoco, 1982), but the precise function of these fatty acids is unknown. Unlike most other mammals, however, the guinea pig has been found to have relatively lower concentrations of 22:6(n-3) and higher concentrations of 22:5(n-6) in their photoreceptor outer segment membranes. This may, in part, explain the absence of changes in the electroretinogram (a measure of retina function) of offspring of guinea pigs fed sunflower oil [high linoleic acid 18:2(n-6), very low α-linolenic acid 18:3(n-3)] treatments for several generations (Leat et al., 1986). Neuringer et al. (1988) speculated that the shift in fatty acid composition of the retina as a result of n-3 fatty acid-deficient diets may affect retinyl function less than in other species that maintain higher concentrations of retinal 22:6(n-3). Essentiality of n-3 fatty acids in the diet of the guinea pig has not been studied.

Signs of EFA Deficiency Classic signs of EFA deficiency (lack of n-6 fatty acids) were reported by Reid (1954b) and Reid and Martin (1959) and include ulcers about the neck and ears, loss of hair on the ventral surface, retarded growth, dermatitis, and mortality. They described additional signs of priapism; underdevelopment of the spleen, testes, and gallbladder; and enlargement of the kidneys, liver, adrenals, and heart. Specific skin changes were found to be confined to the surface layers and, therefore, less extensive than those of the EFA-deficient rat. Fat deprivation was not found to increase water consumption, which also is in contrast to signs described in the EFA-deficient rat.


Sucrose, glucose, lactose, and starch have been used as primary energy sources in purified diets for guinea pigs (Reid and Briggs, 1953; Heinicke and Elvehjem, 1955; Heinicke et al., 1955). Guinea pigs consuming diets that contain lactose as the sole carbohydrate in the diet grew at rates about one-third that of controls fed sucrose-based diets (Heinicke and Elvehjem, 1955). Few differences were observed between guinea pigs fed sucrose- and dextrin-containing diets (Booth et al., 1949; Heinicke et al., 1955). Consuming sucrose or a mixture of glucose and fructose, when added to natural-ingredient diets at concentrations equal to 20 percent of energy, led to equal growth rates (6.6 g/day; Ahrens et al., 1985).

Protein And Amino Acids


The guinea pigs' protein requirement for growth depends on the nitrogen source in the diet (Table 4-4). Woolley and Sprince (1945) observed that the guinea pig had an unusually high protein requirement when casein was the only nitrogen source in a purified diet. Highest weight gains were obtained when the diet contained 300 g casein/kg, but equivalent growth occurred when arginine, cystine, and glycine were added to a diet supplying 180 g casein/kg. These findings have been confirmed (Reid and Briggs, 1953) and extended (Heinicke et al., 1955, 1956; Reid, 1963; Reid and Mickelsen, 1963) to demonstrate that the most limiting amino acid in casein for the growing guinea pig is arginine. As the casein content of the diet is reduced below 300 g/kg, methionine becomes next most limiting followed by tryptophan. Not only does the young guinea pig have a high requirement for arginine, but the arginine in casein is reported to be only about 70 percent available (Heinicke et al., 1955). Supplementing a diet containing 300 g casein/kg (12.6 g arginine/kg) with 3 g L-arginine-HCl/kg resulted in improved growth (Reid and Mickelsen, 1963) that was equivalent to a diet containing 350 g casein/kg (6.5 to 7 g/day; Reid, 1963), although theoretically 300 g casein/kg should meet the arginine requirement. Plant proteins contain generous amounts of arginine, and the herbivorous guinea pig grows well when fed diets that contain 180 to 200 g protein/kg (10.8 g arginine/kg) from plant sources (Lister and McCance, 1965; Shelton, 1971). Soybean protein has been widely used in experimental diets for guinea pigs. Such diets are adequate in arginine but limiting in methionine for maximal growth at concentrations below 300 g soybean protein/kg (Reid and Mickelsen, 1963; Reid, 1966). Supplementation of a diet containing 300 g soybean protein/kg with 5 g DL-methionine/kg re sulted in growth close to 7 g/day (Reid and Mickelsen, 1963; Alberts et al., 1977). A diet containing 200 g soybean protein/kg requires supplementation with 10 g DL-methionine/kg to produce equivalent growth (Reid and Mickelson, 1963).

TABLE 4-4. Protein Requirement for Growth for Various Strains of Guinea Pigs.


Protein Requirement for Growth for Various Strains of Guinea Pigs.

Amino Acids

An early estimate of the requirement for sulfur-containing amino acids of the young guinea pig fed a diet containing 200 g soybean protein/kg supplemented with 1 g tryptophan/kg was found to be 7.1 g/kg diet, with 3.6 g as cystine and 3.5 g as methionine (Reid, 1966). Growth and liver weight were greater with supplementation of 3.75 g L-methionine/kg than with 7.5 g DL-methionine/kg or 3.75 g D-methionine/kg in the diet. Thus, D-methionine does not appear to be as active as L-methionine in the guinea pig (Reid, 1966). Young guinea pigs grew well when a diet containing 190 g heated soybean protein flour/kg diet (Hasdai et al., 1989) provided 5.7 g sulfur-containing amino acids/kg (2.7 g methionine and 3 g cystine/kg). In recent studies in which crystalline amino acid diets were used, the minimum total sulfur amino acid requirement was 5 g/kg with 3 g/kg from L-methionine and 2 g/kg from L-cystine, constituting 40 percent of methionine being replaced by cystine (Typpo et al., 1990b). When corrected for efficiency of use, 6 g total sulfur amino acids with 3.6 g/kg from L-methionine and 2.4 g/kg from L-cystine will meet the requirement (Table 4-5).

TABLE 4-5. Amino Acid Requirements for Growth for Male Hartley Guinea Pigs.


Amino Acid Requirements for Growth for Male Hartley Guinea Pigs.

The tryptophan requirement of the growing guinea pig was reported to be between 1.6 and 2.0 g/kg diet (Reid and Von Sallmann, 1960) to promote maximum growth and prevent cataract development. Signs of tryptophan deficiency were produced by feeding guinea pigs a diet containing 100 grams each of soybean protein and gelatin per kilogram of diet supplemented with an amino acid mixture to the approximate amino acid content of 200 g soybean protein/kg and an ample supply of niacin (200 mg/kg diet). The result of this 1.08 g L-tryptophan/kg diet was poor growth, distended abdomens, alopecia, and cataracts (Reid and Von Sallmann, 1960). Adding 0.3 g L-tryptophan/kg to the diet resulted in maximum growth, but the addition of 1 g L-tryptophan/kg was necessary to obtain complete protection from cataracts. Thus, the requirement for tryptophan to prevent eye lesions was considerably greater than the requirement for maximum growth. Using crystalline amino acid diets, the tryptophan requirement for maximum growth, nitrogen retention, and freedom from cataracts was 1.5 g/kg when niacin was between 0.06 and 0.2 g/kg diet (Smith, 1979). When corrected for efficiency of use, 1.8 g/ kg meets the requirement. Reducing the niacin content of the amino acid diet to 0.05 and 0 g/kg increased the tryptophan requirement to 2 and 3 g/kg, respectively (Smith, 1979).

More recently the development of a basal crystalline L-amino acid diet suitable for studies of individual amino acid requirements in young male guinea pigs has been reported (Jeffery and Typpo, 1982; Typpo et al., 1990b). The basal diet contained 36 g nitrogen/kg as the L form of crystalline amino acids, 3.4 Mcal ME/kg (14.2 MJ ME/kg); sucrose and glucose as the carbohydrates, corn oil, fiber in the form of cellophane; and crystalline vitamins and minerals. The original mixture of indispensable amino acids (the usual 10 plus cystine and tyrosine) was based on the amino acid composition of a number of effective diets that contained natural proteins. Several dispensable amino acids (glutamic acid, asparagine, proline, alanine, aspartic acid, glycine, serine, and sodium glutamate) were included in a mixture. The indispensable nitrogen content of the original diet was 17 g/kg, giving an indispensable-to-total nitrogen ratio of 0.47. In a series of 3-week experiments conducted with guinea pigs of the Hartley strain approximately 2 to 3 weeks old (200 to 250 g), weight gain; nitrogen retention; carcass, liver, and gastrointestinal tract weights; and, for some studies, plasma concentration of the amino acid under test were used to determine the minimum requirement for each individual amino acid. As the requirement for each amino acid was established, this quantity was incorporated into the diet used to determine the requirement for the next amino acid tested. Diets were kept isonitrogenous and isoenergetic by altering the quantity of the dispensable amino acid mixture and sugar mixture, respectively.

A dietary lysine content of 7 g/kg (8.75 g/kg L-lysine-HCl) produced maximal growth and nitrogen retention in 3- to 6-week-old male guinea pigs (Typpo et al., 1985). When corrected for efficiency of use, 8.4 g/kg diet will meet the requirement. Incorporation of up to 20 g lysine/kg in the presence of 18.5 g arginine/kg in the basal diet produced no adverse effects. O'Dell and Regan (1963) found that as little as 5 g arginine/kg added to a diet containing 20 g lysine/kg prevented growth retardation resulting from lysine-arginine antagonism.

Although 12 g phenylalanine/kg was required for maximal growth and nitrogen retention when tyrosine was excluded from the diet (Cho, 1971), in the presence of tyrosine the total minimum requirement for these two amino acids was 9 g/kg (Chueh, 1973). Requirements for L-phenylalanine and L-tyrosine were determined to be 4.5 and 4.5 g/kg diet, respectively, with tyrosine replacing up to 50 percent of the total requirement (Chueh, 1973). When corrected for efficiency of use, these values become 5.4 and 5.4 g/kg diet. Raising the phenylalanine content of the diet to 6 g/kg permitted reduction of the tyrosine content to 3 g/kg, or 33 percent of the total phenylalanine plus tyrosine requirement.

Minimum amounts for maximal growth and nitrogen retention of young guinea pigs have been determined for several other amino acids: threonine, 5 g/kg (Horstkoetter, 1974); histidine, 3 g/kg (Anderson and Typpo, 1977); isoleucine, 5 g/kg (Ayers et al., 1987); leucine, 9 g/kg (Mueller, 1978); and valine, 7 g/kg (Typpo et al., 1990b). These values have been corrected for efficiency of use in Table 4-1. Although antagonisms among the branched-chain amino acids have not been investigated, dietary leucine at 14 g/kg produced some growth inhibition when dietary isoleucine and valine concentrations were 6 and 7 g/kg, respectively.

A dietary arginine concentration of 8 g/kg resulted in maximum growth and nitrogen retention, while 9 g/kg was required for minimum orotic acid excretion in urine, and a requirement of 10 g arginine/kg diet was required to maintain plasma arginine (Yoon, 1977). When corrected for efficiency of use, 12 g arginine/kg diet will meet the requirement.

In these individual amino acid studies, the requirement was determined to be the lowest concentration of the test amino acid that supported a performance (weight gain and nitrogen retention) not significantly different from that resulting from the higher concentrations. Using this criterion results in requirement values that lie somewhere between the linear, slope-ratio, or broken-line models (Hegsted and Chang, 1965a,b; Robbins et al., 1979) and the nonlinear models (Finke et al., 1987; Gahl et al., 1991) for selecting requirements (see Chapter 2, Proteins and Amino Acids). In test diets the amino acid under study was first limiting at the lowest concentrations fed, but as the dietary concentration was raised and approached the requirement, while concentrations of the other indispensable amino acids remained constant, other indispensable amino acids could become limiting. This method of estimating the "requirements" of amino acids does not provide an accurate representation of the "diminishing return" area of the response curve and promotes an inaccurate estimate of the requirement (Gahl et al., 1991). Choosing this procedure could conceivably result in underestimating the requirement. When the determined requirement concentrations of the 10 indispensable amino acids were combined in the diet containing 36 g total nitrogen/kg, weight gain was »5.0 g/day (Condon, 1980; Blevins, 1983). Increasing the quantity of the 10 indispensable amino acids by 20 percent raised weight gain to near 7 g/day, suggesting that the requirement concentrations were all equally limiting and, in combination, were used with lower efficiency. Therefore, the values presented in Table 4-1 reflect an adjustment of 20 percent for each indispensable amino acid.

Maximum growth and nitrogen retention in the young growing guinea pig were obtained when the crystalline amino acid diet contained 36 g total nitrogen/kg, 11.7 g indispensable amino acid nitrogen/kg, an indispensable-to-total nitrogen ratio of 0.325, and 3.4 Mcal ME/kg (14.2 MJ ME/kg). However, the total nitrogen requirement may be lowered from 36 to 28.6 g/kg by reducing the dispensable amino acid component of the chemically defined diet without reducing growth (Typpo et al., 1990a,b).


Although amino acid requirements for the pregnant/lactating and nonpregnant/nonlactating adult guinea pig have not been specifically determined, natural-ingredient diets that provide 18 to 20 percent protein result in satisfactory reproduction (Lister and McCance, 1965; Shelton, 1971) and maintenance of adults (Shelton, 1971). Apgar and Everett (1991b) obtained adequate and similar weight gains and reproductive performance in pregnant guinea pigs fed either a casein-agar diet containing 300 g casein/kg without added arginine or a commercial plant protein diet containing 185 g protein/kg diet, but fewer neonates from dams fed the casein-agar diet survived. These investigators suggested that the cecal flora as a possible source of essential or unrecognized nutrients may be more critical during pregnancy than during growth. In addition, it has been suggested that the elimination of waste products by the pregnant guinea pig is less difficult when an adequate but not excessive amount of protein is provided. Pregnant guinea pigs often have a fetal mass approaching the nonpregnant weight of the female, possibly making elimination of waste products difficult.


The adult nonpregnant, nonlactating guinea pig's requirement for protein and amino acids may be lower than the amount required for growth. The requirement may be similar to that reported for 770 g males (Schiller, 1977). Nitrogen balance and body weight were maintained when a crystalline amino acid diet containing 11 g indispensable amino acid nitrogen/kg and 25.6 or 18.2 g total nitrogen/kg diet (equivalent to 160 or 114 g crude protein/kg diet) was fed but not when the diet contained 11 g total nitrogen/kg (equivalent to 69 g crude protein/kg).

Signs of Protein and Amino Acid Deficiency Protein deficiency produced in growing guinea pigs fed a diet containing 30 g casein/kg diet for 3 to 4 weeks causes growth retardation, marked reduction in plasma total protein and albumin, profound alterations in the plasma amino acid profile, and mild fatty liver. These animals develop clinical symptoms similar to the Kwashiorkor syndrome, including reduced activity, mild hair loss, and extensive edema of the face and forelimbs (Enwonwu, 1973). A protein deficiency produced in growing guinea pigs consuming 20 g casein/kg diet was accompanied by marked inhibition of local and systemic immune responses to vaccination with bacillus Calmette-Guerin (Bhuyan and Ramalingaswami, 1973). Enwonwu (1973) suggests that guinea pigs are suitable models for the study of human protein-calorie malnutrition.

Reports of protein deficiency produced by lowering the protein content of diets fed to adult guinea pigs during reproduction or maintenance were not found. Reducing the intakes of both protein and energy by restricting the intake of adequate protein diets (300 g casein or 185 g plant protein/kg) to 20 to 50 percent during the last half of gestation resulted in premature delivery, reduced weight for pups, and death of most pups within the immediate postnatal period (Apgar and Everett, 1991b). Reduced litter size was reported when feed was restricted to 40 percent of normal ad libitum intake beginning at day 30 of gestation (Young and Widdowson, 1975).



Calcium and Phosphorous

The calcium, phosphorus, potassium, and magnesium requirements of the guinea pig, like those of the rat, appear to reflect interactions among these elements. Morris and O'Dell (1961, 1963) and O'Dell et al. (1956, 1960) found that adequate dietary concentrations of calcium (8 to 10 g Ca/kg), phosphorus (4 to 7 g P/kg), magnesium (1 to 3 g Mg/kg), and potassium (5 to 14g K/kg) varied as the concentrations of the other three elements varied. Van Hellemond et al. (1988) observed that guinea pigs fed purified diets containing 8.4 g Ca/kg with 7.7 g P/kg and 1.0 g Mg/kg retained more calcium than those fed the same concentrations of calcium but with less phosphorus (4.4 g P/kg) and more magnesium (1.9 g Mg/kg). Thus 8 g Ca/kg and 4 g P/kg diet will meet requirements for these minerals.

There is no obvious physiological explanation for the higher apparent requirement of guinea pigs than rats for calcium and phosphorus. Further work is needed to assess growth and bone and kidney accumulation of calcium when guinea pigs are fed concentrations of calcium and phosphorus more consistent with those recommended for rats.

Signs of Calcium and Phosphorus Deficiency Signs of calcium deficiency have been produced in young guinea pigs fed a purified diet containing 0.28 g Ca/kg, 0.20 g P/kg, and a low concentration of vitamin D (Howe et al., 1940). Nine of 21 animals fed this diet survived for 60 days. These guinea pigs lost weight and developed rachitic lesions in ribs and long bones. Generally the younger animals devel oped more bone abnormalities than the older animals. The teeth of all animals developed extreme enamel hypoplasia. As there were no control animals in this study, interpretation of these data is difficult.

Prevention of soft tissue calcification caused by imbalances among dietary calcium, phosphorus, potassium, and magnesium is of more concern in the formulation of practical diets for guinea pigs than the prevention of overt deficiencies. Hogan and Regan (1946) implicated excess phosphorus as a cause of soft tissue calcification in guinea pigs. These findings were confirmed when 90 percent of the guinea pigs fed a diet containing 8 g Ca/kg and 9 g P/kg developed soft tissue mineral deposits, whereas the incidence was less than 10 percent when the diet contained only 5 g P/kg (Hogan et al., 1950). In subsequent experiments, supplemental magnesium and potassium prevented the effects of excess dietary phosphorus, including soft tissue calcification, in guinea pigs (House and Hogan, 1955). These observations seem to be consistent with those for rats (see Chapter 2, Nephrocalcinosis in Rats Fed Purified Diets.)

Chloride, Sodium, and Sulfur

No published data could be found on the requirements of chloride, sodium, or sulfur for the guinea pig. The concentrations of chloride and sodium in purified diets used for rats should be used as a first approximation of the dietary concentrations of these nutrients.


The magnesium requirement of guinea pigs depends on the dietary concentrations of calcium, phosphorus, and potassium. Morris and O'Dell (1963) concluded that an excess of calcium or phosphorus independently increased the minimum magnesium requirement and that the effects were additive. As dietary phosphorus increased from 8 g to 17 g/kg diet, the minimum requirement for magnesium increased from 1 g to 4 g/kg diet. Similarly, as dietary calcium increased from 9 g to 25 g/kg diet, the requirement for magnesium increased.

Interactions of magnesium with potassium and fluoride are also important. Magnesium-deficient guinea pigs not only have reduced muscle extracellular and intracellular magnesium concentration (20 percent and 80 percent of control values, respectively) but also have reduced muscle potassium and increased intracellular sodium and water concentrations (Grace and O'Dell, 1970a). Supplementing the diets of magnesium-deficient guinea pigs with potassium stimulated growth, lowered blood phosphorus concentrations, decreased calcium concentrations in muscle, extended survival times, and decreased mortality. Guinea pigs appeared to use cations rather than ammonia to neutralize and excrete acid in the urine (O'Dell et al., 1956).

Adding 0.1 to 0.4 g fluorine/kg diet to a magnesium-deficient diet (0.4 g/kg diet) significantly improved growth, increased serum magnesium concentrations, reduced incidence of soft tissue calcification, and reduced calcium concentrations in kidney, heart, and liver (Pyke et al., 1967). When magnesium was severely limiting (0.1 g/kg diet), 0.2 g fluorine/kg diet was toxic and caused lameness and swollen feet; but adequate magnesium largely overcame the deleterious effects of excess fluorine in weanling guinea pigs (O'Dell et al., 1973).

On the basis of no new research, the magnesium requirement is 1 to 3 g/kg diet, 1 g/kg diet being the minimum requirement. However, if additional work were to demonstrate that current estimates of the requirements for calcium and phosphorus are high, the magnesium requirements would also need to be reevaluated.

Signs of Magnesium Deficiency Clinical signs of magnesium deficiency in young guinea pigs include poor growth, hair loss, decreased activity, poor muscular coordination and stiffness of hind limbs, elevated serum phosphorus, and anemia (Maynard et al., 1958; O'Dell et al., 1960; Morris and O'Dell, 1963). Convulsions, which characterize magnesium deficiency in some species, are uncommon in guinea pigs (O'Dell et al., 1960; Grace and O'Dell, 1970a), but one study reported tetany (Thompson et al., 1964). Gross tissue changes at necropsy were enlarged pale kidneys, white foci and streaks in liver, soft tissue calcification, and incisors that were darkened, eroded, and soft (Maynard et al., 1958; O'Dell et al., 1960; Morris and O'Dell, 1961). In addition, Grace and O'Dell (1970b) concluded that magnesium deficiency probably affected appetite and/or membrane transport of nutrients.


The potassium requirements of guinea pigs depend on the dietary concentrations of calcium and phosphorus. Mortality was 100 percent within 4 weeks when young guinea pigs were fed a purified diet (30 percent casein) that supplied excess cations but only 1 g K/kg diet. The requirement for maximal growth under these circumstances was 4 to 5 g K/kg diet supplied as potassium acetate (Grace and O'Dell, 1968). Additional dietary potassium, up to 14 g K/kg diet, has been found to be required when diets combined very high concentrations of calcium, phosphorus, and magnesium (O'Dell et al., 1956; Morris and O'Dell, 1963). With moderate dietary concentrations of calcium, phosphorus, and magnesium, the requirement for potassium is 5 g/kg diet and should be considered generous.

Signs of Potassium Deficiency Luderitz et al. (1971) found that membrane potentials in striated muscle cells from young guinea pigs fed a potassium-deficient diet were higher than in control animals. These effects were accompanied by a significant, and apparently quantitative, increase in Na+, K+-ATPase activity in heart muscle cells (Erdmann et al., 1971).

Trace Minerals

Copper and Iron

Diets containing 6 mg Cu/kg diet have been reported to be adequate for normal growth and development of the guinea pig (Everson et al., 1967, 1968). If guinea pigs are fed diets containing less than 1 mg Cu/kg during pregnancy and early postnatal development, the offspring are characterized by growth retardation, cardiovascular defects, and severe abnormalities of the central nervous system including agenesis of cerebellar folia, cerebral edema, and delayed myelination (Everson et al., 1968). The dietary requirement for copper is increased if there are high concentrations of molybdenum (Suttle, 1974). Offspring of dams given 0.18 percent CuSO4 in their drinking water from day 21 of gestation on were characterized by high liver copper concentrations and subtle evidence of liver pathology (Chesta et al., 1989).

Dietary iron requirements of the guinea pig have not been directly addressed. Based on an evaluation of previous and current diets used for guinea pigs, it is estimated that a diet containing 50 mg Fe/kg will satisfy the iron requirements for reproduction, growth, and development. Dietary iron at high concentrations (200 to 300 mg/kg) can result in significant tissue iron concentration, although overt tissue pathology has not been reported (Smith and Bidlack, 1980; Caulfield and Rivers, 1990).


A dietary concentration of 40 mg Mn/kg diet has been shown to be adequate for normal growth and development of the guinea pig (Everson et al., 1959). Similar to the mouse and rat (Hurley and Keen, 1987), diets containing 3 mg Mn/kg or less are inadequate for the guinea pig during growth and development. Although the manganese dietary requirement for the guinea pig is probably less than 40 mg/kg, in the absence of studies evaluating dietary manganese concentrations between 3 and 40 mg/kg diet, the recommended concentration is 40 mg/kg diet for all stages of life.

Signs of Manganese Deficiency In a series of studies by Everson (Tsai and Everson, 1967; Everson, 1968; Everson and Shrader, 1968; Everson et al., 1968; Shrader and Everson, 1968) it was established that signs of prenatal and early postnatal manganese deficiency include reduced litter size, abortions or stillbirths, congenital ataxia, skeletal abnormalities, and pancreatic pathology that resulted in a diabetes-like syndrome. The pancreatic pathology and diabetic syndrome can be reversed with manganese supplementation; the ataxia, however, is irreversible (Everson and Shrader, 1968; Shrader and Everson, 1968).


Alberts et al. (1977) reported that casein-based diets containing 12 mg Zn/kg and soybean protein-based diets containing 20 mg Zn/kg were adequate to support optimal growth rate without evidence of deficiency signs in the young guinea pig. These values are consistent with the report by Navia and Lopez (1973) that purified gel diets containing 19 mg Zn/kg diet support normal growth and development. The requirement for zinc is 20 mg/kg diet for all stages of life.

Signs of Zinc Deficiency Guinea pigs fed diets containing less than 1.25 mg Zn/kg are characterized by low plasma zinc concentration, depressed ability to elicit a delayed-type hypersensitivity, low gamma-globulin concentrations, altered glycosaminoglycan metabolism, abnormal posture, skin lesions, anorexia, and excessive vocalization (McBean et al., 1972; Hsieh and Navia, 1980; Quarterman and Humphries, 1983; Gupta et al., 1988; Verma et al., 1988; O'Dell et al., 1989). If a zinc-deficient diet (≤2 mg Zn/kg) is given during pregnancy, it can result in premature delivery or abortion (Apgar and Everett, 1991b).

Iodine, Molybdenum, and Selenium

Diets unsupplemented with iodine, selenium, or molybdenum have been shown conclusively to have negative effects on the physiological or biochemical status of mammals. No systematic effort has been made to establish the requirements of iodine, molybdenum, and selenium for the guinea pig. Most of the research to establish requirements has been done with the laboratory rat. (For an indepth discussion, see Chapter 2.)

The dietary requirement for selenium of the rat and mouse has been determined by using the maximization of liver glutathione peroxidase activity (GSH-Px). This procedure may prove difficult in the guinea pig because the activity of this enzyme in the liver of the guinea pig is less than 10 percent of that in other species such as hamsters, rats, and mice. Apparently this phenomenon is not related to the amount of dietary selenium. Even if guinea pigs are fed commercial natural-ingredient diets containing more selenium (140 to 200 µg/kg) than the amount required by rats, GSH-Px activities in various tissues are very low.

Lawrence and Burk (1978) found no GSH-Px activity in livers of guinea pigs fed natural-ingredient diets, while Toyoda et al. (1989) found that liver, kidney, and heart had only 4 to 6 percent of the activity normally observed in similar tissues of mice or rats. In spite of low liver GSH-Px activity, excellent reproductive performance has been observed for many years in experimental and commercial guinea pig colonies fed commercially available natural-ingredient diets containing 140 to 330 µg Se/kg (Boyd O'Dell, University of Missouri, Columbia, MO, and Dennis Renner, Sasco Inc., Lincoln, NE, 1993, personal communications). These diets are reported to contain 400 to 1,000 µg I/kg but no added molybdenum. Although liver GSH-Px activity is lower in tissues of guinea pigs than in those of other species, liver selenium concentrations are comparable (Toyoda et al., 1989).

Although no work has been done to directly establish the iodine, molybdenum, or selenium requirements for the guinea pig, some evidence indicates that these requirements might be similar to those of rats and mice. Therefore, until more research is conducted, concentrations established for the rat can be used as a first estimate for requirement in the guinea pig. By no means, however, should this be construed to indicate that guinea pigs metabolize these elements exactly as do rats. The requirement for iodine at all stages of life is 150 µg/kg diet and that for molybdenum is 150 µg/kg diet. The requirement for selenium, as selenite, for all stages of life is 150 µg/kg diet with the exception of pregnancy and lactation, for which a dietary concentration of 400 µg Se/kg diet is suggested.


Fat-Soluble Vitamins

Vitamin A

Guinea pigs apparently have a high vitamin A requirement. Bentley and Morgan (1945) reported that 21 µmol vitamin A/kg diet maintained growth and a very modest store of vitamin A in the liver. Gil et al. (1968) found that 11.5 µmol/kg diet would maintain growth, but that normal tissue histology, and storage of vitamin A in the liver were only found with diets containing 23 µmol/kg diet or more. Intermediate concentrations were not tested. Although they did not measure liver vitamin A reserves, Howell et al. (1967) found that a dose of vitamin A equivalent to 18 µmol/kg diet was adequate to maintain vision, reproduction, and growth for 460 days. Reid and Briggs (1953) found that 18 µmol/kg diet was satisfactory for optimal growth in guinea pigs fed a purified diet.

β-Carotene is used by the guinea pig as a source of vitamin A (Chevallier and Choron, 1935, 1936; Woytkiw and Esselbaugh, 1951); however, the molar efficiency of utilization may be only 40 percent that of preformed vitamin A (Bentley and Morgan, 1945) when consumed at amounts near the requirement. The reason for this low efficiency of utilization has not been identified. In rats, an intake at this concentration would have a similar efficiency. The lower efficiency of β-carotene utilization at higher intakes is mainly caused by poor absorption from the intestine. β-Carotene is a pure hydrocarbon that is very difficult to solubilize at the higher concentrations.

Diets that contain 21,960 IU retinol/kg diet (23 µmol or 6.6 mg/kg diet) appear to maintain optimal health and a slightly positive vitamin A balance in guinea pigs. If β-carotene is used as the source of vitamin A activity, then 47,425 IU β-carotene/kg diet (53 µmol or 28 mg/kg) would be needed to maintain a slightly positive vitamin A balance.

Signs of Vitamin A Deficiency Time before onset of deficiency signs varies widely with age, liver vitamin A concentrations, and stress conditions. Young guinea pigs may develop deficiency signs in 2 weeks, whereas older pigs may require nearly 10 weeks when fed a diet devoid of vitamin A or provitamin A. The first evidence of vitamin A deficiency is poor growth, then weight loss, followed by incrustations of eyelids and severe dermatitis resulting from bacterial infection (Bentley and Morgan, 1945). Gross pathology studies often reveal accumulation of organic debris in the bile ducts and gallbladder, clouding of the cornea, and xerophthalmia. Often animals develop pneumonia prior to death. Histologically, epithelia of various organs showed squamous metaplasia and some keratinization (Howell et al., 1967).

The primary effect of a vitamin A deficiency on the incisors of guinea pigs is mainly on odontogenic epithelium with incomplete differentiation of cells, loss of organization, and formation of defective dentin by atrophic odontoblast (Wolbach, 1954). The incisors had a distinctive appearance characterized by thickened dentin on the labial side and thin dentin on the lingual and lateral sides.

Signs of Vitamin A Toxicity Excessive amounts of vitamin A given to guinea pigs caused degenerative changes in the cartilaginous epiphyseal plates of long bones (Wolbach, 1947), and there was increased bone resorption interfering with normal remodeling. Gil et al. (1968) reported "loss of weight" in guinea pigs fed diets containing 121 mg/kg diet (230 µmol/kg) or more of retinyl palmitate. Teratogenic effects were noted by Robens (1970) when a single oral dose (210 µmol/kg BW) given to pregnant guinea pigs during fetal organogenesis (days 14 to 20) caused soft tissue and skeletal anomalies in the offspring. The most frequent defects recorded were agnathia, synotia, malpositioning of teeth, and microstomia. Administration of the same dose between days 17 and 20 frequently produced changes in the tibias and fibulas, but fetal growth was not affected.

Vitamin D

A quantitative requirement for vitamin D has not been established for guinea pigs, but currently used natural-ingredient and purified diets contain between 20 and 180 nmol/kg diet (Reid and Briggs, 1953; Navia and Lopez, 1973; O'Dell et al., 1989). These amounts seem to promote growth at rates that were average for the colony. The requirement for growth is set at 1,000 IU vitamin D/kg diet (65 nmol/kg diet; 0.025 mg/kg diet).

Signs of Vitamin D Deficiency Guinea pigs fed diets with a normal calcium-to-phosphorus ratio do not develop gross signs of vitamin D deficiency (Kodicek and Murray, 1943). However, Sergeev et al. (1990) observed many changes in vitamin D status of guinea pigs fed a vitamin D-deficient diet containing 6 g calcium/kg diet and 6 g phosphorus/kg diet. Serum calcium and phosphorus concentrations were reduced, serum alkaline phosphatase was increased, serum 25-hydroxycholecalciferol concentrations were extremely low, kidney 1-α-hydroxylase activity was more than twice the normal concentrations, active transport of calcium in the duodenum was decreased, and bone calcium content was about four-fifths the control concentrations. Administering 5.2 nmol (15 IU) of cholecalciferol per animal every other day prevented the development of these signs. This is about twice the amount available from typical diets. Lower amounts were not used. A deficiency of ascorbic acid also altered the animal's ability to metabolize vitamin D. Howe et al. (1940) housed guinea pigs in a darkened room and fed them a low-vitamin D purified diet with 0.28 g Ca/kg and 2 g P/kg. In addition to retarded growth, typical lesions occurred in the zone of cartilage proliferation at the epiphyseal plate of long bones and ribs. Also, incisors exhibited a high degree of enamel hypoplasia, and enamel and dentin were disorganized and irregular with poor calcification.

Signs of Vitamin D Toxicity Guinea pigs show a response to excessive vitamin D intake. An extract of the poisonous plant Solanum malacoxylon caused hypercalcemia and calcification of kidney, aorta, muscles, spleen, heart, and liver (Camberos et al., 1970). This plant has been shown to contain derivatives of the active metabolites of vitamin D, which are responsible for the toxicity (Boland et al., 1987).

Vitamin E

No precise quantitative requirement for vitamin E can be given, in spite of studies with guinea pigs involving vitamin E and related nutrients. The earliest estimate of a minimum requirement for the growing guinea pig, eating a vitamin E-deficient diet containing 20 g cod liver oil/kg, is equivalent to 2.6 µmol RRR-α-tocopherol/day (Shimotori et al., 1940). Assuming a feed intake of 20 g/day, this is equivalent to 128 µmol/kg diet (82 IU or 55 mg RRR-α-tocopherol/kg diet. (See Chapter 2 for a discussion of the forms and potency of vitamin E.) Farmer et al. (1950) reported that 5.1 µmol/day was required for normal reproduction in the female guinea pig receiving cod liver oil. Assuming a feed intake of 30 g/day, this is equivalent to 170 µmol/kg diet (74 mg/kg). Several popular diets have been developed for the guinea pig that do not contain cod liver oil. Reid and Briggs (1953) originally developed their diet to contain a vitamin E activity equivalent to 34 µmol RRR-α-tocopherol/kg diet, but later Reid (1963) modified the diet to contain 82 µmol/kg diet. The diet described by Hsieh and Navia (1980) contained a vitamin E activity equivalent to 62 µmol RRR-α-tocopherol per kg diet. Based on the above, a diet containing 40 IU/kg diet (62 µmol or 26.7 mg/kg diet) should meet the needs of growing guinea pigs. There have been no reports of vitamin E deficiency with these diets.

Signs of Vitamin E Deficiency Diet-induced muscular dystrophy was produced in the guinea pig when 5 to 20 g cod-liver oil/kg was included in the diet. The research of Shimotori et al. (1940) related vitamin E deficiency to muscular dystrophy. An average oral dose of 1.5 mg of synthetic α-tocopherol per day provided protection against sign of muscular dystrophy during a 200-day period. Pappenheimer and Goettsch (1941) confirmed the role of vitamin E for maintenance of normal muscle and extended the observations to show the need for vitamin E during pregnancy. Schottelius et al. (1959) reported that vitamin E deficiency in guinea pigs precipitated a decrease in muscle myoglobin concentration. Reduced myoglobin concentration was observed before the appearance of severe tissue lesions or increased creatine excretion. Supplementation with vitamin E reduced the magnitude of the myoglobin change. Elmadfa and Feldheim (1971) have shown that creatine phosphokinase activity in skeletal muscle of young male guinea pigs was reduced significantly by feeding them a vitamin E-deficient diet for 2 weeks. The serum creatine phosphokinase activity increased during the same period. At about 4 weeks, creatine excretion in the urine increased, and by 6 weeks erythrocyte hemolysis increased, reaching a maximum at 8 weeks. Soon thereafter, the guinea pigs became prostrate with severe body weight loss and degeneration of skeletal muscle. In males, testes atrophied and developed degenerative changes in the seminiferous tubules, with clumping or complete disappearance of spermatozoa and spermatids. Fetal malformations, resorption, and death occurred in pregnant females.

Vitamin K

The information to develop a specific recommendation for the vitamin K requirement of guinea pigs does not exist. The menadione content of some of the more frequently used diets ranges from 12 to 58 µmol/kg diet (Reid and Briggs, 1953; Navia and Lopez, 1973; O'Dell et al., 1989). These diets appear to be adequate to prevent hemorrhages, but no information is available about more sensitive indicators of vitamin K status. Based on limited information, a concentration of 5 mg phylloquinone/kg diet (11 µmol phylloquinone/kg diet) is suggested.

Signs of Vitamin K Deficiency The drug Warfarin prevents the normal recycling of vitamin K and thereby rapidly causes a nonfunctional form of vitamin K to accumulate in the tissues. In guinea pigs treated with Warfarin, prothrombin concentrations dropped to 14 percent of control concentrations within 24 hours (Carlisle et al., 1975); and a greatly reduced amount of γ-carboxyglutamic acid in plasma proteins was noted (Stenflo and Fernlund, 1984). Thus, Warfarin and vitamin K appear to interact in guinea pigs much the same as they do in rats.

Water-Soluble Vitamins

Ascorbic Acid

The ascorbic acid requirement of the guinea pig has been reviewed by Mannering (1949). Navia and Hunt (1976) summarized the major metabolic roles for ascorbic acid in this animal. The daily requirement of ascorbic acid varied from 0.4 to 25 mg/day according to the criterion used to evaluate adequacy. Values reported to support growth were 0.4 to 2 mg/day in 250 to 350 g guinea pigs; reproduction was supported by 2 to 5 mg/day (Mannering, 1949). Scurvy was prevented by 1.3 to 2.5 mg/day; odontoblast growth, wound healing, and bone regeneration were supported by 2 mg/day; and tissue saturation occurred at 25 to 30 mg/day. Approximately 7 mg of ascorbic acid/kg BW was adequate to maintain adrenal size and odontoblast height in male guinea pigs ranging from 110 to 840 g BW (Pfander and Mitchell, 1952). Collins and Elvehjem (1958) found 5 mg/kg BW sufficient for growth of immature guinea pigs.

The liver, kidney, plasma, lens, and aqueous humor concentration of ascorbic acid reflected the amount of ascorbic acid fed (0.8 to 60 mg/animal/day) to both young and old guinea pigs. The half-life of tissue ascorbate was reported to be the same in guinea pigs provided a maintenance dose (0.5 mg/day) or a higher dose (30 mg/100 g BW/day) (Ginter et al., 1982). A concentration of 50 mg/kg diet was marginal for survival. At 200 mg/kg diet, hepatic ascorbic acid accumulated in the liver. Adrenal and splenic concentrations increased with concentrations of 900 mg/kg diet (Degkwitz and Boedeker, 1989). Higher tissue concentrations were achieved by mixing the vitamin in the diet (500 mg/kg) than by daily oral administration (Ginter et al., 1979). An intake of 5 mg/day provides adequate amounts of ascorbic acid for growth and reproduction; normal intake of 200 mg/kg diet (1,135 µmol/kg diet) will fulfill this need.

Ascorbic acid absorption was reported to be sodium dependent and involve a transporter molecule (Siliparandi et al., 1979). Dehydroascorbic acid was readily absorbed and reduced by dehydroascorbic acid reductase to ascorbic acid in the intestinal mucosa. Transport of endogenous ascorbate across the basolateral membrane assures the mucosal cell access to the vitamin in the absence of a dietary supply (Rose et al., 1988).

The stability of ascorbic acid in diets varies with the composition of the diet, storage temperature, and humidity. Approximately one-half of the initial ascorbic acid may be oxidized and lost 90 days after the diet has been mixed. Aqueous solutions may lose vitamin C potency rapidly.

Ascorbic acid at 0.5 mg/kg BW prevented rapid fatal scurvy and 55 percent of guinea pigs survived, but after 16 weeks these animals exhibited a marked increase in serum cholesterol, LDL-cholesterol, VLDL-cholesterol, triglycerides, and total lipids. The LDL:HDL ratio rose from 1.13 to 19.02 with cholesterol added at 3 g/kg diet (Kothari and Sharma, 1988) and stimulated the oxidation of ascorbic acid to carbon dioxide (Ginter and Zloch, 1972). Magnesium L-ascorbic acid phosphate has been shown to cure scurvy in the guinea pig (Machlin et al., 1979), but L-ascorbic acid 2-sulfate did not have antiscorbutic activity (Tsujimura, 1978).

Signs of Ascorbic Acid Deficiency Early signs of vitamin C deficiency in guinea pigs were reduced diet intake and weight loss, followed by anemia and widespread hemorrhages. An impaired clotting mechanism, as indicated by increased prothrombin time, also contributes to hemorrhaging with vitamin C deficiency. Resting body temperatures were higher in scorbutic guinea pigs than normal animals (Green et al., 1980). Deficiency resulted in muscle damage but not neuropathy (Sillevis Smitt et al., 1991). Ascorbic acid-deficient animals were dead within 3 to 4 weeks from the causes noted above or from secondary bacterial infections, to which guinea pigs are susceptible. Ascorbate deficiency has been linked to an impairment in carnitine synthesis, increased urinary carnitine excretion, and prolonged survival time with carnitine supplementation (Jones and Hughes, 1982; Alkonyi et al., 1990).

Vitamin C deficiency resulted in decreased vitamin B12 absorption; increased absorption of alanine and leucine; enhanced activity of brush border sucrase, alkaline phosphatase, and leucine aminopeptidase; and higher concentrations of intestinal membrane sialic acid and total lipids (Dulloo et al., 1982). Deficiency also reduced oxalate absorption (Farooqui et al., 1983). Growth and maintenance of connective tissue in skin, fetal tissues, and repairing wounds required a supply of dietary ascorbic acid (Barnes et al., 1969a,b, 1970; Rivers et al., 1970). The characteristic hemorrhages in subcutaneous tissues, joints, skeletal muscle, and intestine of scorbutic guinea pigs result in defects in connective tissue. Ascorbic acid is essential in hydroxylase reactions for the formation of hydroxyproline and hydroxylysine in the collagen molecule (Stone and Meister, 1962; Udenfriend, 1966). General weight loss in scorbutic guinea pigs resulted in decreased proteoglycan and collagen synthesis (Chojkier et al., 1983; Spanheimer and Peterkofsky, 1985; Bird et al., 1986a,b). Impaired synthesis of collagen had many effects on the guinea pig, including enlarged costochondral junctions, disturbed epiphyseal growth centers of long bones, bone loss, altered dentin, and gingivitis. Deficiency in ascorbic acid reduced cytochrome P-450 more than 50 percent (Rikans et al., 1977). Urinary excretion of fluoride was greater in guinea pigs on low ascorbic acid and protein diets (Parker et al., 1979).

Vitamin C deficiency has been reported to result in elevated serum copper and ceruloplasmin and liver copper concentrations (Milne and Omaye, 1980). Ascorbate deficiency has been reported to reduce thymus size, lower the delayed type hypersensitivity response, and active and total rosette-forming cells against sheep red blood cells (Majumder and Rahim, 1987). During the progression of a deficiency, the percentage of B lymphocytes increased and T lymphocytes decreased (Fraser et al., 1980). Leukocyte chemotaxis was impaired in guinea pigs fed 0.5 mg/kg BW compared to 20 mg/kg BW (Johnston and Huang, 1991). Antibody response to an injected antigen occurred more rapidly and was more pronounced in deficiency (Prinz et al., 1980). Splenic cell cyclic GMP and erythrocyte ATPase were depressed by a deficiency of vitamin C (Barkagan and Gelashvili, 1970; Haddox et al., 1979).


No quantitative requirement for biotin has been demonstrated for normal healthy guinea pigs. Reid (1954b) observed no significant change in growth of young guinea pigs fed a purified diet with biotin omitted. Feeding guinea pigs a biotin-deficient diet containing raw egg white produced weight loss, alopecia, and depigmentation of the hair (Coots et al., 1959). Based on limited information a concentration of 0.2 mg biotin/kg diet (0.82 µmol/kg diet) is suggested as the requirement for all stages of the life cycle.


The inclusion of 7.2 mmol choline as 1.8 g choline bitartrate/kg diet supported acceptable growth of young guinea pigs fed a diet containing 30 percent casein (Reid, 1955). Although methionine does seem to have some sparing effect on the choline requirement, methionine could not be used to replace choline.

Signs of Choline Deficiency Choline deficiency has been characterized in young guinea pigs (Reid, 1954b, 1955). When 2- to 4-week-old guinea pigs were fed a 30 percent casein diet lacking added choline, but adequate in folic acid and vitamin B12 (23 and 0.03 µmol/kg diet, respectively), poor growth, anemia, and muscle weakness were observed. Some adrenal and subcutaneous hemorrhages occurred, but no renal hemorrhage or marked fatty infiltration of liver were reported.


The young guinea pig appears to have a high requirement for folic acid, on the order of 3 to 6 mg/kg diet (6.8 to 13.6 µmol/kg diet) (Mannering, 1949; Woodruff et al., 1953; Reid 1954a; Reid et al., 1956). Guinea pigs practice coprophagy and may obtain folic acid from bacterial synthesis in the gastrointestinal tract. As the animal matures, less folic acid is required.

Signs of Folate Deficiency Young guinea pigs fed a folic acid-deficient diet grew slowly initially and became weaker as diet intake declined. Anemia and leukopenia developed. Hemoglobin and hematocrit values decreased, and the bone marrow became aplastic. Fatty livers and adrenal hemorrhages were prominent at necropsy (Woodruff et al., 1953; Reid, 1954a; Reid et al., 1956).


Guinea pigs require a dietary intake of niacin (Reid, 1954b). However, because they can produce niacin from tryptophan, the niacin requirement is influenced by quantity and quality of dietary protein, especially tryptophan content and availability. According to Reid (1961), 10 mg niacin/kg diet (81 µmol/kg diet) was adequate in a purified diet containing 30 percent casein or 20 percent casein supplemented with 1 percent L-arginine and 0.25 percent DL-methionine.

Signs of Niacin Deficiency The most definitive reports on niacin deficiency in the guinea pig are those of Reid (1954b, 1961). When niacin was omitted from a purified diet containing 30 percent casein, deficiency signs were observed in 3 to 4 weeks. All niacin-deficient animals exhib ited poor growth; small appetite; pale feet, nose, and ears; drooling; anemia; and a tendency to diarrhea. The animals also had lowered hemoglobin and hematocrit. No oral or ocular lesions and no dermatitis were observed.

Pantothenic Acid

Reid and Briggs (1954) reported that 20 mg or 42 µmol calcium pantothenate/kg diet was adequate for optimal growth. They did not indicate whether calcium d-pantothenate or calcium dl-pantothenate was used. The adult requirement has not been established. It is projected to be similar to that of young animals, as nonpregnant or pregnant adults can be depleted rather rapidly (Hurley et al., 1965).

Signs of Panthothenic Acid Deficiency Young guinea pigs fed a purified, pantothenic acid-deficient diet developed signs of deficiency such as decreased growth rate, anorexia, weight loss, rough coat, diarrhea, weakness, and death (Reid and Briggs, 1954). Hair pigmentation was unaffected, and the adrenals were enlarged and sometimes hyperemic or hemorrhagic. Adult animals fed a pantothenic acid-deficient diet died within 10 to 41 days (Hurley et al., 1965). Many of them had adrenal and gastrointestinal hemorrhages.


Based on weight gain and general appearance of the growing guinea pig, the quantitative requirement of pyridoxine is 2 to 3 mg/kg diet (9.7 to 14.6 µmol/kg diet) (Reid, 1964).

Signs of Pyridoxine Deficiency When fed a purified diet containing 30 percent casein with no pyridoxine added, 15 of 27 animals lived for 8 weeks (Reid, 1964). These animals grew slowly, but showed no specific signs of deficiency. Some pyridoxine may have been present in the casein used in the diet.


The limited research by Slanetz (1943), Reid (1954b), and Hara (1960) is inadequate to establish a riboflavin requirement for the guinea pig. The best estimate is 3 mg riboflavin/kg diet (8 µmol riboflavin/kg diet) (Slanetz, 1943).

Signs of Riboflavin Deficiency By feeding young guinea pigs a purified diet deficient in riboflavin, Reid (1954b) found that they exhibited poor growth; rough hair; pale feet, nose and ears; and early death (2 weeks). Later, Hara (1960) described microscopic lesions, such as corneal vascularization, skin atrophy and chromatolysis, and myelin degeneration in the pons and spinal cord. Myocardial alterations included hemorrhage and edema accompanied by vacuolar degeneration and atrophy.


The thiamin requirement of the young guinea pig is 2 mg thiamin-HCl/kg diet (5.9 µmol/kg diet) (Liu et al., 1967; Reid and Bieri, 1967). No reports are available to support a definite quantitative requirement for gestation and lactation.

Signs of Thiamin Deficiency Young growing guinea pigs fed a thiamin-deficient diet exhibited reduced food intake and weight loss, followed by the development of central nervous system disorders. An unsteady gait and some retraction of the head also occurred as the condition progressed. Death occurred within 4 weeks (Liu et al., 1967; Reid, 1954b; Reid and Bieri, 1967).

Potentially Beneficial Dietary Constituents


It has long been recognized that fiber is an important ingredient in the diet of the guinea pig. Booth et al. (1949) observed low growth rates (1.9 g/day) for guinea pigs fed synthetic diets containing no fiber; additions of pectin, agar, oat straw, cellulose, and cellophane stimulated growth to some extent, but gum arabic was found to produce the best response (growth rates more than 5 g/day). Other researchers observed that cellulose was more effective in stimulating growth than either gum arabic or cellophane when added at 150 g/kg diet (Heinicke and Elvehjem, 1955). The cecum of the guinea pig contains short-chain fatty acids in concentrations comparable to those found in the rumen (Henning and Hird, 1970), and digestion of cellulose in this organ may contribute to meeting energy requirements. Hirsh (1973) showed that dilution of the diet 1:1 with cellulose did not alter food intake or body weight of guinea pigs, supporting the use of cellulose as an energy source (see ''Energy" section).

Trace Minerals

It has been suggested that many of the minor elements, which may be supplied in minute amounts, are essential for laboratory animals, including the guinea pig. These elements include cobalt, chromium, arsenic, boron, nickel, vanadium, silicon, tin, fluorine, lead, and cadmium. Cobalt is essential but only as a part of vitamin B12. For additional comments see the discussion on this subject in Chapter 2.



There is no evidence that the guinea pig requires a dietary source of inositol. Reid (1954b) did not observe significant growth retardation when inositol was omitted from a purified diet.

Vitamin B12

There is no evidence that the growing guinea pig requires a dietary source of vitamin B12 (Reid, 1954b). Guinea pigs may ingest a significant amount of this vitamin during coprophagy.


  • Ahrens, R. A., S. L. Garland, H. N. Kigutha, and E. Russek. 1985. The disaccharide effect of sucrose feeding on glucuronide excretion and bile concentration of injected phenolphthalein in guinea pigs. J. Nutr. 115:288–291. [PubMed: 3968593]
  • Alberts, J. C., J. A. Lang, P. A. Reyes, and G. M. Briggs. 1977. Zinc requirement of the young guinea pig. J. Nutr. 107:1517–1527. [PubMed: 560431]
  • Alkonyi, I., J. Cseko, and A. Sandor. 1990. Role of the liver in carnitine metabolism: The mechanism of development of carnitine-deficient status in guinea-pigs. J. Clin. Chem. Clin. Biochem. 28:319–321. [PubMed: 2380669]
  • Anderson, H. A., and J. T. Typpo. 1977. Histidine requirement of the growing guinea pig. Fed. Proc. 36:11-53 (abstr.).
  • Apgar, J., and G. A. Everett. 1991. a. The guinea pig as a model for effects of maternal nutrition on pregnancy outcome. Nutr. Res. 11:929–939.
  • Apgar, J., and G. A. Everett. 1991. b. Low zinc intake affects maintenance of pregnancy in guinea pigs. J. Nutr. 121:192–200. [PubMed: 1847415]
  • Argenzio, R. A., J. A. Liacos, and M. J. Allison. 1988. Intestinal oxalate-degrading bacteria reduce oxalate absorption and toxicity in guinea pigs. J. Nutr. 118:787–792. [PubMed: 3373343]
  • Ayers, L. S., J. T. Typpo, and G. F. Krause. 1987. Isoleucine requirement of young growing male guinea pigs. J. Nutr. 117:1098–1101. [PubMed: 3598719]
  • Barkagan, T. S., and S. S. Gelashvili. 1970. Guinea pig erythrocyte ATPase activity and nutritional vitamin C factor. Uch. Zap. Gor's Gos. Univ. 111:75–78.
  • Barnes, M. J., B. J. Constable, and E. Kodicek. 1969. a. Excretion of hydroxyproline and other amino acids in scorbutic guinea pigs. Biochim. Biophys. Acta 184:358–365. [PubMed: 5809720]
  • Barnes, M. J., B. J. Constable, and E. Kodicek. 1969. b. Studies in vivo on the biosynthesis of collagen and elastin in ascorbic acid-deficient guinea pigs. Biochem. J. 113:387–397. [PMC free article: PMC1184646] [PubMed: 4309121]
  • Barnes, J. J., B. J. Constable, L. F. Morton, and E. Kocicek. 1970. Studies in vivo on the biosynthesis of collagen and elastin in ascorbic acid-deficient guinea pigs: Evidence for the formation and degradation of a partially hydroxylated collagen. Biochem. J. 119:575–585. [PMC free article: PMC1179389] [PubMed: 5500318]
  • Bentley, L. S., and A. F. Morgan. 1945. Vitamin A and carotene in the nutrition of the guinea pig. J. Nutr. 30:159–168.
  • Berger, J., D. Shepard, F. Morrow, and A. Taylor. 1989. Relationship between dietary intake and tissue levels of reducing and total vitamin C in the nonscorbutic guinea pig. J. Nutr. 119:734–740. [PubMed: 2723822]
  • Bhuyan, U. N., and V. Ramalingaswami. 1973. Immune responses of the protein-deficient guinea pig to BCG vaccination. Am. J. Pathol. 72:489–500. [PMC free article: PMC1904034] [PubMed: 4728896]
  • Bird, T. A., R. G. Spanheimer, and B. Peterkofsky. 1986. a. Coordinate regulation of collagen and proteoglycan synthesis in costal cartilage of scorbutic and acutely fasted, vitamin C-supplemented guinea pigs. Arch. Biochem. Biophys. 246:42–51. [PubMed: 3963829]
  • Bird, T. A., N. B. Schwartz, and B. Peterkofsky. 1986. b. Mechanism for the decreased biosynthesis of cartilage proteoglycan in the scorbutic guinea pig. J. Biol. Chem. 261:11166-11172. [PubMed: 3733750]
  • Blevins, B. G. 1983. Amino acid requirements of guinea pigs. XII. The indispensable amino acid component at levels of total nitrogen near or above the requirement. M.S. thesis. University of Missouri, Columbia, Mo.
  • Boland, R. L., M. I. Skliar, and A. W. Norman. 1987. Isolation of Vitamin D3 metabolites from Solanum malacoxylon leaf extracts incubated with ruminal fluid. Toxicol. Lett. 53:161–164. [PubMed: 3602141]
  • Booth, A. N., C. A. Elvehjem, and E. B. Hart. 1949. The importance of bulk in the nutrition of the guinea pig. J. Nutr. 37:263–274. [PubMed: 18112978]
  • Breazile, J. E., and E. M. Brown. 1976. Anatomy. Pp. 53–62 in Biology of the Guinea Pig, J. E. Wagner, editor; , and P. J. Manning, editor. , eds. New York: Academic Press.
  • Camberos, H. R., G. K. Davis, M. I. Djafar, and C. F. Simpson. 1970. Soft tissue calcification in guinea pigs fed the poisonous plant Solanum malacoxylon. Am. J. Vet. Res. 31:685–696. [PubMed: 5437108]
  • Carlisle, T. L., D. V. Shah, R. Schelegel, and J. W. Suttie. 1975. Plasma abnormal prothrombin and microsomal prothrombin precursor in various species. Proc. Soc. Exp. Biol. Med. 148:140–144. [PubMed: 1129252]
  • Caulfield, J. E., and J. M. Rivers. 1990. Effect of increasing storage iron on ascorbic acid metabolism in the guinea pig. Am. J. Clin. Nutr. 52:529–533. [PubMed: 2393011]
  • Chesta, J., S. K. S. Srai, A. K. Burroughs, P. J. Scheuer, and O. Epstein. 1989. Copper overload in the developing guinea pig liver: A historical, histochemical and biochemical study. Liver 9:198–204. [PubMed: 2770433]
  • Chevallier, A., and Y. Choron. 1935. Sur la teneur du foie en vitamin A et ses variations. C. R. Soc. Biol. 120:1223–1225.
  • Chevallier, A., and Y. Choron. 1936. Accumulation of vitamin A reserves in the guinea pig. C. R. Soc. Biol. 121:1015–1016.
  • Cho, E. S. 1971. Amino acid requirements of guinea pigs. III. The phenylalanine requirement. M.S. thesis. University of Missouri, Columbia, Mo.
  • Chojkier, M., R. Spanheimer, and B. Peterkofsky. 1983. Specifically decreased collagen biosynthesis in scurvy dissociated from an effect on proline hydroxylation and correlated with body weight loss: In vitro studies in guinea pig calvarial bones. J. Clin. Invest. 72:826–835. [PMC free article: PMC1129247] [PubMed: 6309911]
  • Chueh, L. M. 1973. Amino acid requirements of guinea pigs. IV. The phenylalanine and tyrosine requirements. M.S. thesis. University of Missouri, Columbia, Mo.
  • Collins, M., and C. A. Elvehjem. 1958. Ascorbic acid requirements of the guinea pig, using growth and tissue ascorbic acid concentrations as criteria. J. Nutr. 64:503–511. [PubMed: 13549984]
  • Condon, A. E. 1980. Amino acid requirements of guinea pigs. XII. The total essential amino acid requirement. M.S. thesis. University of Missouri, Columbia, Mo.
  • Coots, M. C., A. E. Harper, and C. A. Elvehjem. 1959. Production of biotin deficiency in the guinea pig. J. Nutr. 67:525–530. [PubMed: 13642142]
  • Degkwitz, E., and R. H. Boedeker. 1989. Indications for adaptation to differently high vitamin C supplies in guinea pigs. 1. Development of ascorbic acid levels after altered dosing. Zeit. Ernaehrung. 28:327–337. [PubMed: 2618109]
  • Dulloo, R. M., S. Majumdar, R. N. Chakravarti, and A. Mahmood. 1982. Intestinal brush border membrane structure and function effect of chronic vitamin C deficiency in guinea-pigs. Biochem. Med. 27:325–333. [PubMed: 7052074]
  • Dunkin, G. W., P. Hartley, E. Lewis-Faning, and W. T. Russell. 1930. Comparative biometric study of albino and coloured guinea-pigs from the point of view of their stability for experimental use. J. Hyg. 30:311–319. [PMC free article: PMC2170564] [PubMed: 20475067]
  • Ediger, R. D. 1976. Care and management. Pp. 5–12 in Biology of the Guinea Pig, J. E. Wagner, editor; and P. J. Manning, editor. , eds. New York: Academic Press.
  • Elmadfa, I., and W. Feldheim. 1971. Enzyme activity, metabolites and clinically demonstrable changes in guinea pigs in tocopherol deficiency. Int. J. Vitam. Nutr. Res. 41:490–503. [PubMed: 5152355]
  • Enwonwu, C. O. 1973. Experimental protein-calorie malnutrition in the guinea pig and evaluation of the role of ascorbic acid status. Lab. Invest. 29:17–26. [PubMed: 4728354]
  • Erdmann, E., H. D. Bolte, and B. Ludentz. 1971. The Na+,K+-ATPase activity of guinea pig heart muscle in potassium deficiency. Arch. Biochem. Biophys. 145:121–125. [PubMed: 4256440]
  • Everson, G. J. 1968. Preliminary study of carbohydrates in the urine of manganese-deficient guinea pigs at birth. J. Nutr. 96:283–288. [PubMed: 5725885]
  • Everson, G. J., and R. E. Shrader. 1968. Abnormal glucose tolerance in manganese-deficient guinea pigs. J. Nutr. 94:89–94. [PubMed: 5638643]
  • Everson, G. J., L. S. Hurley, and J. F. Geiger. 1959. Manganese deficiency in the guinea pig. J. Nutr. 68:49–56. [PubMed: 13655125]
  • Everson, G. J., H. C. Tsai, and T. Wang. 1967. Copper deficiency in the guinea pig. J. Nutr. 93:533–540. [PubMed: 6082665]
  • Everson, G. J., R. E. Shrader, and T. Wang. 1968. Chemical and morphological changes in the brains of copper-deficient guinea pigs. J. Nutr. 96:115–125.
  • Farmer, F. A., B. C. Mutch, J. M. Bell, L. D. Woolsey, and E. W. Crampton. 1950. The vitamin E requirement of guinea pigs. J. Nutr. 42:309–318. [PubMed: 14795280]
  • Farooqui, S., S. K. Thind, R. Nath, and A. Mohmood. 1983. Intestinal absorption of oxalate in scorbutic and ascorbic acid supplemented guinea pigs. Acta Vitaminol. Enzymol. 5:235–241. [PubMed: 6673575]
  • Fernandez, M. L., and D. J. McNamara. 1991. Regulation of cholesterol and lipoprotein metabolism in guinea pigs mediated by dietary fat quality and quantity. J. Nutr. 121:934–943. [PubMed: 1646873]
  • Fernandez, M. L., A. Trejo, and D. J. McNamara. 1990. Pectin isolated from prickly pear (Opuntia sp.) modifies low density lipoprotein metabolism in cholesterol fed guinea pigs. J. Nutr. 120:1283–1290. [PubMed: 2231018]
  • Finke, M. D., G. R. Defoliart, and N. J. Benevenga. 1987. Use of simultaneous curve fitting and a four-parameter logistic model to evaluate the nutritional quality of protein sources at growth rates of rats from maintenance to maximum gain. J. Nutr. 117:1681–1688. [PubMed: 3668681]
  • Fraser, R. C., S. Pavlovic, C. G. Kurahara, A. Murata, N. S. Peterson, K. B. Taylor, and G. A. Feigen. 1980. The effect of variations in vitamin C intake on the cellular immune response of guinea pigs. Am. J. Clin. Nutr. 33:839–847. [PubMed: 7361703]
  • Gahl, M. J., M. D. Finke, T. D. Crenshaw, and N. J. Benevenga. 1991. Use of a four-parameter logistic equation to evaluate the response of growing rats to ten levels of each indispensable amino acid. J. Nutr. 121:1720–1729. [PubMed: 1941179]
  • Gil, A., G. M. Briggs, J. Typpo, and G. MacKinney. 1968. Vitamin A requirement of the guinea pig. J. Nutr. 96:359–362. [PubMed: 5725892]
  • Ginter, E., and Z. Zloch. 1972. Raised ascorbic acid consumption in cholesterol-fed guinea pigs. Int. J. Vitam. Nutr. Res. 42:72–79. [PubMed: 5019181]
  • Ginter, E., P. Bobek, and D. Vargova. 1979. Tissue levels and optimum dosage of vitamin C in guinea pigs. Nutr. Metab. 23:217–226. [PubMed: 424088]
  • Ginter, E., E. Drobna, and L. Ramacsay. 1982. Kinetics of ascorbate depletion in guinea pigs after long-term high vitamin C intake. Int. J. Vitam. Nutr. Res. 52:307–311. [PubMed: 7174229]
  • Grace, N. D., and B. L. O'Dell. 1968. Potassium requirement of the weanling guinea pig. J. Nutr. 94:166–170. [PubMed: 5637210]
  • Grace, N. D., and B. L. O'Dell. 1970. a. Interrelationship of dietary magnesium and potassium in the guinea pig. J. Nutr. 100:37–44. [PubMed: 5412129]
  • Grace, N. D., and B. L. O'Dell. 1970. b. Relation of polysome structure to ribonuclease and ribonuclear inhibitor activities in livers of magnesium-deficient guinea pigs. Can. J. Biochem. 48:21–26. [PubMed: 5512540]
  • Green, M. D., J. Hawkins, and S. Omaye. 1980. Effect of scurvy on reserpine induced hypothermia in the guinea pig. Life Sci. 27:111–116. [PubMed: 7401927]
  • Gupta, R. P., P. C. Verma, J. R. Sadana, and R. K. P. Gupta. 1988. Studies on the pathology of experimental zinc deficiency in guinea pigs. J. Comp. Pathol. 98:405–413. [PubMed: 3417909]
  • Haddox, M. K., J. H. Stephenson, M. E. Moser, D. B. Glass, J. G. White, B. Holmes-Gray, and N. D. Goldberg. 1979. Ascorbic acid modulation of splenic cell cyclic GMP metabolism. Life Sci. 24:1555–1566. [PubMed: 39206]
  • Hara, H. 1960. Pathologic study on riboflavin deficiency in guinea pigs. J. Vitaminol. 6:24–42. [PubMed: 14399653]
  • Hasdai, A., Z. Nitsan, and R. Volcani. 1989. Growth, digestibility, and enzyme activities in the pancreas and intestines of guinea pigs fed on raw and heated soya-bean flour. Br. J. Nutr. 62:529–537. [PubMed: 2481492]
  • Hegsted, D. M., and Y. Chang. 1965. a. Protein utilization in growing rats. I. Relative growth index as a bioassay procedure. J. Nutr. 85:159–168. [PubMed: 14259456]
  • Hegsted, D. M., and Y. Chang. 1965. b. Protein utilization in growing rats at different levels of intake. J. Nutr. 87:19–25. [PubMed: 5834571]
  • Heinicke, H. R., and C. A. Elvehjem. 1955. Effect of high levels of fat, lactose, and type of bulk in guinea pig diets. Proc. Soc. Exp. Biol. Med. 90:70–72. [PubMed: 13273355]
  • Heinicke, H. R., A. E. Harper, and C. A. Elvehjem. 1955. Protein and amino acid requirements of the guinea pig. II. Effect of carbohydrate, protein level and amino acid supplementation. J. Nutr. 57:483–496. [PubMed: 13278773]
  • Heinicke, H. R., A. E. Harper, and C. A. Elvehjem. 1956. Protein and amino acid requirements of the guinea pig. II. Effect of age, potassium and magnesium, and type of protein. J. Nutr. 58:269–280. [PubMed: 13295852]
  • Henning, S. J., and F. J. R. Hird. 1970. Concentrations and metabolism of volatile fatty acids in the fermentative organs of two species of kangaroo and guinea pig. Br. J. Nutr. 24:145–155. [PubMed: 5424254]
  • Hirsh, E. 1973. Some determinants of intake and pattern of feeding in the guinea pig. Physiol. Behav. 11:687–704. [PubMed: 4748064]
  • Hogan, A. G., and W. O. Regan. 1946. Diet and calcium phosphate deposits in guinea pigs. Fed. Proc. 5:138 (abstr.). [PubMed: 21026232]
  • Hogan, A. G., W. O. Regan, and W. B. House. 1950. Calcium phosphate deposits in guinea pigs and phosphorus content of the diet. J. Nutr. 41:203–213. [PubMed: 15422410]
  • Holman, R. T. 1960. The ratio of trienoic:tetraenoic acids in the tissue lipids as a measure of essential fatty acid requirement. J. Nutr. 70:405–410. [PubMed: 14402760]
  • Horstkoetter, R. W. 1974. Amino acid requirements of guinea pigs. V. The threonine requirement. M.S. thesis. University of Missouri, Columbia, Mo.
  • House, W. B., and A. G. Hogan. 1955. Injury to guinea pigs that follows a high intake of phosphates. J. Nutr. 55:507–517. [PubMed: 14354482]
  • Howe, P. R., L. G. Wesson, P. E. Boyle, and S. B. Wolbach. 1940. Low calcium rickets in the guinea pig. Proc. Soc. Exp. Biol. Med. 45:298–301.
  • Howell, J. M., J. N. Thompson, and G. A. J. Pitt. 1967. Changes in the tissues of guinea pigs fed on a diet free from vitamin A, but containing methyl retinoate. Br. J. Nutr. 21:37–44. [PubMed: 6024271]
  • Hsieh, H. S., and J. M. Navia. 1980. Zinc deficiency and bone formation in guinea pig alveolar implants. J. Nutr. 110:1581–1588. [PubMed: 7400848]
  • Hunt, C. E., and D. D. Harrington. 1974. Nutrition and nutritional diseases of the rabbit. In The Biology of the Laboratory Rabbit. New York: Academic Press.
  • Hurley, L. S., N. E. Volkert, and J. T. Eichner. 1965. Pantothenic acid deficiency in pregnant and nonpregnant guinea pigs, with special reference to effects on the fetus. J. Nutr. 86:201–208. [PubMed: 14302122]
  • Hurley, L. S., and C. L. Keen. 1987. Manganese. Pp. 185–223 in Trace Elements in Human and Animal Nutrition, W. Mertz, editor. , ed. Orlando, Fla.: Academic Press.
  • Jeffery, D. M., and J. T. Typpo. 1982. Crystalline amino acid diet for determining amino acid requirements of growing guinea pigs. J. Nutr. 112:1118–1125. [PubMed: 7086540]
  • Johnston, C. S. 1989. Effect of single oral doses of ascorbic acid on body temperature in healthy guinea pigs. J. Nutr. 119:407–425. [PubMed: 2921641]
  • Johnston, C. S., and S. Huang. 1991. Effect of ascorbic acid nutriture on blood histamine and neutrophil chemotaxis in guinea pigs. J. Nutr. 121:126–131. [PubMed: 1992049]
  • Jones, E., and R. E. Hughes. 1982. Influence of oral carnitine on the body weight and survival time of avitaminotic-C guinea pigs. Nutr. Rep. Int. 25:201–204.
  • Kodicek, E., and P. D. F. Murray. 1943. Influence of a prolonged partial deficiency of vitamin C on the recovery of guinea pigs from injury to bone and muscles. Nature 151:395–396.
  • Kothari, L. K., and P. Sharma. 1988. Aggravation of cholesterol induced hyperlipidemia by chronic vitamin C deficiency: Experimental study in guinea pigs. Acta Biol. Hung. 39:49–57. [PubMed: 3254010]
  • Labhsetwar, A. P., and M. Diamond. 1970. Ovarian changes in the guinea pig during various reproductive stages and steroid treatments. Biol. Reprod. 2:53–57. [PubMed: 5520112]
  • Lawrence, R. A., and R. F. Burk. 1978. Species, tissue and subcellular distribution of non Se-dependent glutathione peroxidase activity. J. Nutr. 108:211–215. [PubMed: 621577]
  • Leat, W. M. F., R. Curtis, N. J. Millichamp, and R. W. Cox. 1986. Retinyl function in rats and guinea pigs reared on diets low in essential fatty acids and supplemented with linoleic or linolenic acids. Ann. Nutr. Metab. 30:166–174. [PubMed: 2872851]
  • Lister, D., and R. A. McCance. 1965. The effect of two diets on the growth, reproduction and ultimate size of guinea pigs. Br. J. Nutr. 19:311–319. [PubMed: 14292871]
  • Liu, C. T. 1988. Energy balance and growth rate of outbred and inbred male guinea pigs. Am. J. Vet. Res. 49:1752–1756. [PubMed: 3189993]
  • Liu, K. C., J. T. Typpo, J. Y. Lu, and G. M. Briggs. 1967. Thiamine requirement of the guinea pig and the effect of salt mixtures in the diets on thiamine stability. J. Nutr. 93:480–484. [PubMed: 6082661]
  • Luderitz, B., H. D. Bolte, and G. Steinbeck. 1971. Single fiber potentials and cellular cation-concentration of the heart ventricle in chronic potassium deficiency. Klin. Wochenschr. 49:369–371. [PubMed: 5574163]
  • Machlin, L. J., F. Garcia, W. Kuenzig, and M. Brin. 1979. Antiscorbutic activity of ascorbic acid phosphate in the rhesus monkey and the guinea pig. Am. J. Clin. Nutr. 32:325–331. [PubMed: 105621]
  • Majumder, M. S. I., and A. T. M. Rahim. 1987. Cell-mediated immune response of scorbutic guinea pigs. Nutr. Res. 7:611–616.
  • Mannering, G. J. 1949. Vitamin requirements of the guinea pig. Vitam. Horm. 7:201–221.
  • Maynard, L. A., D. Boggs, G. Fisk, and D. Sequin. 1958. Dietary mineral interrelations as a cause of soft tissue calcification in guinea pigs. J. Nutr. 64:85–97. [PubMed: 13514531]
  • McBean, L. D., J. C. Smith, and J. A. Halsted. 1972. Zinc deficiency in guinea pigs. Proc. Soc. Exp. Biol. Med. 140:1207–1209. [PubMed: 5057583]
  • Miller, C. C., V. A. Ziboh, T. Wong, and M. P. Fletcher. 1990. Dietary supplementation with oils rich in (n-3) and (n-6) fatty acids influences in vivo levels of epidermal lipoxygenase products in guinea pigs. J. Nutr. 120:36–44. [PubMed: 2106017]
  • Milne, D. B., and T. Omaye. 1980. Effect of vitamin C on copper and iron metabolism in the guinea pig. Int. J. Vitam. Nutr. Res. 50:301–308. [PubMed: 7429759]
  • Morris, E. R., and B. L. O'Dell. 1961. Magnesium deficiency in the guinea pig. Mineral composition of tissues and distribution of acid-soluble phophorus. J. Nutr. 75:77–85. [PubMed: 13772826]
  • Morris, E. R., and B. L. O'Dell. 1963. Relationship of excess calcium and phosphorus to magnesium requirement and toxicity in guinea pigs. J. Nutr. 81:175–181. [PubMed: 14068933]
  • Mueller, M. J. 1978. Amino acid requirement of growing guinea pigs. IX. The leucine requirement. M.S. thesis. University of Missouri, Columbia, Mo.
  • National Institutes of Health. 1982. NIH Rodents 1980 Catalogue. NIH No. 83–606. Washington, D.C.: Department of Health and Human Services.
  • Navia, J. M., and C. E. Hunt. 1976. Nutrition, nutritional diseases and nutrition research application. Pp. 235–265 in Biology of the Guinea Pig, J. E. Wagner, editor; and P. J. Manning, editor. , eds. New York: Academic Press.
  • Navia, J. M., and H. Lopez. 1973. A purified gel diet for guinea pigs. Lab. Anim. Sci. 23:111–114. [PubMed: 4347749]
  • Neuringer, M., G. J. Anderson, and W. E. Connor. 1988. The essentiality of n-3 fatty acids for the development and function of the retina and brain. Annu. Rev. Nutr. 8:517–541. [PubMed: 3060176]
  • O'Dell, B. L., and W. O. Regan. 1963. Effect of lysine and glycine upon arginine requirement of guinea pigs. Proc. Soc. Exp. Biol. Med. 112:336–337.
  • O'Dell, B. L., J. M. Vandepopuliere, E. R. Morris, and A. G. Hogan. 1956. Effect of a high phosphorus diet on acid-base balance in guinea pigs. Proc. Soc. Exp. Biol. Med. 91:220–223. [PubMed: 13297758]
  • O'Dell, B. L., E. R. Morris, and W. O. Hogan. 1960. Magnesium requirements of guinea pigs and rats. Effect of calcium and phosphorus and symptoms of magnesium deficiency. J. Nutr. 70:103–110. [PubMed: 14428049]
  • O'Dell, B. L., R. I. Moroni, and W. O. Hogan. 1973. Interaction of dietary fluoride and magnesium in guinea pigs. J. Nutr. 103:841–850. [PubMed: 4705270]
  • O'Dell, B. L., J. K. Becker, M. P. Emery, and J. D. Browning. 1989. Production and reversal of the neuromuscular pathology and related signs of zinc deficiency in guinea pigs. J. Nutr. 119:196–201. [PubMed: 2918391]
  • Ostwald, R., W. Yamanaka, and D. Irvin. 1971. Effect of dietary modifications on cholesterol-induced anemia in guinea pigs. J. Nutr. 101:699–712. [PubMed: 5108515]
  • Pappenheimer, A. M., and M. Goettsch. 1941. Death of embryos in guinea pigs on diets low in vitamin E. Proc. Soc. Exp. Biol. Med. 47:268–270.
  • Parker, C. M., R. P. Sharma, and J. L. Shupe. 1979. The interaction of dietary vitamin C, protein and calcium with fluoride toxicity. Fluoride-Quart. Rep. 12:144–154. [PubMed: 509894]
  • Parra, R. 1978. Comparison of foregut and hindgut fermentation in herbivores. Pp. 205–229 in The ecology of arboreal folivores, G. G. Montgomery, editor. , ed. Washington, D.C.: Smithsonian Institution Press.
  • Pfander, W. H., and H. H. Mitchell. 1952. The ascorbic acid requirement of the guinea pig when adrenal weight and odonto-blast height are used as criteria. J. Nutr. 47:503–524. [PubMed: 14955707]
  • Prinz, W., J. Bloch, G. Gilich, and G. Mitchell. 1980. A systematic study of the effect of vitamin C supplementation on the humoral immune response in ascorbate-dependent mammals. I. The antibody response to sheep red blood cells (a T-dependent antigen) in guinea pigs. Int. J. Vitam. Nutr. Res. 50:294–300. [PubMed: 7429758]
  • Pyke, R. E., W. G. Hoekstra, and P. H. Phillips. 1967. Effects of fluoride on magnesium deficiency in the guinea pig. J. Nutr. 92:311–316. [PubMed: 6053739]
  • Quarterman, J., and W. R. Humphries. 1983. The production of zinc deficiency in the guinea pig. J. Comp. Pathol. 93:261–270. [PubMed: 6863612]
  • Reid, M. E. 1954. a. Nutritional studies with the guinea pig. B-vitamins other than pantothenic acid. Proc. Soc. Exp. Biol. Med. 85:547–550. [PubMed: 13167134]
  • Reid, M. E. 1954. b. Production and counteraction of a fatty acid deficiency in the guinea pig. Proc. Soc. Exp. Biol. Med. 86:708–712. [PubMed: 13204330]
  • Reid, M. E. 1955. Nutritional studies with the guinea Pig. III. Choline. J. Nutr. 56:215–229. [PubMed: 14392503]
  • Reid, M. E. 1961. Nutritional studies with the guinea pig. VII. Niacin. J. Nutr. 75:279–286. [PubMed: 14491183]
  • Reid, M. E. 1963. Nutritional studies with the guinea pig. IX. Effect of dietary protein level on body weight and organ weights in young guinea pigs. J. Nutr. 80:33–38. [PubMed: 13973764]
  • Reid, M. E. 1964. Nutritional studies with the guinea pig. XI. Pyridoxine. Proc. Soc. Exp. Biol. Med. 116:289–292. [PubMed: 14189120]
  • Reid, M. E. 1966. Methionine and cystine requirements of the young growing guinea pig. J. Nutr. 88:379–402. [PubMed: 5948868]
  • Reid, M. E., and J. G. Bieri. 1967. Nutritional studies with the guinea pig. VIII. Thiamine. Proc. Soc. Exp. Biol. Med. 126:11–13. [PubMed: 6066150]
  • Reid, M. E., and G. M. Briggs. 1953. Development of a semisynthetic diet for young guinea pigs. J. Nutr. 51:341–354. [PubMed: 13109570]
  • Reid, M. E., and G. M. Briggs. 1954. Nutritional studies with the guinea pig. II. Pantothenic acid. J. Nutr. 52:507–517. [PubMed: 13163737]
  • Reid, M. E., and Martin, M. G. 1959. Nutritional studies with the guinea pig. V. Effects of deficiency of fat or unsaturated fatty acids. J. Nutr. 67:611–622. [PubMed: 13642150]
  • Reid, M. E., and O. Mickelsen. 1963. Nutritional studies with the guinea pig. VIII. Effect of different proteins, with and without amino acid supplements, on growth. J. Nutr. 80:25–32. [PubMed: 13973763]
  • Reid, M. E., and L. Von Sallmann. 1960. Nutritional studies with the guinea pig. VI. Tryptophan (with ample dietary niacin). J. Nutr. 70:329–336. [PubMed: 14437098]
  • Reid, M. E., M. G. Martin, and G. M. Briggs. 1956. Nutritional studies with the guinea pig. IV. Folic acid. J. Nutr. 59:103–119. [PubMed: 13320199]
  • Reid, M. E., J. G. Bieri, P. A. Plack, and E. L. Andrews. 1964. Nutritional studies with the guinea pig. X. Determination of the linoleic acid requirement. J. Nutr. 82:401–408. [PubMed: 14151124]
  • Rikans, L. E., C. R. Smith, and V. G. Zannoni. 1977. Ascorbic acid and heme synthesis in deficient guinea pig liver. Biochem. Pharmacol. 26:797–799. [PubMed: 856210]
  • Bivers, J. M., L. Krook, and A. Cormier. 1970. Biochemical and histological study of guinea pig fetal and uterine tissue in ascorbic acid deficiency. J. Nutr. 100:217–227. [PubMed: 5414418]
  • Robbins, K. D., H. W. Norton, and D. H. Baker. 1979. Estimation of nutrient requirements from growth data. J. Nutr. 109:1710–1714. [PubMed: 490209]
  • Robens, J. R. 1970. Teratogenic effects of hypervitaminosis A in the hamster and the guinea pig. Toxicol. Appl. Pharmacol. 16:88–99. [PubMed: 5416756]
  • Rose, R. C., J. L. Choi, and M. J. Koch. 1988. Intestinal transport and metabolism of oxidized ascorbic acid (dehydroascorbic acid). Am. J. Physiol. 254:G824–G828. [PubMed: 3377081]
  • Schiller, E. L. 1977. Relationships among selected dietary components and plasma transaminase activities in adult miniature swine and guinea pigs and indices of nitrogen status in adult guinea pigs. Ph.D. dissertation. University of Missouri, Columbia, Mo.
  • Schottelius, B. A., D. D. Schottelius, and A. D. Bender. 1959. Effect of vitamin E on myoglobin content of guinea pig skeletal muscle. Proc. Soc. Exp. Biol. Med. 102:581–583. [PubMed: 14443492]
  • Sergeev, I. N., Y. P. Arkhapchev, and V. B. Spirichev. 1990. Ascorbic acid effects of vitamin D hormone metabolism and binding in guinea pigs. J. Nutr. 120:1185–1190. [PubMed: 2170601]
  • Shelton, D. C. 1971. Feeding the guinea pig. Lab. Anim. 7:84–87.
  • Shimotori, N., G. A. Emerson, and H. M. Evans. 1940. The prevention of nutritional muscular dystrophy in guinea pigs with vitamin E. J. Nutr. 19:547–554.
  • Shrader, R. E., and G. J. Everson. 1968. Pancreatic pathology in manganese-deficient guinea pigs. J. Nutr. 94:269–281. [PubMed: 5642191]
  • Siliparandi, L., P. Vanni, M. Kessler, and G. Semena. 1979. Na+ dependent, electroneutral L-ascorbate transport across brush border membrane vesicles from guinea pig small intestine. Biochim. Biophys. Acta 552:129–142. [PubMed: 435492]
  • Sillevis Smitt, P. A., J. M. de Jong, D. Troost, and M. A. Kuipers. 1991. Muscular changes in the guinea pig caused by chronic ascorbic acid deficiency. J. Neurol. Sci. 102:4–10. [PubMed: 1842898]
  • Simboli-Campbell, M., and G. Jones. 1991. Dietary phosphate deprivation increases renal synthesis and decreases renal catabolism of 1,25-dihydroxycholecalciferol in guinea pigs. J. Nutr. 121:1635–1642. [PubMed: 1765829]
  • Singh, K. D., E. R. Morris, W. O. Regan, and B. L. O'Dell. 1968. An unrecognized nutrient for the guinea pig. J. Nutr. 94:534–542. [PubMed: 5653267]
  • Sisk, D. B. 1976. Physiology. Pp. 63–98 in Biology of the Guinea Pig, J. E. Wagner, editor; and P. J. Manning, editor. , eds. New York: Academic Press.
  • Slanetz, C. A. 1943. The adequacy of improved stock diets for laboratory animals. Am. J. Vet. Res. 4:182–189.
  • Smith, C. H., and W. R. Bidlack. 1980. Interrelationship of dietary ascorbic acid and iron on the tissue distribution of ascorbic acid, iron and copper in female guinea pigs. J. Nutr. 110:1398–1408. [PubMed: 7381603]
  • Smith, L. F. 1979. Amino acid requirements of growing guinea pigs. X. The tryptophan requirement and interrelationship with niacin. M.S. thesis. University of Missouri, Columbia, Mo.
  • Spanheimer, R. G., and B. Peterkofsky. 1985. A specific decrease in collagen synthesis in acutely fasted, vitamin C-supplemented, guinea pigs. J. Biol. Chem. 260:3955–3962. [PubMed: 3980462]
  • Stenflo, J., and P. Fernlund. 1984. β-Hydroxyaspartic acid in vitamin K-dependent plasma proteins from scorbutic and warfarin-treated guinea pigs. FEBS Lett. 168:287–292. [PubMed: 6723952]
  • Stone, N., and A. Meister. 1962. Function of ascorbic acid in the conversion of proline to collagen hydroxyproline. Nature 194:555–557. [PubMed: 13917472]
  • Suttle, N. F. 1974. Recent studies of the copper-molybdenum antagonism. Proc. Nutr. Soc. 33:299–305. [PubMed: 4617883]
  • Tinoco, J. 1982. Dietary requirements and functions of α-linolenic acid in animals. Prog. Lipid Res. 21:1–45. [PubMed: 6287500]
  • Thompson, D. J., J. F. Heintz, and P. H. Phillips. 1964. Effect of magnesium, fluoride, and ascorbic acid on metabolism of connective tissue. J. Nutr. 84:27–30. [PubMed: 14210017]
  • Toyoda, H., S. Himens, and N. Imura. 1989. The regulation of glutathione peroxidase gene expression relevant to species difference and the effects of dietary selenium manipulation. Biochim. Biophys. Acta 1008:301–308. [PubMed: 2474322]
  • Tsai, H. C. C., and G. J. Everson. 1967. Effect of manganese deficiency on the acid mucopolysaccharides in the cartilage of guinea pigs. J. Nutr. 91:447–460. [PubMed: 4227162]
  • Tsao, C. S., and P. Y. Leung. 1988. Urinary ascorbic acid levels following the withdrawal of large doses of ascorbic acid in the guinea pigs. J. Nutr. 118:895–900. [PubMed: 3392599]
  • Tsao, C. S., and M. Young. 1989. Effect of dietary ascorbic acid on levels of serum mineral nutrients in guinea pigs. Int. J. Vitam. Nutr. Res. 59:72–76. [PubMed: 2722430]
  • Tsujimura, M. 1978. Studies on the biological activity of L-ascorbic acid 2-sulfate. Joshi Eiyo Daigaku Kiyo 9:213–252.
  • Typpo, J. T., H. L. Anderson, G. F. Krause, and D. T. Yu. 1985. The lysine requirement of young growing male guinea pigs. J. Nutr. 115:579–587. [PubMed: 3923163]
  • Typpo, J. T., J. E. Link, G. F. Krause, and D. Baravati. 1990. a. The total nitrogen requirement of young, growing, male guinea pigs. FASEB J. 4:A804 (abstr.).
  • Typpo, J. T., D. J. Curtis, L. S. Ayers, S. C. Mokros, J. E. Link, and G. F. Krause. 1990. b. Amino acid requirements of guinea pigs using chemically defined diets. Amino Acids 2:1132–1140.
  • Udenfriend, S. 1966. Formation of hydroxyproline in collagen. Science 152:1335–1340. [PubMed: 5327887]
  • Van Hellemond, M. J., A. G. Lemmens, and A. C. Beynen. 1988. Dietary phosphorus and calcuium excretion in guinea pigs. Nutr. Rep. Intl. 37:909–912.
  • Verma, P. C., R. P. Gupta, J. R. Sadana, and R. K. P. Gupta. 1988. Effect of experimental zinc deficiency and repletion on some immunological variables in guinea pigs. Br. J. Nutr. 59:149–154. [PubMed: 2449907]
  • Wagner, J. E., and H. L. Foster. 1976. Germ-free and specific pathogen-free. Pp. 21–30 in Biology of the Guinea Pig, J. E. Wagner, editor; and P. J. Manning, editor. , eds. New York: Academic Press.
  • Wagner, J. E., and P. J. Manning. 1976. The Biology of the Guinea Pig. New York: Academic Press.
  • Weir, B. J. 1974. Notes on the origin of the domestic guinea pig. In The Biology of Hystricomorph Rodents, I. W. Rowlands, editor; and B. J. Weir, editor. , eds. New York: Academic Press.
  • Wolbach, S. B. 1947. Vitamin-A deficiency and excess in relation to skeletal growth. J. Bone Joint Surg. 29:171–192. [PubMed: 20284696]
  • Wolbach, S. B. 1954. Effects of vitamin A deficiency and hypervitaminois A in animals. Pp. 106–137 in The Vitamins, Vol. 1, W. H. Sebrell, Jr., editor; , and R. S. Harris, editor. , eds. New York: Academic Press.
  • Woodruff, C. W., S. L. Clark, and E. B. Bridgeforth. 1953. Folic acid deficiency in the guinea pig. J. Nutr. 51:23–34. [PubMed: 13097223]
  • Woolley, D. W., and H. Sprince. 1945. The nature of some new dietary factors required by guinea pigs. J. Biol. Chem. 157:447–453.
  • Woytkiw, L., and N. C. Esselbaugh. 1951. Vitamin A and carotene absorption in the guinea pig. J. Nutr. 43:451–458. [PubMed: 14851058]
  • Yoon, S. H. 1977. Amino Acid Requirements of Guinea Pigs. VII. The arginine requirement. M.S. thesis. University of Missouri, Columbia, Mo.
  • Young, M., and E. M. Widdowson. 1975. Influence of diet deficiency in energy, or in protein on conceptive weight, and the placental transfer of a non-metabolizable amino acid in the guinea pig. Biol. Neonate 27:184–191. [PubMed: 1182242]
© 1995 by the National Academy of Sciences. All rights reserved.
Bookshelf ID: NBK231932


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