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Montmayeur JP, le Coutre J, editors. Fat Detection: Taste, Texture, and Post Ingestive Effects. Boca Raton (FL): CRC Press/Taylor & Francis; 2010.

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Fat Detection: Taste, Texture, and Post Ingestive Effects.

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Chapter 15Fats and Satiety

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15.1. INTRODUCTION

Dietary fat has frequently been blamed for the increase in prevalence of obesity (Bray et al., 2004). Epidemiological studies have demonstrated a positive relationship between high-fat diets and excess energy intake due to their high energy density and palatability (Prentice and Poppitt, 1996). However, this association is confounded by differences in physical activity, smoking, and food availability and variety (Willett, 1998; Bray et al., 2004). Furthermore, epidemiological studies investigating the association between high fat intake and obesity have been inconsistent (Seidell, 1998; Willett, 1998).

Preload studies have shown that fat exerts the weakest effect on satiety compared to carbohydrate and protein, suggesting that fat may lead to “passive overconsumption” (Blundell et al., 1993). But when preloads were matched for energy density and palatability, differences in satiety were not obvious (Geliebter, 1979; Stubbs and Harbron, 1996; McCrory et al., 2000), pointing to energy density as the key driver of satiety under experimental conditions. Furthermore, lipids suppress later food intake when present in the small intestine of both humans and animals (Welch et al., 1988; Greenberg et al., 1990; Drewe et al., 1992; Woltman and Reidelberger, 1995; Castiglione et al., 1998; Van Wymwlbeke et al., 1998).

Relatively few studies have investigated the responses of specific fats and fatty acids on food intake. Furthermore, studies have used different fats and fatty acids making it almost impossible to draw conclusions. However, it is clear that not all fats are equal in their effect on appetite and associated biological processes.

15.2. DIETARY FATS AND SATIETY: FAT STRUCTURE

The effect of fats on satiety has been investigated in four areas associated with fat structure: chain length, degree of saturation, degree of esterification, and functionality of specific fat molecules, particularly conjugated linoleic acid (CLA) and Olibra® (Lipid Technologies Provider AB, Karishamn, Sweden).

15.2.1. Chain Length

Studies on the effect of fatty acid chain length on satiety have shown that medium-chain triacylglycerols (MCT, 8–12 C) are more satiating than long-chain triacylglycerols (LCT) in animals (Friedman et al., 1983) and humans (Stubbs and Harbron, 1996; Rolls et al., 1988; Van Wymelbeke et al., 1998, 2001; St-Onge et al., 2003). MCT consumed as a preload resulted in lower energy intake 30 min later compared to LCT in healthy individuals (Rolls et al., 1988) (Figure 15.1). A breakfast high in MCT (30%) resulted in lower energy intake (220 kcal) at lunch 4 h later compared to a high oleic acid breakfast (30%) in healthy individuals (St-Onge et al., 2003). A similar study also found that food intake at lunch was lower after a high MCT breakfast (43 g) compared to high oleic or high saturated fat breakfast in men (Van Wymelbeke et al., 1998). The same authors found lower intake at dinner when a high MCT lunch was consumed (Van Wymelbeke et al., 2001).

FIGURE 15.1. Mean energy intake (kcal) from an ad libitum lunch in 12 individuals.

FIGURE 15.1

Mean energy intake (kcal) from an ad libitum lunch in 12 individuals. Lunch was offered 30 min after a preload of 100 (10 g), 200 (20 g), and 300 (30 g) kcal of MCT or LCT. There was a significant reduction in calories (14%–15% fewer calories) (more...)

Studies on weight loss have shown that adding MCT to a very low calorie diet improved satiety and resulted in a higher rate of weight loss without affecting fat-free mass (FFM) compared to LCT in the first 2 weeks of the diet in obese women (Krotkiewski, 2001). As well, consumption of 18–24 g/day of MCT with a weight reduction diet resulted in lower endpoint body weight and a trend toward greater fat mass loss after 16 weeks compared to LCT in overweight subjects (St-Onge and Bosarge, 2008).

Mode of intake (oral vs. gastrointestinal infusions) plays an important role on the effect of chain length on appetite. MCT is more satiating compared to LCT when taken orally in humans (Stubbs and Harbron, 1996; Rolls et al., 1988; Van Wymelbeke et al., 1998, 2001; St-Onge et al., 2003). However, when infused in the stomach, fatty acids with different chain lengths did not show different effects on satiety in rats (Maggio and Koopmans, 1982). On the other hand, intraduodenal infusion of long-chain fatty acids (sodium oleate) inhibited food intake, whereas infusion of medium-chain fatty acids (sodium caprylate) had no effect on food intake in humans (Matzinger et al., 2000).

The time between fat ingestion and subsequent meal has been shown to be an important variable on the effect of chain length on appetite. In diabetic rats, 1.5 mL of MCT suppressed subsequent food intake in the first 2 h after the preload, whereas the reduction in intake with 1.5 mL LCT occurred after 2–4 h compared to a no preload control (Friedman et al., 1983). The difference is proposed to be due to a differential rate of delivery of the ingested lipid to the liver (Friedman et al., 1983). MCT have an advantage over triacylglycerols in getting hydrolyzed and absorbed. Furthermore, MCT are absorbed into the portal system and are rapidly taken up and oxidized by the liver, whereas, LCT are packed into chylomicrons that bypass the liver via the lymphatic system, favoring uptake of LCT into the adipose tissue and muscle. In the mitochondria, MCT do not require acylcarnitine transferase to cross the inner mitochondrial membrane, and therefore, it is not a rate-limiting step in MCT oxidation as it is for LCT (Bremer, 1983). As a result, plasma ketone bodies are increased, which is an indication of enhanced hepatic acid oxidation (Krotkiewski, 2001; Van Wymelbeke et al., 2001). Satiety has been associated with increased fatty acid oxidation in the liver (Langhans, 1996).

Fatty acid chain length seems to be a determinant of gut hormone secretion. Only fatty acids with a chain length greater than C12 are able to stimulate the secretion of Cholecystokinin (CCK), Gastric Inhibitory Peptide (GIP), neurotensin, and pancreatic polypeptide (PP) (McLaughlin et al., 1999; Barbera et al., 2000; Drewe et al., 2008). MCT (<C12) ingested or given intraduodenally did not stimulate CCK or neurotensin release in humans (Matzinger et al., 2000; Drewe et al., 2008). Peptide YY (PYY) secretion is stimulated by both MCT and LCT, but the magnitude and concentration was greater after LCT compared to MCT (Maas et al., 1998).

Overall, when compared to LCT, MCT suppress energy intake when consumed in high amounts. However, intake of high quantities of MCT has been linked to adverse events such as nausea, vomiting, gastrointestinal discomfort, and abdominal discomfort, which limits the amount of MCT that can be incorporated in the diet.

15.2.2. Saturation

Within the same chain length, a greater degree of unsaturation is associated with enhanced satiety, but studies have been inconsistent. In the C-18 fatty acids, linoleic acid resulted in lower appetite and short-term food intake compared to oleic and stearic acids when administered intraduodenally in human subjects (French et al., 2000) (Figure 15.2) or incorporated in foods (Lawton et al., 2000). In weanling Zucker rats, a daily gavage of 100 μL of γ-linolenic acid suppressed food intake and weight gain compared to soy oil (Phinney et al., 1993; Thurmond et al., 1993). γ-Linolenic acid (890 mg/day) has been shown to reduce weight regain in formerly obese humans compared to oleic acid after 1 year of supplementation (Schirmer and Phinney, 2007). On the other hand, a 2-week study of ingestion of oils with different degrees of saturation has reported no difference in satiety scores, energy intake, or weight in overweight subjects consuming a diet high in oleic or γ-linoleic or α-linolenic acid (45 mL oil) (Kamphuis et al., 2001). In overweight subjects, polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA) in a preload (63–87 g) suppressed appetite and short-term food intake to the same extent (Flint et al., 2003). Similarly, muffins rich in MUFA (40 g) decreased food intake and appetite in a similar manner to muffins rich in saturated fatty acids (40 g) in lean subjects (Alfenas and Mattes, 2003). However, a recent study found that in rats, MUFA (600 mg/kg/12 h) were able to suppress food intake and decrease body weight to a larger extent compared to PUFA (Vogler et al., 2008).

FIGURE 15.2. The effect of upper intestine infusion of C-18 fatty acid-enriched oils on food intake.

FIGURE 15.2

The effect of upper intestine infusion of C-18 fatty acid-enriched oils on food intake. Infusions were given for 100 min at a rate of 1 mL (8.3 kJ)/min (200 mL/L emulsions). At 90 min after the start of the infusion, subjects were given a liquid meal (more...)

Several mechanisms have been suggested for the association between the degree of unsaturation of fatty acids and satiety. These mechanisms include both peripheral and central pathways for appetite regulation. In the periphery, plasma CCK in humans (Beardshall et al., 1989) and apolipoprotein A-IV (ApoA-IV) in rats (Kalogeris et al., 1996) have been shown to be more potently released following ingestion of linoleic acid-containing oils compared to other less unsaturated fatty acids. Diunsaturated oil resulted in the highest release of CCK followed by monounsaturated oil with saturated fat showing no effect on plasma CCK release (Beardshall et al., 1989). However, other studies have failed to show a relationship between plasma CCK concentrations and degree of unsaturation (French et al., 2000). Another gut hormone, GLP-1, is increased with α-linolenic acid, an unsaturated long-chain free fatty acid (FFA), in a dose-dependent manner in vitro, whereas medium-chain and saturated long-chain fatty acids did not have any effect (Hirasawa et al., 2005). In the same study but in rats, α-linolenic acid resulted in the highest plasma GLP-1 secretion compared to other unsaturated and saturated fatty acids of same chain length (Hirasawa et al., 2005). Centrally, serotonin (5HT), a neurotransmitter, has also been implicated in the association between appetite and unsaturation (Friedman et al., 1986; Mullen and Martin, 1992). In diet-induced obese mice, Neuropeptide Y (NPY) mRNA in the arcuate nucleus was decreased and pro-opiomelanocortin mRNA was increased with the administration of n – 3 PUFA (Huang et al., 2004). Furthermore, it was suggested that n – 3 PUFA (α-linolenic, eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA]) can exert anorexigenic effects in the peripheral endocannabinoid system by acting as antagonists to n – 6 PUFA (Oda, 2007). n – 3 PUFA competes with the n – 6 PUFA derivatives, anandamide and 2-arachidonoyl glycerol, which are major agonists for the endocannabinoid system (CB1) (Oda, 2007). In mice, the concentration of n – 3 PUFA in the brain of mice is inversely related to 2-arachidonoyl glycerol concentrations (Watanabe et al., 2003).

In conclusion, a greater number of double bonds seems to be associated with enhanced satiety when given in high amounts, but large amounts of fat cannot be recommended for human nutrition. Whether moderate amounts of PUFA can affect food intake remains to be established.

15.2.3. Esterification

The degree of esterification of dietary fats seems to play a role in satiety, but only a limited number of studies address it. One-monoglycerides infused into the duodenum of pigs suppressed subsequent intake in excess of its energy content compared to oleic acid. CCK was shown to be the mediator of this effect by administering a CCK antagonist and abolishing the reported suppression of intake by monoglycerides (Gregory and Rayner, 1987; Gregory et al., 1989). However, in humans, one-monoglycerides, given at 25% of daily energy intake, behaved in a similar manner to triglycerides with regard to appetite and energy intake in the short term and on the subsequent day (Johnstone et al., 1998a,b).

Diacylglycerols (DG), more specifically the 1,3-diacylglycerol isomer, have been reported to lower hunger, appetite, and desire-to-eat over 12 h compared to triacylglycerols when incorporated in foods (~26 g) (Kamphuis et al., 2003b). In terms of weight control, DG consumption is associated with decreased total and visceral body fat accumulation in both rats (Murase et al., 2001) and humans (Nagao et al., 2000; Maki et al., 2002). Suggested mechanisms include enhanced β-oxidation and greater energy expenditure due to the availability of free fatty acids in the portal circulation (Murata et al., 1997). DG have a similar energy value to triacylglycerols (9 kcal/g) (Taguchi et al., 2001). Similar to MCT, DG are incorporated into the portal vein and transported to the liver where they are mostly oxidized (Breckenridge and Kuksis, 1975). However, the potential effect of DG on satiety still requires further investigation.

15.2.4. Functional Fats

15.2.4.1. Conjugated Linoleic Acid

CLAs are a group of geometric and positional isomers of linoleic acid that occur naturally in food (e.g., dairy products, beef). CLA intake from dietary sources is generally <600 mg/day (Kovacs and Mela, 2006). CLA has been implicated with a number of potential health benefits including weight control. Most of the physiologic effects of CLA rest with the trans-10, cis-12 and cis-9, trans-11 isomers, linked to weight control effects; and trans-10, cis-12, associated with body composition changes (Pariza et al., 2001).

The few studies assessing the effect of long-term CLA supplementation on appetite have found inconsistent results in human subjects. Two studies found no effect (Blankson et al., 2000; Medina et al., 2000), while another study found that 13 weeks of mixed isomer CLA intake (1.8 and 3.6 g) increased fullness and satiety compared to baseline (Kamphuis et al., 2003a).

Studies on CLA supplementation and weight control in human subjects have shown that daily intake of 3.4 g of CLA (equal parts of both isomers) reduced total body fat (Blankson et al., 2000) and abdominal fat (Riserus et al., 2001). Furthermore, two other studies have also shown significant reductions in plasma leptin concentrations with daily intake of 3 g of CLA (isomer mix) for 64 days (Medina et al., 2000) and an inverse association with plasma leptin concentrations after 8 weeks of CLA intake (isomer mix) (Belury et al., 2003). Increased β-oxidation has been suggested as a mechanism. For example, infusion of 1% CLA mixture into perfused livers of rats for 2 weeks produced more ketone bodies than 1% linoleic acid-fed rats (Sakano et al., 1999), suggesting that fatty acid oxidation was increased.

While further explorations are required into the effect of CLA on appetite regulation, it is worthwhile noting that CLA trans-10, cis-12 has been shown to induce inflammation and hyperinsulinemia in animal models (Poirier et al., 2006) and impair insulin sensitivity in a few clinical trials (Riserus et al., 2002, 2004; Moloney et al., 2004), which raises concerns regarding supplementation with CLA trans-10, cis-12. Further research is needed in order to asses the health benefits or risks of CLA on the long term.

15.2.4.2. Olibra

Olibra is a novel fat emulsion consisting of a mixture of fractionated palm oil (40%) and fractionated oat oil (2.5%) in water. Olibra has been associated with increased satiety and decreased energy intake (~1 MJ difference) at a meal 4 h later when added to yogurt (5 g) in nonobese, overweight, and obese subjects. The decrease in intake was maintained for the rest of the day (Burns et al., 2000, 2001, 2002). However, a recent study has failed to find an effect on food intake and appetite (Logan et al., 2006). Speculated mechanisms include the physiochemical stability of the emulsion resulting in delayed digestion and stimulation of distal small intestine receptors and gut hormone secretion, but there is no supporting evidence in the literature. One study reported an increase in plasma GLP-1 response but only at 180 min after 25 weeks consumption of 10 g of Olibra (Diepvens et al., 2007). However, the mechanism of action requires further clarification.

15.3. FAT IN RELATION TO OTHER MACRONUTRIENTS AND SATIETY

15.3.1. Fiber

Combining fat with fiber has been shown to increase the satiating potential of fat (French and Read, 1994; Burton-Freeman, 2000; Burton-Freeman et al., 2002). Fiber intake is associated with enhanced satiety and reduced food intake (Howarth et al., 2001; Samra and Anderson, 2007). The properties of some fibers that prolong the contact of dietary fats with the intestinal mucosa and retard fat digestion may contribute to enhanced satiety. Partially hydrolyzed guar gum (PHGG) (6 g) added to yogurt has been shown to decrease bioaccessibility of fat in a dynamic model of the gastrointestinal tract (Minekus et al., 2005). Accordingly, PHGG was able to suppress postprandial serum lipid concentrations in healthy volunteers with moderate hypertriglyceridemia after a high-fat high-cholesterol meal (Kondo et al., 2004). Viscous fiber (12 g guar gum) added to high-fat treatment prolonged satiety and slowed gastric emptying compared to a high-fat treatment without fiber (French and Read, 1994). This effect may be partly mediated through enhanced release of cholecystokinin. Adding fiber (20 g) to a low-fat treatment (16–23 g) increased plasma CCK secretion and subjective satiety to a similar extent as a high-fat treatment (31–40 g) without fiber in healthy individuals (Burton-Freeman et al., 2002).

Combining fat with fiber is an interesting venue to enhance the satiating potential of fat-containing products and therefore merits further exploration.

15.3.2. Carbohydrate

Short-term studies investigating satiety after meals varying in fat-to-CHO ratios have been inconsistent (Fryer et al., 1955; Driver, 1988; van Amelsvoort et al., 1989; Foltin et al., 1990). Meals with a high-fat–carbohydrate ratio either show a weaker suppression of hunger (van Amelsvoort et al., 1989; Cotton et al., 2007) or have the same effect (van Amelsvoort et al., 1989; Foltin et al., 1990; de et al., 1992; Stubbs et al., 1995) compared to meals with a low-fat–carbohydrate ratio. Such inconsistencies could result from diverse experimental parameters and not upon actual differences in the metabolic properties of the macronutrients themselves. For example, variations in the type of fat and carbohydrate used, palatability and energy density of the test meal, population studied (gender, age, dietary restraint, body mass index, etc.), and the mode of test food delivery could result in different outcomes between studies.

15.4. FACTORS BEHIND THE IMPACT OF FAT ON SATIETY

15.4.1. Physical Properties

The chemical composition of fatty acids affects the physical properties of the triacylglycerol molecule. For example, the melting point of the fatty acid is inversely related to its degree of unsaturation (Table 15.1). Therefore, the degree of unsaturation is likely to affect the ease of emulsification of the triacylglycerol in the digestive tract, which is predicted to markedly affect the ease of digestion and absorption of fatty acids. The result is modulation of the rate of interaction between fatty acids and satiety signals on the intestinal wall (Small, 1991).

TABLE 15.1

TABLE 15.1

Effect of Increasing Unsaturation of Component Fatty Acids on the Melting Point of Pure Long-Chain Triacylglycerols

15.4.2. Cephalic Modulation

Cephalic stimulation with fat is associated with modulation of digestive processes and appetite. Gilbertson et al. have shown that different fatty acids can be discriminated by taste receptors on the tongue of rats (Gilbertson et al., 1997). K+ currents on the tongue were shown to be markedly inhibited by linoleic and linolenic acids but not by stearic or oleic acid. These findings seem to parallel the human food intake data (Figure 15.1). K+ currents are identified in other tissues including the duodenum (Gilbertson, 1998), suggesting that similar signaling from the small intestine in response to fatty acids may occur. In general, presence of food in the mouth is associated with modulation of digestive processes (Helman, 1988; Teff and Engelman, 1996). Cephalic stimulation with fats, particularly long-chain unsaturated fatty acids, elicit several digestive processes including gastric lipase (Wojdemann et al., 1997) and pancreatic digestive enzymes secretion (Hiraoka et al., 2003), CCK release (Wisen et al., 1992), and pancreatic polypeptide secretion (Crystal and Teff, 2006). Stimulation of the human tongue with full-fat soft cheese increases the serum lipid response to an intragastric load of triacylglycerol when compared with nonfat soft cheese or no stimulation (Mattes, 1996). Subjects were blinded on the nature of the cheese and were not able to distinguish between the cheese samples in sensory tests suggesting that a specific chemosensory or tactile mechanism from the mouth mediated this change.

Few studies have investigated the association between oral stimulation of fat and satiety. A study has shown that oral stimulation with different fats by modified-sham-feeding (MSF) resulted in increased feelings of satiety compared with water in human subjects, with linoleic acid showing the strongest response (Smeets and Westerterp-Plantenga, 2006). On the other hand, sham feeding a high-fat cake increased food intake at the next meal compared to nonfat cake in restrained eaters (Crystal and Teff, 2006).

15.4.3. Oxidative Qualities

Fatty acid oxidation in the liver seems to be associated with appetite and food intake (Friedman and Tordoff, 1986; Friedman et al., 1986; Langhans and Scharrer, 1987; Stubbs et al., 1995). Studies on the effect of fat oxidation on food intake suggest that fat that is oxidized generates a satiety signal and, in contrast, fat that is stored is less satiating (Friedman, 1998). In rats, feeding is stimulated when the oxidation of long-chain fatty acids is inhibited by methyl palmoxirate, which blocks carnitine palmitoyl-transferase-1 and decreases transport of long-chain fatty acids to the mitochondria (Friedman and Tordoff, 1986; Friedman et al., 1990). Perhaps because MCT do not require carnitine palmitoyltransferase-1 for their transport into the mitochondria, they are more readily oxidized in the mitochondria compared to LCT, which need carnitine palmitoyltransferase-1 (Williams et al., 1968). The fast oxidation rate may partly explain the reported reduced feeding response after MCT intake compared to LCT (Friedman et al., 1990).

15.4.4. Gut Hormones

Regulation of appetite upon fat consumption has been shown to be mediated by a number of gut hormones. Administration of the CCK-A receptor antagonist loxiglumide suppressed the reduction of food intake resulting from intraduodenal fat administration; suggesting that CCK is a candidate mediator of this interaction (Matzinger et al., 2000). Duodenal fat administration in animals has been shown to result in elevated concentrations of plasma CCK (Schwartz et al., 1999). Another candidate peptide is enterostatin, which is produced from pancreatic colipase in equimolar amounts to colipase in the intestine (Erlanson-Albertsson and York, 1997). Furthermore, long-chain triglycerides have been shown to suppress plasma ghrelin (Heath et al., 2004) and stimulate secretion of CCK, GIP, neurotensin, PP, and PYY in humans (Spiller et al., 1984; Maas et al., 1998; Barbera et al., 2000) and ApoA-IV (Liu et al., 2003) in rats. PUFA stimulated the release of plasma GLP-1 in mice (Hirasawa et al., 2005).

15.4.5. Delayed Fat Digestion

Dietary fat is usually digested and absorbed in the duodenum, but if digestion and absorption of fat occurs in the distal sections of the small intestine, it stimulates a strong feedback signal associated with slowing of gastrointestinal transit and release of various satiety hormones (Read et al., 1984; Spiller et al., 1984; Welch et al., 1985; Van Citters and Lin, 1999). Infusion of corn oil into the jejunum induced early satiety and reduced energy intake in healthy volunteers compared to infusion in the duodenum (Welch et al., 1985, 1988). Furthermore, administration of a compound that retards fat digestion, by inhibiting the lipase–colipase-mediated fat hydrolysis, was associated with reduced food intake and elevated concentrations of plasma CCK and enterostatin in rats (Mei et al., 2006). Therefore, delaying fat digestion might be a promising method to enhance the satiating effect of fats and deserves further research.

15.4.6. Inhibited Fat Digestion

Products of fat digestion seem to be essential for a fat-induced satiety response. Inhibition of fat digestion by administration of a lipase inhibitor (tetrahydrolipstatin) has been shown to decrease proximal gastric relaxation (Feinle et al., 2001) and antropyloroduodenal motility (Feinle et al., 2003) resulting from intraduodenal fat administration. Furthermore, the suppression of fat breakdown modulates gut hormone release by decreasing the secretion of CCK, GLP-1, PP, and PYY and the suppression of ghrelin (Feinle et al., 2001, 2003; Feinle-Bisset et al., 2005) resulting from intraduodenal infusion of triacylglycerol. When Orlistat, a lipase inhibitor, was administered with a high-fat preload (70% fat), suppression of food intake at the next meal was prevented (Feinle et al., 2003) and the fat-induced increase in circulating neurotensin and CCK was blocked in healthy subjects (Drewe et al., 2008). These observations suggest that digestion of fats with the consequent release of free fatty acids into the small intestine is important for the effects of fat on gastrointestinal function and energy intake (Little et al., 2007).

15.4.7. Length of Small Intestine Exposed to Fat

Gastric emptying rate and intestinal transit time seem to be dependent on the length and region of small intestine exposed to dietary fats. Studies on dogs implanted with intestinal fistulae have demonstrated that regardless of the region exposed, gastric emptying was inhibited only when more than 15 cm of the small intestine was exposed to fat (sodium oleate) with the highest degree of inhibition achieved after exposure of more than 150 cm (Lin et al., 1989, 1990). However, exposure of the proximal small intestine to fat produced a stronger inhibition of gastric emptying compared to the distal small intestine (Lin et al., 1990).

Intestinal transit is inhibited by fat in both the proximal (jejunal brake) (Lin et al., 1996a) and distal gut (ileal brake) (Read et al., 1984; Spiller et al., 1984). However, contrary to gastric emptying, intestinal transit was more potently inhibited by fat in the distal than in the proximal small intestine in dogs implanted with intestinal fistulae (Lin et al., 1997). PYY has been suggested as the primary mediator of fat-induced ileal brake (Lin et al., 1996b). PYY releasing cells are located in the ileum and colon (Adrian et al., 1985; Taylor, 1985); therefore, fat in the proximal gut can release PYY indirectly via CCK (McFadden et al., 1992) or by direct stimulation of these endocrine cells in the distal small intestine (Aponte et al., 1988).

Suppression of energy intake has also been reported to be dependent on the length of small intestine exposed to fat. In rats, energy intake was decreased only when the entire small intestine was exposed to fat. Exposing only 35 cm of the jejunum to fat did not affect energy intake (Meyer et al., 1998).

15.5. CONCLUSION

In the present chapter, we tried to answer the question: Is dietary fat satiating? Within a controlled environment, yes, fats do have an effect on satiety and appear to regulate appetite through several mechanisms including the release of appetite hormones and inhibition of gastric emptying and intestinal transit. Certain types of fats are more satiating than others. However, in free-living conditions, the situation is complicated. Several genetic, psychological, and behavioral factors interact with physiological and metabolic systems on their effect on food behavior in free-living individuals. For instance, it has been found that certain individuals are genetically “immune” to the effects of a high-fat diet, suggesting that the consumption of a high-fat diet does not universally lead to weight gain. These individuals habitually consume a high-fat diet and remain lean and are therefore labeled as having “high-fat phenotypes” while others gain weight and are labeled as having “low-fat phenotypes” (Cooling and Blundell, 2001). Furthermore, in a free-living environment, the presence of highly palatable foods, a characteristic of high-fat foods, could chronically activate the hedonic system which would promote higher appetite and more energy intake (Lowe and Levine, 2005). The hedonic system is regarded as pleasure associated with eating palatable foods. In an environment with unlimited availability of highly palatable foods, there is a concern of how much the homeostatic appetite regulatory mechanisms can override the hedonic components and hyperresponsiveness to palatable foods (Blundell et al., 2005).

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