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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 5Peripheral Gustatory Processing of Free Fatty Acids

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It is well known that obesity is a major health problem, with approximately 66% of adults in the United States considered overweight and more than 1 billion overweight adults worldwide (Ogden et al., 2006) (World Health Organization). In addition to the impact on the joints and bones caused by increased body mass, obesity can also lead to heart disease, hypertension, diabetes, and stroke (Wong and Marwick, 2007). Given the severity and consequences of these conditions, it is not surprising that there is a large body of research exploring factors that contribute to the development of obesity, including diet and, more specifically, the proportion of certain foods in the diet.

Vilified in the media as “Public Enemy Number One in the Battle of the Bulge,” dietary fat, and in particular the over consumption of fat, is considered by many to be the greatest contributing factor to obesity. Yet, is fat the enemy? Clearly, high fat ingestion, along with lack of exercise, has the potential to negatively impact a healthy lifestyle. At the same time, however, fats are critical for many biological processes.

As the lipid bilayer of cells, fat is a building block for life and, in the form of myelin, enables fast electrical communication between neurons. Fat provides insulation that helps conserve body heat in cold climates and also can protect organs, like those necessary for reproduction, from damage. Fats and the main component of fats, free fatty acids, are essential for the growth and development of vital organs, including the brain (Spector, 2001). Clearly, fat is crucial for life, yet the body cannot synthesize certain kinds of fats. Rather, these fats are obtained from ingested food. Thus, the ability to detect certain kinds of fat in food sources is necessary for survival.

Fortunately, there is strong motivation to find and subsequently consume fat because fat is preferred by many animals, including humans. What is it about fat that is so alluring? In the past, the palatability of fat was thought to be the result of smell and/or texture. For example, impairment of the ability to smell (either by bilateral transection of the olfactory nerve or by destruction of the olfactory mucosa with ZnSO4) eliminates the preference for high-fat foods in mice (Mela, 1988; Kinney and Antill, 1996). Moreover, increasing the texture of low-fat dairy products also increases the perceived fat content. Interestingly, sensitivity to the texture of fat seems to be related to the number of functional taste buds on the tongue, as people with the greatest number of taste buds (i.e., so-called “super tasters”) are the best at discriminating between solutions with varying fat contents (Bartoshuk et al., 1994). Moreover, there are even cells in a specialized primate brain area called the orbitofrontal cortex that respond only to the texture of fats (Verhagen et al., 2003). Clearly, smell and texture are important for fat perception.

However, rats can discriminate between different kinds of oils that, presumably, have a similar texture and continue to prefer fat solutions when texture and smell are minimized in behavioral tests (Larue, 1978; Fukuwatari et al., 2003). Furthermore, ingested fats are rapidly (within 1–5 s) broken down into free fatty acids in the oral cavity by lingual lipase (Kawai and Fushiki, 2003). In fact, rats have a robust preference for free fatty acids; however, prevention of the breakdown of fats into free fatty acids by the addition of a lingual lipase inhibitor greatly reduces rats’ preference for fat solutions. Thus, fat and in particular the building blocks of fats—free fatty acids—have a taste component that plays a strong role in our fat preference.


Free fatty acids are organized into three broad categories with respect to their saturation degree: (1) monounsaturated, (2) polyunsaturated, and (3) saturated. Monounsaturated free fatty acids, such as oleic acid and palmitoleic acid, and polyunsaturated free fatty acids, including linoleic acid (LA) and arachidonic acid, together are classified as essential free fatty acids—such named because these fats are not synthesized by the body, but rather must be obtained from the foods we eat. On the other hand, saturated free fatty acids (such as lauric acid and stearic acid) are easily made by the body and, thus, do not need to be consumed (Galli and Patrizia, 2006). Therefore, the body must discriminate between different types of free fatty acids in order to detect, and subsequently consume unsaturated, essential free fatty acids.

In fact, it appears that the taste of free fatty acids may be important for this discrimination because essential free fatty acids act on taste cells by inhibiting delayed rectifying potassium channels (Gilbertson, 1998; Gilbertson et al., 1998); nonessential free fatty acids do not. These potassium channels are important because they are responsible for bringing taste cells back to resting state after activation (Chen et al., 1996). However, the effect of this inhibition on taste processing and perception remains not fully understood (see Section 5.7).


Although there are many essential free fatty acids, gustatory processing of LA is the most studied of all. One reason that LA is the focus of so much taste research is because, as the main component of corn oil, this polyunsaturated essential free fatty acid is a large component of the American diet (e.g., fried foods, baked goods, etc.). Surprisingly, little is known about whether and how the gustatory system detects LA. In fact, do animals (including humans) use their taste receptors to respond to and consume LA?

Historically, taste perception has been studied since the time of the ancient Greeks when Aristotle first described taste as a form of touch—thus called because taste molecules must directly act on (i.e., “touch”) taste receptors in the tongue (Johansen, 1997). In modern times, the advancement of technology led to a sundry of ways to explore taste perception in depth, including the development of ways to measure the detection threshold for tastes, such as LA. One way to measure the detection threshold for LA is by using a conditioned taste aversion design, which has the advantage of being comparatively straightforward to administer and requiring little animal training as compared to other training—intensive behavioral paradigms, such as conditioned shock avoidance (Spector et al., 1995). In a conditioned taste aversion protocol, rats are placed on a water restriction schedule that gradually gives them access to 10 min of water in the morning (training) and 30 min of water in the afternoon daily. Once they drink reliable quantities of deionized water (≥7 mL) in the 10 min training sessions, all rats are given 88 μM LA in a graduated drinking tube (conditioning day). After 10 min, fluid intake is recorded and half of the rats are then injected with lithium chloride (LiCl) and the other half are injected with physiological saline.

Rats injected with LiCl experience general malaise (i.e., feel “sick”) and associate this with the taste of LA. Thus, these animals will not consume LA solutions in which they can taste LA. Rats are given a 10 min two-bottle preference test between water and 88 μM LA to verify that the LiCl-treated animals developed a conditioned aversion to LA. The generalization of the conditioned aversion to less concentrated LA solutions (44, 22, 11, and 5.5 μM) is tested using additional two-bottle (LA and water) tests. During these generalization tests, one LA concentration is given each day with presentation in descending order of concentration. Preference scores are calculated as intake of LA/total fluid intake. A preference score of 0.5 indicates that animals consumed equal amounts of both solutions and preference scores >0.5 indicate that animals consumed more LA than water; whereas preference scores <0.5 indicate that animals consumed less LA than water. The point at which LiCl-treated animals consume significant amounts of LA, suggests that these animals cannot detect LA at this concentration and, thus, indicates the approximate LA detection threshold. To ensure that the results obtained do not reflect an extinction of the conditioned aversion, the aversion to 88 μM LA is again assessed after the final day of generalization testing. Using this procedure Stratford et al. (2006) found that the LA detection threshold is ~11 μM LA (Figure 5.1, top). It is important to note that, olfaction and texture were not explicitly controlled in this experiment, suggesting that these sensory attributes may contribute to LA detection in this protocol. However, this is unlikely because free fatty acids have minimal viscosity (McCormack et al., 2006) and impairment of the ability to smell by removal of the olfactory bulbs does not prevent the discrimination of free fatty acids even at very low concentrations (Smith, 2004).

FIGURE 5.1. LA taste discrimination threshold by CT-intact (a) and CTX (b) male rats.


LA taste discrimination threshold by CT-intact (a) and CTX (b) male rats. Open circles, NaCl treated closed squares, LiCl-treated. (*) LiCl treated significantly different from NaCl treated (p < 0.05). Black boxes indicate the approximate LA taste (more...)


Clearly, rats are able to develop a conditioned aversion to LA and generalize this aversion to weaker LA concentrations until they reach a concentration they no longer can detect. However, if LA’s taste is indeed its salient component, through what neural pathways is this information transmitted from chemoreceptors on the tongue to the brain? Three sensory nerves carry information about taste from the tongue and palate to the brain. Specifically, two gustatory branches of the facial nerve, the chorda tympani (CT) and the greater superficial petrosal nerves, innervate chemoreceptors on the anterior 2/3 of the tongue and palate, respectively. The glossopharyngeal nerve innervates taste receptors on the posterior 1/3 of the tongue. Together, these nerves convey different sensory information about taste quality from the tongue and palate (Frank and Pfaffmann, 1969; Krimm et al., 1987; Frank, 1991; St John and Spector, 1996) to the nucleus of the solitary tract, located in the hindbrain which then relays this information to higher brain areas such as the parabrachial nucleus, thalamic taste area, and gustatory cortex (Norgren and Leonard, 1973; Norgren, 1976; Norgren et al., 1989).

5.4.1. Role of the Glossopharyngeal and Greater Superficial Petrosal Nerves in Linoleic Acid Taste Processing

Based on numerous factors, the glossopharyngeal nerve appears to be ideally suited to transmit fat taste information from chemoreceptors to the brain. First, lingual lipase (the enzyme that breaks triglycerides into free fatty acids in the mouth) is secreted by the von Ebner’s glands found within circumvallate papillae in the back of the tongue. Second, CD36 (a fatty acid transporter/translocase) is highly expressed in circumvallate papillae which are also located in the back part of the tongue and are innervated by the glossopharyngeal nerve (Doty, 2003; Laugerette et al., 2005). However, little is known about the role of the glossopharyngeal nerve in free fatty acid recognition. For example, bilateral transection of the glossopharyngeal nerve impairs the ability of mice to discriminate 2% LA from a control solution, using a 30 min, conditioned aversion two-bottle choice test (Gaillard et al., 2008). Unfortunately, this is the only behavioral study conducted so far and there has been only one electrophysiological investigation exploring the role of the glossopharyngeal nerve in fat taste. Kitagawa et al., 2007, found that the pharyngeal branch of the glossopharyngeal nerve responds to oleic acid ~20 times better than it does to safflower oil (an oil rich in LA). However, this branch of the glossopharyngeal nerve innervates receptors in the pharynx that are most likely important for the control of reflexes, rather than for the identification of taste stimuli (Kitagawa et al., 2007). To date, no study has explored the effect of transection of the pharyngeal branch of the glossopharyngeal nerve on LA detection. Moreover, no one has conducted an electrophysiological study of the LA responses of the lingual (gustatory) branch of the glossopharyngeal nerve that innervates the chemoreceptors located in the circumvallate papillae on the posterior tongue. Finally, the role of the greater superficial petrosal nerve in free fatty acid taste sensitivity has not been explored.

5.4.2. Role of the Chorda Tympani in Linoleic Acid Taste Processing Behavioral Studies

There is strong evidence that the CT is important for fat taste detection, focusing primarily on the polyunsaturated free fatty acid, LA. Using a conditioned aversion protocol (see 5.3), two recent studies found that the detection threshold for LA is ~10 μM (Figure 5.1A), but that bilateral transection of the CT (CTX) prior to development of a LA conditioned aversion prevents rats from discriminating LA from water at concentrations more dilute than 44 μM (Figure 5.1B) (Stratford et al., 2006; Pittman et al., 2007). Thus, these two nerve cut experiments indicate that the CT is important for LA detection. Importantly, transection of the CT does not completely eliminate the ability to detect LA, suggesting that other gustatory nerves are also involved or that rats can detect LA using sensory attributes other than taste (i.e., texture or smell). However, the latter two possibilities are unlikely because free fatty acids have a minimal viscosity (only about 1.5% greater than that of water) and little smell as bulbectomized rats can discriminate LA even at 10 μM (Smith, 2004; McCormack et al., 2006). Electrophysiological Studies

Removal of sensory input by CTX suggests that the CT is important for the detection of LA, but does not provide the resolution to determine what kind of information the CT carries. One approach to address this question is to record electrophysiological responses from the CT of anesthetized rats in response to LA stimulation of the tongue. By using a solenoid fluid delivery system that delivers taste solutions at a constant flow rate of 50 μL/s, this approximates the fluid volume consumed by a rat licking from a drinking spout obtaining ~5–7 μL/lick at a rate of 6–7 licks/s (Lundy and Contreras, 1999). A custom computer program controls input to a mixing platform that allows rapid switching and/or mixing while maintaining continuous solution flow. Between stimuli, the tongue is continuously rinsed to minimize transient thermal or tactile responses and each taste stimulus is followed by a 90 s rinse to ensure that nerve activity returns to stable baseline levels.

Surprisingly, application of LA to the tongue does not produce a detectable CT response (Figure 5.2). Moreover, individual neurons in the geniculate ganglion (the location of the cell bodies of chorda tympani gustatory sensory neurons) are also unresponsive to LA stimulation (Breza et al., 2007). What could account for this discrepancy? LA detection may depend upon the interaction of multiple gustatory sensory nerves. This is supported by the fact that removal of CT sensory input does not completely prevent the detection of LA (Figure 5.1B). However, the role of other gustatory nerves—individually or in combination—in LA detection remains unknown.

FIGURE 5.2. CT whole nerve activity (μV) in response to lingual application of LA (11, 22, 44, and 88 μM).


CT whole nerve activity (μV) in response to lingual application of LA (11, 22, 44, and 88 μM). Gray, raw nerve activity; black, integrated, rectified activity.


An intriguing possibility is that fat is not an effective taste stimulus when presented alone. Rather, fat is a taste stimulus only when there is an “active background,” such as in the presence of saliva in the mouth. Importantly, this could explain the discrepancy between behavioral CTX data (in which saliva is present) and electrophysiological data (in which saliva is washed off during rinses). Moreover, CTX secondarily results in a decrease in saliva (via denervation of the submaxillary and sublingual salivary glands). Thus, impairment of LA taste discrimination seen after CTX (see Sections 5.4.2 and may result from transection of the chorda tympani nerve itself, a secondary decrease in saliva, or both. What in saliva could be important for LA taste processing? Saliva is made of a large number of proteins, ions (e.g., K+ and Cl) and enzymes (Hart, 1998). Thus, at present it is unknown what component of saliva may be important for LA taste processing, but ongoing studies are addressing this idea.


If LA taste processing requires the action of another stimulus, such as saliva, this suggests that fats may also exert a powerful influence by complementing, modulating, or enhancing other taste stimuli as well. Indeed, work in isolated taste cells shows that essential unsaturated free fatty acids, but not saturated free fatty acids, inhibit delayed rectifying potassium channels (Gilbertson et al., 1998, 2005). This inhibition presumably leads to a broadening of action potentials and prolongation of the release of neurotransmitters. Thus, unsaturated free fatty acids may increase the perceived intensity of other taste stimuli. In this regard, the addition of LA increases both licking responses to sucrose (Pittman et al., 2006; Stratford et al., 2006) as well as the preference for monosodium glutamate (MSG), especially at lower (40 and 100 mM) concentrations in behavioral studies (Stratford et al., 2008).

These behavioral results are further supported by recent electrophysiological experiments which found that the addition of LA increases CT responses to MSG (Figure 5.3). Importantly, this enhancement occurs at the same MSG concentration whose preference is also increased by LA (i.e., 40 and 100 mM). Because MSG is generally preferred—especially at lower concentrations—it is likely that LA increases the behavioral preference for MSG, in part, by increasing the intensity of MSG. However, whether the effects seen by coapplication of MSG and LA are specific to MSG (or one of its components), or rather, reflects a global enhancement of taste by fats, remains unexplored.

FIGURE 5.3. CT whole nerve activity in response to lingual application of monosodium glutamate MSG (40, 100, and 300 mM) mixed with water (left) or 88 μM LA (right) in a male rat.


CT whole nerve activity in response to lingual application of monosodium glutamate MSG (40, 100, and 300 mM) mixed with water (left) or 88 μM LA (right) in a male rat. Gray, raw nerve activity; black, integrated, rectified activity. Percentages (more...)


Given these diverse results, the obvious question is whether free fatty acids such as LA have their own taste or, rather, only increase the intensity of other tastes. In other words, is LA simply a flavor enhancer? Although LA increases behavioral preference for some taste stimuli, fatty acids do not enhance responses to taste stimuli in all conditions. For example, LA increases licking to sucrose and glucose, but decreases licking to sodium chloride, citric acid, and quinine hydrochloride solutions in rats (Pittman et al., 2006). In humans, the addition of 1% LA significantly decreases the intensity of sodium chloride, citric acid, and caffeine, but does not change intensity perceptions of sweet and sour solutions (Mattes, 2007). Thus, it remains unclear whether LA either (1) requires the action of other taste stimuli to have a behavioral effect, but has its own taste quality, (2) increases only the perception and/or intensity of other taste stimuli, or (3) perhaps, fulfills both roles in certain situations.

An intriguing idea first proposed by Laugerette et al. (2007) suggests that free fatty acids play different roles depending on which part of the tongue they stimulate. Free fatty acids may enhance the intensity of other taste stimuli via taste-free fatty acid interactions on the anterior part of the tongue (as seen in regard to the CT). However, free fatty acids may also directly activate the gustatory system to produce their own “fatty” taste in the posterior oral cavity. In support of this latter idea, free fatty acid stimulation of circumvallate papillae in the back part of the tongue results in increased intracellular Ca2+ as well as neurotransmitter release (El-Yassimi et al., 2008). Moreover, these effects may depend on the fatty acid transporter/translocase, CD36, which is highly expressed in circumvallate papillae, as inactivation of the CD36 gene abolishes the preference for free fatty acids in mice (Laugerette et al., 2005).

On the other hand, CD36 is not present in CT-innervated fungiform papillae (Laugerette et al., 2005). Moreover, stimulation of the tongue with LA alone neither activates the CT (Figure 5.2) nor the geniculate ganglion (Breza et al., 2007). However, LA does increase CT responses to MSG (Figure 5.3). Moreover, the addition of LA (but not the saturated free fatty acid, lauric acid) to a subthreshold saccharine concentration makes saccharine detectable (Gilbertson et al., 2005). Furthermore, unsaturated free fatty acids inhibit delayed rectifying potassium channels in the taste cells of fungiform papillae, as mentioned previously, (Gilbertson et al., 1998), which presumably broadens action potentials and prolongs neurotransmitter release.


To complicate this issue further, there are sex differences in the detection of LA. Female rats discriminate a weaker (more dilute) concentration of LA from water than can male rats (i.e., ~2.75 vs. 11 μM LA; Figure 5.4a). In addition, female rats also increase their licking to a lower concentration of LA when it is mixed with sucrose as compared to males (Stratford et al., 2006). Moreover, CTX impairs LA taste discrimination in female rats and in fact shifts the discrimination threshold to the same LA concentration as observed after CTX in male rats (Figure 5.4b). However, because females have a lower LA taste discrimination threshold, the magnitude of the shift seen after CTX is greater in females. Together, these results suggest that the CT is important for LA taste discrimination in both male and female rats, but that the CT may play a greater role in LA taste discrimination and fat taste responses by females.

FIGURE 5.4. Sex differences in LA taste discrimination thresholds.


Sex differences in LA taste discrimination thresholds. (a) LA taste discrimination threshold by CT-intact female rats. Open circles, NaCl treated; closed squares, LiCl treated. Solid lined black box indicates the approximate LA taste discrimination threshold (more...)

To explore further sex differences in fat taste, Stratford et al. (2008) first recorded electrophysiological responses from the CT in response to application of LA to the tongue of anesthetized rats. Similar to the effect seen in male rats, the CT was unresponsive to LA stimulation (Stratford et al., 2006). Moreover, the addition of LA increased CT responses to MSG (Stratford et al., 2008). However, LA increased CT responses to 100 mM MSG in females only (Figure 5.5); whereas it increased CT responses to 40 and 100 mM MSG in males (Figure 5.4). More strikingly, data collected from behavioral preference tests paralleled these results (i.e., LA increased the preference for 100 mM MSG only in females, but increased the preference for 40 and 100 mM MSG in males) (Stratford et al., 2008).

FIGURE 5.5. CT whole nerve activity in response to lingual application of monosodium glutamate MSG (40, 100, and 300 mM) mixed with water (left) or 88 μM LA (right) in a female rat.


CT whole nerve activity in response to lingual application of monosodium glutamate MSG (40, 100, and 300 mM) mixed with water (left) or 88 μM LA (right) in a female rat. Gray, raw nerve activity; black, integrated, rectified activity. Percentage (more...)

These results are perplexing: females appear to have a lower LA detection threshold and are more sensitive to LA when it is mixed with sucrose, but are less sensitive to LA mixed with MSG than males. A simple explanation is that sex differences in fat taste may depend on the taste stimulus with which the fat is mixed. For instance, males prefer MSG solutions at lower concentrations than do females, which could explain why LA increases CT responses to and behavioral preference for MSG at a lower concentration in males than in females (Hiji and Masayasu, 1967; Ohara and Naim, 1977). On the other hand, females have a greater preference for sucrose than do males, which may result in females increasing their licking to a lower LA–sucrose concentration than do males. However, what could account for observed sex differences in the detection of LA when it is mixed “alone?” If saliva is important for LA taste processing (see Section 5.5), sex differences in LA detection may be the result of sex differences in the detection of one of the components of saliva. In this regard, there are sex differences in the detection of sodium, as females detect lower concentrations of NaCl than do male rats (Curtis and Contreras, 2006). Thus, sex differences in the detection of LA may result from sex differences in salivary sodium. Moreover, how and to what extent this differing sensitivity to fats affects the perception and subsequent ingestion of other tastes and foods remains unknown.

What evolutionary function could an enhanced sensitivity to certain kinds of fatty foods (such as “sweet-fats”) for females serve? It is well known that many evolutionary adaptations promote reproduction, in part, by optimizing survival of the offspring. For example, enhanced sensitivity to environmental stimuli during pregnancy may improve the ability to detect resources necessary to support a viable pregnancy. In this regard, energy dense foods such as fats are essential to good maternal health during pregnancy (Decsi and Koletzko, 2005; Facchinetti et al., 2005). Thus, the detection of fat may have intrinsic survival value and, in fact, preferences for fats increase during pregnancy. However, although estrogen levels change during pregnancy, it appears that sex differences in LA taste responses is not the result of acute estrogen effects, as estradiol benozoate treatment of ovariectomized rats does not alter licking responses to sucrose–LA mixtures (Stratford et al., 2006). The role of other reproductive hormones (i.e., testosterone and progesterone)—alone or in combination—remains unexplored. Moreover, estrogen may still play a role in sex differences in LA taste responses during the development of the gustatory system. Finally, sex differences in peripheral input do not preclude the possibility of sex differences in the central processing of LA-taste mixtures as well.


The field of fat taste is still in its infancy and, as such, much is left unexplored. Several ground-breaking discoveries provided important insight into not only how fat taste information travels from the tongue to the brain, but also what the nature of this sensory information may be. Fat taste detection begins with the initial break down of fat into free fatty acids in the mouth. In turn, free fatty acids, especially the essential unsaturated free fatty acid linoleic acid, activate gustatory receptor cells on the tongue. Moreover, both the glossopharyngeal nerve and the chorda tympani nerve are involved in free fatty acid detection. Yet, the nature of this information remains the subject of debate and may be dependent upon which part of the tongue is stimulated by free fatty acids. Finally, there are sex differences in both behavioral responses and electrophysiological responses to free fatty acids. However, the mechanisms that underlie these differences remain unknown.

More importantly, the implications for this research are far-reaching as taste plays a significant role in food choices. Given the obesity epidemic that many industrialized nations currently face, it is essential to understand and explore every factor that could contribute to the development of this chronic and debilitating disease, including the taste of fat. However, obesity is certainly a multidimensional disorder, which requires a corresponding multifaceted treatment plan. Thus, the future of fat taste research relies on the ability to integrate current and future findings into existing obesity treatments.


This chapter is the culmination of a decade’s worth of work. As such, many people contributed to the ideas presented. First, we thank those whose work is presented in this chapter for having the courage to explore interesting questions. We wish you well in all future endeavors. Second, we also thank Dr. Kath Curtis for encouraging the exploration of sex differences in fat taste, which led to many interesting and unexpected discoveries. Finally, we extend a special note of thanks to Dr. Jim Smith for his pioneering work on fat taste at Florida State University as well as providing useful comments on this book chapter. We are indebted to him for all he has done and continues to do. The National Institute on Deafness and Communication Disorders of the NIH supported this research (DC-004785, DC-00044, and DC-008934).


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Bookshelf ID: NBK53553PMID: 21452479


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