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Experience with activity based anorexia affects conditioned taste aversion in rats
Abstracts / Appetite 54 (2010) 631–683
Watching TV food commercials increases food consumption of snacks, but not meals D.A. LEVITSKY ∗ , B. WARACH, N. TRIVEDI Division of Nutritional Sciences and Department of Psychology, Cornell University, Ithaca, NY, USA Watching food commercials on television has been shown to cause an increase in food consumption. Almost all of the published work has used consumption of snacks as the dependent variable and children as subjects. We tested the generalizabilty of the finding by examining the effect of watching three, 14 min, TV commercials involving, (a) food, (b) cars, or (c) people eating, in young adults just prior to being served lunch. Fifteen males and 21 females, ages 8 to 57 volunteered for a study. Lunch was served from a buffet table and food intake was measured. No effect of watching any of the commercials on the amount consumed was observed. A very similar study using 19 females and 7 males was then performed but instead of consuming a meal, snacks were placed in front of the participants as they watched the commercials. Watching the food advertisements significantly increased intake by about 25% (p = 0.04). The results indicate that watching food advertisements increases snacking behavior in young adults and does not affect spontaneous eating of a meal when served after watching the advertisements. doi:10.1016/j.appet.2010.04.113
Experience with activity based anorexia affects conditioned taste aversion in rats N.-C. LIANG ∗ , N.T. BELLO, A.S. GUARDA, T.H. MORAN Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA Activity based anorexia (ABA) is a model of anorexia nervosa (AN). In this model, rats reduce food intake and lose weight dramatically as a result of enhanced running wheel (RW) activity during conditions of restricted food access. The aim of this study was to investigate whether ABA alters food reward. We compared the acquisition and extinction of a conditioned taste aversion (CTA) in naive (ad lib with no access to RW), ABA, and pair-fed to ABA (with access to a locked RW) in female Sprague–Dawley rats. The CTA conditioning was conducted after the ABA and pair-fed rats had recovered to pre-ABA body weights. There was no difference in the rate of a CTA acquisition to 0.3 M sucrose paired with low dose LiCl (0.009 M and 0.018 M at 1.33 ml/100 g of body weight, i.p.). However, ABA rats suppressed sucrose intake more than the controls. After 10 conditioning trials, 67% ABA rats completely avoided the sucrose while 43% naive and 20% pair-fed rats showed the same degree of aversion. When extinction was assessed by 1-bottle tests, the ABA rats tended to extinguish more slowly. The results of 2 bottle tests (sucrose and water simultaneously) confirmed that the ABA rats recovered their reference for sucrose more slowly than the pair-fed (p < 0.007) and naive (p = 0.06) controls. These data suggest that experience with AN-like symptoms could cause a devaluation of food reward thereby affecting the strength of CTA learning and retention. Supported by NIH grant DK19302. doi:10.1016/j.appet.2010.04.114
657
Imaging glucose-induced gut-to-brain signalling pathways in humans. Role of the CCK1 receptor T.J. LITTLE ∗ , S. MCKIE, R.B. JONES, N. ASTBURY, M. D’AMATO Glucose inhibits neuronal activity in the hypothalamus, measured as a decrease in Blood Oxygenation Level-Dependent (BOLD) signal using magnetic resonance imaging (phMRI). However, the signalling pathway by which glucose exerts this effect is unclear. This study determined the effects of glucose on BOLD signal over the whole brain, and whether the effects of glucose on CNS activity are mediated by the CCK1 receptor. The CNS responses to intragastrically administered 1 M glucose or 0.9% saline were studied in 12 healthy subjects on 3 occasions in a blinded, randomised fashion using phMRI. Blood glucose levels and subjective appetite perceptions were also assessed. The experiment was conducted with and without the CCK1 receptor antagonist dexloxiglumide (600 mg orally). We identified that glucose modulated BOLD signal in the same brainstem and hypothalamic areas that we had previously demonstrated in response to lipid. However, in contrast to our previous results with lipid, glucose decreased, rather than increased, BOLD signal, suggesting neuronal inhibition. This effect of glucose was blocked by pre-treatment with dexloxiglumide. There was no effect of treatment on appetite perceptions. Blood glucose levels were higher, and equivalent, during glucose and glucose + dexloxiglumide conditions when compared with saline (P < 0.05). We have identified that glucose activates a CCK-mediated gut-brain activation matrix. Changes in BOLD signal appeared independent of changes in blood glucose concentrations. doi:10.1016/j.appet.2010.04.115
Effects of fat on appetite and energy intake in humans T.J. LITTLE University of Adelaide Discipline of Medicine, Adelaide, Australia There is a strong positive relationship between the intake of dietary fat with total energy intake and body weight. Dietary fat contributes to overeating hence recommendations for reduced dietary fat intake as a first line treatment for obesity. However, the sensing of dietary fat, and particularly of free fatty acids, by receptors in the tongue and intestine induces potent effects on gastrointestinal motility and gut peptide secretion that favour suppression of hunger and energy intake. In humans, oral hyposensitivity to fatty acids has been associated with higher energy intake and body mass index suggesting that impairment of fat taste sensing mechanisms may contribute to overeating and obesity. Furthermore, while in humans small intestinal triglycerides modulate gastrointestinal motility, stimulate gastrointestinal hormone release, including cholecystokinin (CCK) and peptide YY (PYY) and suppress subsequent energy intake; recent data from our lab indicate that these effects of fat are attenuated in individuals with reduced oral sensitivity to fat, and following consumption of a highfat diet. This presentation will focus on emerging aspects of fat sensing in both the tongue, and the intestine, and the physiological mechanisms induced by dietary fat which may mediate dietary fat preference, satiation and satiety. A particular focus will be on the translational aspects of this research for the treatment of obesity. doi:10.1016/j.appet.2010.04.116
Watching TV food commercials increases food consumption of snacks, but not meals D.A. LEVITSKY ∗ , B. WARACH, N. TRIVEDI Division of Nutritional Sciences and Department of Psychology, Cornell University, Ithaca, NY, USA Watching food commercials on television has been shown to cause an increase in food consumption. Almost all of the published work has used consumption of snacks as the dependent variable and children as subjects. We tested the generalizabilty of the finding by examining the effect of watching three, 14 min, TV commercials involving, (a) food, (b) cars, or (c) people eating, in young adults just prior to being served lunch. Fifteen males and 21 females, ages 8 to 57 volunteered for a study. Lunch was served from a buffet table and food intake was measured. No effect of watching any of the commercials on the amount consumed was observed. A very similar study using 19 females and 7 males was then performed but instead of consuming a meal, snacks were placed in front of the participants as they watched the commercials. Watching the food advertisements significantly increased intake by about 25% (p = 0.04). The results indicate that watching food advertisements increases snacking behavior in young adults and does not affect spontaneous eating of a meal when served after watching the advertisements. doi:10.1016/j.appet.2010.04.113
Experience with activity based anorexia affects conditioned taste aversion in rats N.-C. LIANG ∗ , N.T. BELLO, A.S. GUARDA, T.H. MORAN Department of Psychiatry and Behavioral Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA Activity based anorexia (ABA) is a model of anorexia nervosa (AN). In this model, rats reduce food intake and lose weight dramatically as a result of enhanced running wheel (RW) activity during conditions of restricted food access. The aim of this study was to investigate whether ABA alters food reward. We compared the acquisition and extinction of a conditioned taste aversion (CTA) in naive (ad lib with no access to RW), ABA, and pair-fed to ABA (with access to a locked RW) in female Sprague–Dawley rats. The CTA conditioning was conducted after the ABA and pair-fed rats had recovered to pre-ABA body weights. There was no difference in the rate of a CTA acquisition to 0.3 M sucrose paired with low dose LiCl (0.009 M and 0.018 M at 1.33 ml/100 g of body weight, i.p.). However, ABA rats suppressed sucrose intake more than the controls. After 10 conditioning trials, 67% ABA rats completely avoided the sucrose while 43% naive and 20% pair-fed rats showed the same degree of aversion. When extinction was assessed by 1-bottle tests, the ABA rats tended to extinguish more slowly. The results of 2 bottle tests (sucrose and water simultaneously) confirmed that the ABA rats recovered their reference for sucrose more slowly than the pair-fed (p < 0.007) and naive (p = 0.06) controls. These data suggest that experience with AN-like symptoms could cause a devaluation of food reward thereby affecting the strength of CTA learning and retention. Supported by NIH grant DK19302. doi:10.1016/j.appet.2010.04.114
657
Imaging glucose-induced gut-to-brain signalling pathways in humans. Role of the CCK1 receptor T.J. LITTLE ∗ , S. MCKIE, R.B. JONES, N. ASTBURY, M. D’AMATO Glucose inhibits neuronal activity in the hypothalamus, measured as a decrease in Blood Oxygenation Level-Dependent (BOLD) signal using magnetic resonance imaging (phMRI). However, the signalling pathway by which glucose exerts this effect is unclear. This study determined the effects of glucose on BOLD signal over the whole brain, and whether the effects of glucose on CNS activity are mediated by the CCK1 receptor. The CNS responses to intragastrically administered 1 M glucose or 0.9% saline were studied in 12 healthy subjects on 3 occasions in a blinded, randomised fashion using phMRI. Blood glucose levels and subjective appetite perceptions were also assessed. The experiment was conducted with and without the CCK1 receptor antagonist dexloxiglumide (600 mg orally). We identified that glucose modulated BOLD signal in the same brainstem and hypothalamic areas that we had previously demonstrated in response to lipid. However, in contrast to our previous results with lipid, glucose decreased, rather than increased, BOLD signal, suggesting neuronal inhibition. This effect of glucose was blocked by pre-treatment with dexloxiglumide. There was no effect of treatment on appetite perceptions. Blood glucose levels were higher, and equivalent, during glucose and glucose + dexloxiglumide conditions when compared with saline (P < 0.05). We have identified that glucose activates a CCK-mediated gut-brain activation matrix. Changes in BOLD signal appeared independent of changes in blood glucose concentrations. doi:10.1016/j.appet.2010.04.115
Effects of fat on appetite and energy intake in humans T.J. LITTLE University of Adelaide Discipline of Medicine, Adelaide, Australia There is a strong positive relationship between the intake of dietary fat with total energy intake and body weight. Dietary fat contributes to overeating hence recommendations for reduced dietary fat intake as a first line treatment for obesity. However, the sensing of dietary fat, and particularly of free fatty acids, by receptors in the tongue and intestine induces potent effects on gastrointestinal motility and gut peptide secretion that favour suppression of hunger and energy intake. In humans, oral hyposensitivity to fatty acids has been associated with higher energy intake and body mass index suggesting that impairment of fat taste sensing mechanisms may contribute to overeating and obesity. Furthermore, while in humans small intestinal triglycerides modulate gastrointestinal motility, stimulate gastrointestinal hormone release, including cholecystokinin (CCK) and peptide YY (PYY) and suppress subsequent energy intake; recent data from our lab indicate that these effects of fat are attenuated in individuals with reduced oral sensitivity to fat, and following consumption of a highfat diet. This presentation will focus on emerging aspects of fat sensing in both the tongue, and the intestine, and the physiological mechanisms induced by dietary fat which may mediate dietary fat preference, satiation and satiety. A particular focus will be on the translational aspects of this research for the treatment of obesity. doi:10.1016/j.appet.2010.04.116