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Viscosity and sweet taste as determinants of caloric compensation in rats
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T.H. Moran / Appetite 51 (2010) 350–412
Mercaptoacetate (MA) stimulates feeding after infusion into the hepatic portal vein (HPV) or vena cava (VC), but not after infusion into the descending aorta A. MANSOURI ∗ , M. ARNOLD, N. GEARY, M. LEONHARDT, W. LANGHANS. Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Zurich, Switzerland
Viscosity and sweet taste as determinants of caloric compensation in rats A.A. MARTIN ∗ , J.J. FIELDS, M.A. WATERS, R.C. KENNEDY, S.E. SWITHERS, T.L. DAVIDSON. Department of Psychological Sciences and the Ingestive Behavior Research Center, Purdue University, West Lafayette, USA
Intraperitoneal injections of mercaptoacetate (MA) inhibit hepatic fatty acid oxidation and stimulate feeding. Abdominal vagal afferents mediate the feeding-stimulatory effect of MA, but it is unclear where in the abdomen this effect originates. We addressed this question by assessing the feeding-stimulatory effects of MA infusions into the hepatic portal vein (HPV), the vena cava (VC), and the descending aorta near the beginning of the celiac artery (NCA). In separate experiments, ad lib-fed male Sprague–Dawley rats (>400 g body weight (BW)) received HPV, VC, or HPV vs. NCA infusions (40 l/min) of MA (45.6 mg/kg; 15 mM) or saline in the middle of the light phase. Food intake was measured for 12 h. MA stimulated feeding similarly after HPV and VC infusions, but had not effect on feeding after NCA infusion. To our knowledge, this is the first report of a stimulation of feeding after intravenous MA infusion in rats. The data do not disclose the origin of MA’s feeding-stimulatory effect, but suggest that MA does not increase food intake by acting either in the liver or in the intestine. doi:10.1016/j.appet.2008.04.157
Energy and weight regulation depend, in part, on an animal’s ability to compensate for excess calories consumed on one occasion by decreasing energy intake at another time. Recent research suggests that this type of caloric compensation may be strongly influenced by the orosensory properties of foods. For example, compensation is usually weaker following consumption of low viscosity than high viscosity foods. Similarly, rats exposed to sweet taste paired occasionally without calories eat more food after consuming a sweet, high calorie premeal than rats only exposed to sweet taste paired with calories. Thus, both viscosity and sweet taste can influence compensatory ability when tested separately. However, it is unknown how these cues determine compensation when both are presented simultaneously. We investigated this interaction using adult, male Sprague–Dawley rats in a standard preload test paradigm. Animals received 10 g, equicaloric, premeals that factorially combined high and low viscosity with sweet and bland taste, and amount of lab chow eaten during a subsequent test meal was measured. Weaker caloric compensation was found following low compared to high viscosity premeals independent of sweet taste. A follow up study that manipulated prior experience with sweet taste, viscosity, and calories did not abolish the effects of viscosity on caloric compensation. These data suggest that the effects of viscosity on caloric compensation may occur independently of variations in sweet taste. doi:10.1016/j.appet.2008.04.159
Hyperphagia-induced obesity in young male and female OLETF rats: A developmental study A. MARCO 1,∗ , M. SCHROEDER 1 , L. SHBIRO 1 , T.H. MORAN 2 , A. WELLER 1 . 1 Bar-Ilan University, Ramat-Gan, Israel 2 Johns Hopkins University, Baltimore, USA OLETF rats lack the expression of functional CCK1 receptors and are a model of hyperphagia-induced obesity used to study the early origins and neurobiology of obesity. OLETF pups are heavier than LETO controls from birth and develop pre-obese characteristics early in life. In the present study, we aimed to examine the development of young males and females towards obesity. Rats were weighed every 5th day from the time of weaning, intake was assessed daily and feeding efficiency was calculated. Animals were sacrificed at four different time-points: weaning (postnatal day [PND] 22), PND 38, 65 and 90. Blood plasma was collected for leptin analysis. Brown, retroperitoneal, inguinal and epididymal fat pads were collected and weighed. Adipocyte cell size was assessed from the inguinal fat pad. The estrous cycle of the females was monitored from PND 40 until PND 75. Patterns of intake and sugar preference were measured at critical times. Results show pre-obese characteristics in the OLETF strain since childhood and appear to show a specific time-point at PND 65 where obesity sharply increases. The high and sudden accumulation of white fats observed here in both sexes are accompanied by hypertrophic adipocyte development and very high leptin levels. While intake was about 30–40% higher in the OLETF strain, the feeding efficiency did not differ between the strains, further suggesting that obesity in this strain develops following life-long abnormalities in eating behavior and not as a consequence of a metabolic disorder. Acknowledgment: Support: US-Israel BSF. doi:10.1016/j.appet.2008.04.158
Blocking of branch chain amino acid metabolism decreases hypothalamic POMC and increases AgRP expression in mice on a low fat diet R.J. MARTIN 1,2,∗ , S. LI 1 , J. ZHOU 1 , C.D. MORRISON 1 , S.M. HUTSON 3 . 1 Pennington Biomedical Research Center, Baton Rouge, USA 2 LSU AgCenter, Baton Rouge, USA 3 Wake Forest, Winston-Salem, USA High protein diets lower the expression of AGRP and suppress appetite. In addition, the branch chain amino acid, leucine acts locally within the hypothalamus to regulate hypothalamic neuropeptide expression and feeding behavior. Nonetheless, the role of branched-chain amino acid metabolism in this signaling remains unclear. To further investigate the role of BCAA metabolism in neuronal function, we utilized mice deficient for BCATm, which is the enzyme catalyzing the first step in peripheral BCAA metabolism. BCATm−/− mice exhibit elevated plasma leucine and reduced adiposity and body weight despite eating more food, along with increased energy expenditure. The wild type and knock out mice were fed either a high fat or a low fat diet to determine if the lack of leucine metabolism would alter the response to a high fat diet. Arcuate nucleus (ARC) micropunches were collected for five continuous coronal sections, and levels of agouti-related protein (AgRP), neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA in the ARC were determined using real-time reverse transcriptase polymerase chain reaction. Compared with wildtype mice, POMC expression was significantly decreased and AgRP expression increased in the arcuate nucleus of BCATm−/− mice (p < 0.05) on the low fat diet but not on mice receiving the high fat diet. It is proposed that the high fat diet increased the levels of leptin in the KO mice and reversed the effects of low leucine utilization on neuropeptide expression. doi:10.1016/j.appet.2008.04.160
T.H. Moran / Appetite 51 (2010) 350–412
Mercaptoacetate (MA) stimulates feeding after infusion into the hepatic portal vein (HPV) or vena cava (VC), but not after infusion into the descending aorta A. MANSOURI ∗ , M. ARNOLD, N. GEARY, M. LEONHARDT, W. LANGHANS. Institute of Animal Sciences, ETH Zurich, Schwerzenbach, Zurich, Switzerland
Viscosity and sweet taste as determinants of caloric compensation in rats A.A. MARTIN ∗ , J.J. FIELDS, M.A. WATERS, R.C. KENNEDY, S.E. SWITHERS, T.L. DAVIDSON. Department of Psychological Sciences and the Ingestive Behavior Research Center, Purdue University, West Lafayette, USA
Intraperitoneal injections of mercaptoacetate (MA) inhibit hepatic fatty acid oxidation and stimulate feeding. Abdominal vagal afferents mediate the feeding-stimulatory effect of MA, but it is unclear where in the abdomen this effect originates. We addressed this question by assessing the feeding-stimulatory effects of MA infusions into the hepatic portal vein (HPV), the vena cava (VC), and the descending aorta near the beginning of the celiac artery (NCA). In separate experiments, ad lib-fed male Sprague–Dawley rats (>400 g body weight (BW)) received HPV, VC, or HPV vs. NCA infusions (40 l/min) of MA (45.6 mg/kg; 15 mM) or saline in the middle of the light phase. Food intake was measured for 12 h. MA stimulated feeding similarly after HPV and VC infusions, but had not effect on feeding after NCA infusion. To our knowledge, this is the first report of a stimulation of feeding after intravenous MA infusion in rats. The data do not disclose the origin of MA’s feeding-stimulatory effect, but suggest that MA does not increase food intake by acting either in the liver or in the intestine. doi:10.1016/j.appet.2008.04.157
Energy and weight regulation depend, in part, on an animal’s ability to compensate for excess calories consumed on one occasion by decreasing energy intake at another time. Recent research suggests that this type of caloric compensation may be strongly influenced by the orosensory properties of foods. For example, compensation is usually weaker following consumption of low viscosity than high viscosity foods. Similarly, rats exposed to sweet taste paired occasionally without calories eat more food after consuming a sweet, high calorie premeal than rats only exposed to sweet taste paired with calories. Thus, both viscosity and sweet taste can influence compensatory ability when tested separately. However, it is unknown how these cues determine compensation when both are presented simultaneously. We investigated this interaction using adult, male Sprague–Dawley rats in a standard preload test paradigm. Animals received 10 g, equicaloric, premeals that factorially combined high and low viscosity with sweet and bland taste, and amount of lab chow eaten during a subsequent test meal was measured. Weaker caloric compensation was found following low compared to high viscosity premeals independent of sweet taste. A follow up study that manipulated prior experience with sweet taste, viscosity, and calories did not abolish the effects of viscosity on caloric compensation. These data suggest that the effects of viscosity on caloric compensation may occur independently of variations in sweet taste. doi:10.1016/j.appet.2008.04.159
Hyperphagia-induced obesity in young male and female OLETF rats: A developmental study A. MARCO 1,∗ , M. SCHROEDER 1 , L. SHBIRO 1 , T.H. MORAN 2 , A. WELLER 1 . 1 Bar-Ilan University, Ramat-Gan, Israel 2 Johns Hopkins University, Baltimore, USA OLETF rats lack the expression of functional CCK1 receptors and are a model of hyperphagia-induced obesity used to study the early origins and neurobiology of obesity. OLETF pups are heavier than LETO controls from birth and develop pre-obese characteristics early in life. In the present study, we aimed to examine the development of young males and females towards obesity. Rats were weighed every 5th day from the time of weaning, intake was assessed daily and feeding efficiency was calculated. Animals were sacrificed at four different time-points: weaning (postnatal day [PND] 22), PND 38, 65 and 90. Blood plasma was collected for leptin analysis. Brown, retroperitoneal, inguinal and epididymal fat pads were collected and weighed. Adipocyte cell size was assessed from the inguinal fat pad. The estrous cycle of the females was monitored from PND 40 until PND 75. Patterns of intake and sugar preference were measured at critical times. Results show pre-obese characteristics in the OLETF strain since childhood and appear to show a specific time-point at PND 65 where obesity sharply increases. The high and sudden accumulation of white fats observed here in both sexes are accompanied by hypertrophic adipocyte development and very high leptin levels. While intake was about 30–40% higher in the OLETF strain, the feeding efficiency did not differ between the strains, further suggesting that obesity in this strain develops following life-long abnormalities in eating behavior and not as a consequence of a metabolic disorder. Acknowledgment: Support: US-Israel BSF. doi:10.1016/j.appet.2008.04.158
Blocking of branch chain amino acid metabolism decreases hypothalamic POMC and increases AgRP expression in mice on a low fat diet R.J. MARTIN 1,2,∗ , S. LI 1 , J. ZHOU 1 , C.D. MORRISON 1 , S.M. HUTSON 3 . 1 Pennington Biomedical Research Center, Baton Rouge, USA 2 LSU AgCenter, Baton Rouge, USA 3 Wake Forest, Winston-Salem, USA High protein diets lower the expression of AGRP and suppress appetite. In addition, the branch chain amino acid, leucine acts locally within the hypothalamus to regulate hypothalamic neuropeptide expression and feeding behavior. Nonetheless, the role of branched-chain amino acid metabolism in this signaling remains unclear. To further investigate the role of BCAA metabolism in neuronal function, we utilized mice deficient for BCATm, which is the enzyme catalyzing the first step in peripheral BCAA metabolism. BCATm−/− mice exhibit elevated plasma leucine and reduced adiposity and body weight despite eating more food, along with increased energy expenditure. The wild type and knock out mice were fed either a high fat or a low fat diet to determine if the lack of leucine metabolism would alter the response to a high fat diet. Arcuate nucleus (ARC) micropunches were collected for five continuous coronal sections, and levels of agouti-related protein (AgRP), neuropeptide Y (NPY) and proopiomelanocortin (POMC) mRNA in the ARC were determined using real-time reverse transcriptase polymerase chain reaction. Compared with wildtype mice, POMC expression was significantly decreased and AgRP expression increased in the arcuate nucleus of BCATm−/− mice (p < 0.05) on the low fat diet but not on mice receiving the high fat diet. It is proposed that the high fat diet increased the levels of leptin in the KO mice and reversed the effects of low leucine utilization on neuropeptide expression. doi:10.1016/j.appet.2008.04.160