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Oxytocin knockout (OT KO) mice overconsume palatable carbohydrate solutions, but not palatable lipid solutions.
ARTICLE IN PRESS Abstracts / Appetite 49 (2007) 272–341
Effects of chronic intermittent intraperitoneal infusion of salmon calcitonin on food intake and adiposity in diet-induced obese rats
R.D. REIDELBERGER, P.K. CHELIKANI, A.C. HAVER. VA Nebraska Western Iowa Health Care System, Omaha, NE 68105, USA Chronic administration of anorexigenic substances to experimental animals by injections or continuous infusion typically produces either no effect or a transient reduction in daily food intake and body weight, outcomes that are likely to occur in obese humans as well. Our aim here was to identify an intermittent dosing strategy for IP infusion of salmon calcitonin (sCT) that would produce a sustained reduction in daily food intake (25–35%) and adiposity in diet-induced obese rats. Rats (650711 g, 2771% body fat) with IP catheters tethered to infusion swivels had free access to a 45% fat diet. Results showed that (i) vehicle-treated rats (n=16) regulated their food intake, body weight and adiposity during the 6-week test period; (ii) none of 11 dosing strategies in sCT-treated rats (n=18) produced a sustained 25–35% reduction in daily food intake for Z2 week, although body weight and adiposity were reduced across the 6week period by 13% (583712 vs. 666719 g) and 26% (10477 vs. 167715 g), respectively; (iii) transient effects of sCT on daily food intake when inter-infusion intervals were Z3 h appeared to be due to development of compensatory hyperphagia between infusions; (iv) transient effects of sCT on daily food intake when interinfusion interval was reduced to 2 h suggested possible sCT receptor down-regulation; however, food intake increased dramatically when sCT treatments were discontinued for 1 day following apparent loss in treatment efficacies. Together, these results demonstrate the development of a powerful homeostatic response to increase food intake when sCT treatments reduce energy reserves in diet-induced obese rats.
323
densely innervated by the sympathetic nervous system (SNS), the activation of which is generally required to stimulate UCP1 activity. Molecules such as PPAR-gamma agonists, which increase expression of BAT UCP1 while reducing SNS, do not promote energy expenditure. SNS-mediated thermogenesis is controlled by several neurosystems that include the melanocortin system. Activation of the melanocortin receptor 4 stimulates BAT thermogenesis. The brain site of this activation remains to be clarified. There is also evidence that cannabinoid receptor 1 antagonists can also stimulate BAT thermogenesis. The circulating hormone leptin stimulates UCP1 expression, which is blunted by corticosteroids in rats. Intriguingly, the gastrointestinal anorectic hormones glucagon-like peptide-1 and peptide tyrosine–tyrosine do not have major effects on UCP1 activity. 10.1016/j.appet.2007.03.166
Oxytocin knockout (OT KO) mice overconsume palatable carbohydrate solutions, but not palatable lipid solutions
L. RINAMAN, A. SCLAFANI, R.R. VOLLMER, J. MIEDLAR, J.A. AMICO. Departments of Neuroscience, Pharmaceutical Sciences, and Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Psychology, CUNY Brooklyn College, Brooklyn, NY, USA
10.1016/j.appet.2007.03.165
The control of the sympathetic nervous system (SNS)-mediated uncoupling 1 (UCP1) activity D. RICHARD. Laval Hospital
Research Center and Laval University, Que., Canada Despite the progresses made, the complex etiology of obesity remains poorly understood. Etymologically derived from the Latin word ‘obedere’—to eat in excess—obesity has to be first and foremost seen as an energy-balance-regulation disorder and the pathways whereby energy balance is regulated through complex neural controls on food intake and energy expenditure have yet to be fully delineated. Compared to the control of energy intake, that of energy expenditure has received only mitigated attention. The importance of energy expenditure in energy balance regulation in rodents as well as in humans has been emphasized in conditions leading to energy deficits. Also, the energy expenditure component has been reported to be of particular importance in laboratory rodents, which possess brown adipose tissue (BAT), a very efficient thermogenesis effector. BAT expresses uncoupling protein 1 (UCP1), which is a mitochondrial protein having an enormous thermogenic capacity. BAT is
OT KO mice display enhanced intake of nutritive and nonnutritive sweet solutions (i.e., sucrose and saccharin) compared to wild-type (WT) mice of the same C57BL/6 background strain. The present study further investigated the differential behavioral response of OT KO and WT mice to sucrose solutions, and also examined intake preferences of OT KO and WT mice for palatable but non-sweet isocaloric solutions of carbohydrate and fat. A progressive ratio operant licking procedure demonstrated that OT KO and WT mice display similar motivational drive to consume 10% sucrose. A series of two-bottle intake tests revealed that OT KO mice consume significantly larger amounts of sweet and non-sweet carbohydrate solutions (i.e., sucrose, polycose, and cornstarch) compared to WT cohorts. Intake pattern analyses revealed that OT KO mice overconsume carbohydrate solutions by initiating more drinking bouts compared to WT mice; bout sizes did not differ between the genotypes. In contrast, OT KO and WT mice did not differ in their daily or hourly evening intake of Intralipid, a palatable soybean oil emulsion, except on the first day of exposure. These findings indicate that the absence of OT in mice does not affect their appetitive drive to consume palatable sucrose solutions. Instead, the absence of OT may increase daily intake of palatable sweet and non-sweet solutions of carbohydrate (but not fat) by selectively blunting or masking processes that contribute to postingestive satiety. Research supported by National Institutes of Health Grants HD 44898 (JAA) and DK 31135 (AS). 10.1016/j.appet.2007.03.167
Effects of chronic intermittent intraperitoneal infusion of salmon calcitonin on food intake and adiposity in diet-induced obese rats
R.D. REIDELBERGER, P.K. CHELIKANI, A.C. HAVER. VA Nebraska Western Iowa Health Care System, Omaha, NE 68105, USA Chronic administration of anorexigenic substances to experimental animals by injections or continuous infusion typically produces either no effect or a transient reduction in daily food intake and body weight, outcomes that are likely to occur in obese humans as well. Our aim here was to identify an intermittent dosing strategy for IP infusion of salmon calcitonin (sCT) that would produce a sustained reduction in daily food intake (25–35%) and adiposity in diet-induced obese rats. Rats (650711 g, 2771% body fat) with IP catheters tethered to infusion swivels had free access to a 45% fat diet. Results showed that (i) vehicle-treated rats (n=16) regulated their food intake, body weight and adiposity during the 6-week test period; (ii) none of 11 dosing strategies in sCT-treated rats (n=18) produced a sustained 25–35% reduction in daily food intake for Z2 week, although body weight and adiposity were reduced across the 6week period by 13% (583712 vs. 666719 g) and 26% (10477 vs. 167715 g), respectively; (iii) transient effects of sCT on daily food intake when inter-infusion intervals were Z3 h appeared to be due to development of compensatory hyperphagia between infusions; (iv) transient effects of sCT on daily food intake when interinfusion interval was reduced to 2 h suggested possible sCT receptor down-regulation; however, food intake increased dramatically when sCT treatments were discontinued for 1 day following apparent loss in treatment efficacies. Together, these results demonstrate the development of a powerful homeostatic response to increase food intake when sCT treatments reduce energy reserves in diet-induced obese rats.
323
densely innervated by the sympathetic nervous system (SNS), the activation of which is generally required to stimulate UCP1 activity. Molecules such as PPAR-gamma agonists, which increase expression of BAT UCP1 while reducing SNS, do not promote energy expenditure. SNS-mediated thermogenesis is controlled by several neurosystems that include the melanocortin system. Activation of the melanocortin receptor 4 stimulates BAT thermogenesis. The brain site of this activation remains to be clarified. There is also evidence that cannabinoid receptor 1 antagonists can also stimulate BAT thermogenesis. The circulating hormone leptin stimulates UCP1 expression, which is blunted by corticosteroids in rats. Intriguingly, the gastrointestinal anorectic hormones glucagon-like peptide-1 and peptide tyrosine–tyrosine do not have major effects on UCP1 activity. 10.1016/j.appet.2007.03.166
Oxytocin knockout (OT KO) mice overconsume palatable carbohydrate solutions, but not palatable lipid solutions
L. RINAMAN, A. SCLAFANI, R.R. VOLLMER, J. MIEDLAR, J.A. AMICO. Departments of Neuroscience, Pharmaceutical Sciences, and Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Psychology, CUNY Brooklyn College, Brooklyn, NY, USA
10.1016/j.appet.2007.03.165
The control of the sympathetic nervous system (SNS)-mediated uncoupling 1 (UCP1) activity D. RICHARD. Laval Hospital
Research Center and Laval University, Que., Canada Despite the progresses made, the complex etiology of obesity remains poorly understood. Etymologically derived from the Latin word ‘obedere’—to eat in excess—obesity has to be first and foremost seen as an energy-balance-regulation disorder and the pathways whereby energy balance is regulated through complex neural controls on food intake and energy expenditure have yet to be fully delineated. Compared to the control of energy intake, that of energy expenditure has received only mitigated attention. The importance of energy expenditure in energy balance regulation in rodents as well as in humans has been emphasized in conditions leading to energy deficits. Also, the energy expenditure component has been reported to be of particular importance in laboratory rodents, which possess brown adipose tissue (BAT), a very efficient thermogenesis effector. BAT expresses uncoupling protein 1 (UCP1), which is a mitochondrial protein having an enormous thermogenic capacity. BAT is
OT KO mice display enhanced intake of nutritive and nonnutritive sweet solutions (i.e., sucrose and saccharin) compared to wild-type (WT) mice of the same C57BL/6 background strain. The present study further investigated the differential behavioral response of OT KO and WT mice to sucrose solutions, and also examined intake preferences of OT KO and WT mice for palatable but non-sweet isocaloric solutions of carbohydrate and fat. A progressive ratio operant licking procedure demonstrated that OT KO and WT mice display similar motivational drive to consume 10% sucrose. A series of two-bottle intake tests revealed that OT KO mice consume significantly larger amounts of sweet and non-sweet carbohydrate solutions (i.e., sucrose, polycose, and cornstarch) compared to WT cohorts. Intake pattern analyses revealed that OT KO mice overconsume carbohydrate solutions by initiating more drinking bouts compared to WT mice; bout sizes did not differ between the genotypes. In contrast, OT KO and WT mice did not differ in their daily or hourly evening intake of Intralipid, a palatable soybean oil emulsion, except on the first day of exposure. These findings indicate that the absence of OT in mice does not affect their appetitive drive to consume palatable sucrose solutions. Instead, the absence of OT may increase daily intake of palatable sweet and non-sweet solutions of carbohydrate (but not fat) by selectively blunting or masking processes that contribute to postingestive satiety. Research supported by National Institutes of Health Grants HD 44898 (JAA) and DK 31135 (AS). 10.1016/j.appet.2007.03.167