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James E Blevins - One of the best experts on this subject based on the ideXlab platform.
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chronic cns oxytocin signaling preferentially induces fat loss in high fat diet fed rats by enhancing Satiety Responses and increasing lipid utilization
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2016Co-Authors: James E Blevins, Benjamin W Thompson, Vishwanath T Anekonda, James L Graham, Zachary S Roberts, Bang H Hwang, Kayoko Ogimoto, Tami Woldenhanson, Jarrell T NelsonAbstract:Based largely on a number of short-term administration studies, growing evidence suggests that central oxytocin is important in the regulation of energy balance. The goal of the current work is to determine whether long-term third ventricular (3V) infusion of oxytocin into the central nervous system (CNS) is effective for obesity prevention and/or treatment in rat models. We found that chronic 3V oxytocin infusion between 21 and 26 days by osmotic minipumps both reduced weight gain associated with the progression of high-fat diet (HFD)-induced obesity and elicited a sustained reduction of fat mass with no decrease of lean mass in rats with established diet-induced obesity. We further demonstrated that these chronic oxytocin effects result from 1) maintenance of energy expenditure at preintervention levels despite ongoing weight loss, 2) a reduction in respiratory quotient, consistent with increased fat oxidation, and 3) an enhanced Satiety Response to cholecystokinin-8 and associated decrease of meal size. These weight-reducing effects persisted for approximately 10 days after termination of 3V oxytocin administration and occurred independently of whether sucrose was added to the HFD. We conclude that long-term 3V administration of oxytocin to rats can both prevent and treat diet-induced obesity.
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a new oxytocin saporin cytotoxin for lesioning oxytocin receptive neurons in the rat hindbrain
Endocrinology, 2010Co-Authors: Denis G Baskin, Michael W. Schwartz, Gregory J Morton, Francis Kim, Richard W Gelling, Brian J Russell, Hyagriv N Simhan, Daniel H Moralejo, James E BlevinsAbstract:Evidence suggests that release of oxytocin in the nucleus tractus solitarius (NTS) of the hindbrain from descending projections that originate in the paraventricular nucleus can inhibit food intake by amplifying the Satiety Response to cholecystokinin (CCK). To further evaluate this mechanism in rats, we used a novel cytotoxin, saporin conjugated to oxytocin (OXY-SAP), a compound designed to destroy cells that express oxytocin receptors (OXYr). OXY-SAP was injected directly into the NTS to lesion neurons that express OXYr and that are implicated in potentiating CCK's Satiety effects. The control consisted of injection of saporin conjugated to a nonsense peptide. We found that OXY-SAP was cytotoxic to human uterine smooth muscle cells in vitro, demonstrating that OXY-SAP can lesion cells that express OXYr. Using laser capture microdissection and real-time quantitative PCR, we demonstrated that OXYr mRNA levels were reduced in the NTS after OXY-SAP administration. Moreover, we found that OXY-SAP attenuated the efficacy of CCK-8 to reduce food intake and blocked the actions of an OXYr antagonist to stimulate food intake. The findings suggest that OXY-SAP is an effective neurotoxin for in vivo elimination of cells that express OXYr and is potentially useful for studies to analyze central nervous system mechanisms that involve the action of oxytocin on food intake and other physiological processes.
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forebrain melanocortin signaling enhances the hindbrain Satiety Response to cck 8
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: James E Blevins, Michael W. Schwartz, Gregory J Morton, D J L Williams, David W Caldwell, Lloyd S Bastian, Brent E Wisse, Denis G BaskinAbstract:Melanocortin 4 receptors (MC4R) are hypothesized to mediate the central nervous system actions of leptin to enhance the Satiety effects of cholecystokinin (CCK). To further elucidate this mechanism, we confirmed that peripheral administration of CCK-8 is less effective in producing this effect in MC4R-deficient mice (MC4R−/−). Whereas intraperitoneal (ip) CCK-8 at 0.75 nmol/kg lean body mass (lbm) suppressed food intake in wild-type mice, CCK-8 doses of 7.5 nmol/kg lbm were required to attenuate food intake in MC4R−/− mice. To determine whether melanocortin signaling in the hypothalamic paraventricular nucleus (PVN) participates in regulating this CCK Satiety Response, we administered the MC3/MC4R antagonist, SHU9119, into the PVN of rats before ip CCK-8 administration. PVN administration of SHU9119 attenuated the ability of CCK-8 to reduce 30-min food intake by 20%. To determine whether MC4R are expressed by PVN neurons that project directly to hindbrain nuclei involved in the Satiety Response to ip CCK-8, the retrograde tracer fluorescent cholera toxin subunit B was injected into the nucleus tractus solitarius (NTS) of the hindbrain. After 4 days, labeled PVN neurons were collected by laser capture microdissection and found to express MC4R mRNA by quantitative RT-PCR analysis. These data provide evidence for a neuroanatomical link between hypothalamic melanocortin signaling in the PVN and NTS neurons that regulate food intake. These findings highlight the contribution of melanocortin signaling in the PVN toward regulating the Satiety effects of CCK-8 while acknowledging that melanocortin-dependent pathways in other brain regions and/or melanocortin-independent mechanisms are also important in this mechanism.
Britt Burtonfreeman - One of the best experts on this subject based on the ideXlab platform.
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short term effects of chewing gum on Satiety and afternoon snack intake in healthy weight and obese women
Physiology & Behavior, 2016Co-Authors: Eunyoung Park, Indika Edirisinghe, Taichi Inui, Sophie Kergoat, Michael Kelley, Britt BurtonfreemanAbstract:Afternoon snacking contributes significantly to total energy intake. Strategies to enhance the Satiety value of lunch and reduce afternoon snacking are of interest for body weight management. To assess whether between-meal gum chewing would enhance the Satiety Response to a fixed lunch meal; and assess the role of cholecystokinin (CCK) as a potential mediator of the Response in non-obese healthy weight and obese women. Fifty unrestrained obese (n=25) and non-obese healthy weight (n=25) women participated in a two-arm cross-over study assessing multiple (15min per hour×3h) gum chewing (GUM) occurrences or no gum (Control) on subjective ratings of Satiety, subsequent sweet and salty snack intake, CCK and general metabolic Responses. GUM compared to Control resulted in significant suppression of hunger, desire to eat and prospective consumption (p<0.05). Total snack energy intake was reduced ~9.3% by GUM, but not significantly different from Control (p=0.08). However, overall carbohydrate intake was reduced by GUM (p=0.03). This was consistent with a reduction in snacks characterized as high carbohydrate, low fat (p=0.02). BMI specific effects indicated GUM reduced pretzel intake in obese women (p=0.05) and Oreo cookie intake in healthy weight women (p=0.03) 3h after lunch. Metabolic Responses and CCK did not differ between experimental conditions. Chewing gum intermittently post-lunch enhances perceptions of Satiety and may have important implications in reducing afternoon high carbohydrate-snack intake.
Rajadurai Akilen - One of the best experts on this subject based on the ideXlab platform.
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the effects of potatoes and other carbohydrate side dishes consumed with meat on food intake glycemia and Satiety Response in children
Nutrition & Diabetes, 2016Co-Authors: Rajadurai Akilen, N Deljoomanesh, Sascha Hunschede, Christopher E Smith, Muhammad Umair Arshad, Ruslan Kubant, G H AndersonAbstract:The effect of carbohydrate (CHO) foods on blood glucose (BG) is ranked by their glycemic index (GI). Boiled and mashed potatoes (BMPs) are ranked as high GI foods, whereas pasta and rice have moderate GI rankings. The objective of this study was to compare ad libitum consumption of common CHO dishes consumed with meat on meal-time food intake and post-meal Satiety, BG, insulin and gut hormones in 11- to 13-year-old normal weight children. Two randomized crossover studies were conducted. At weekly intervals, children (experiment 1: 12 males (M), 8 females (F); experiment 2: 6M, 6 F) received in random order 1 of 5 CHO side dishes of rice, pasta, BMP, fried French fries (FFF) or baked French fries (BFF) eaten freely together with a fixed amount of lean beef (100 g). In experiment-1, food intake over 30 min and subjective appetite were measured for 120 min. In experiment-2, the same outcomes were measured along with BG, plasma insulin and gut hormones. The results for boys and girls were pooled as sex was not a factor. In both experiments, children consumed 30–40% less calories at meals with BMP (P<0.0001) compared with all other treatments, which were similar. BMP increased Satiety, expressed as a change in appetite per kilocalorie, more than all other treatments (P<0.0001). FFF resulted in the lowest (P<0.0001) glucose and insulin at meal end and post-meal and peptide YY (PYY) post-meal. Blood measures were similar among all other treatments. The physiological functions of CHO foods consumed ad libitum at meal time on food intake, appetite, BG, insulin and gut hormone Responses in children is not predicted by the GI.
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the effects of potatoes and other carbohydrate side dishes on meal time food intake blood glucose and Satiety Response in lean healthy children
The FASEB Journal, 2015Co-Authors: Rajadurai Akilen, N Deljoomanesh, Khulood Aldabous, Muhammad Arshad, Chris M Smith, Jill Hamilton, Harvey AndersonAbstract:Background: The effect of carbohydrate foods on blood glucose is ranked by their glycemic index. Boiled-mashed-potatoes (BMP) are ranked as high GI but pasta and rice have moderate GI ranking. Objectives: To compare ad libitum consumption of common carbohydrate dishes on meal-time Satiety, food-intake blood glucose and insulin in 11 to 13 year normal weight children. Methods: Two studies were conducted. At weekly intervals, children (experiment-1: 12M, 8F; experiment-2: 6M, 3F) randomly received 1 of 5 ad libitum carbohydrate meals of rice, pasta, BMP, fried-french-fries (FFF) or baked-french-fries (BFF) together with 100g lean beef as a lunch time meal. In experiment-1, food intake over 30 minutes and subjective appetite was measured for120 minutes. In experiment-2, the same outcomes were measured along with blood glucose and plasma insulin. Results: The results for both boys and girls were pooled as sex was not a factor(P=0.51). In both experiments, children consumed the 30% less calories at meals with ...
John E Blundell - One of the best experts on this subject based on the ideXlab platform.
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The effects of exercise-induced weight loss on appetite-related peptides and motivation to eat
2010Co-Authors: Catia Martins, Neil A King, Bård Kulseng, Jens J. Holst, John E BlundellAbstract:Context: The magnitude of exercise-induced weight loss depends on the extent of compensatory Responses. An increase in energy intake is likely to result from changes in the appetite control system toward an orexigenic environment; however, few studies have measured how exercise impacts on both orexigenic and anorexigenic peptides. ---------- Objective: The aim of the study was to investigate the effects of medium-term exercise on fasting/postprandial levels of appetite-related hormones and subjective appetite sensations in overweight/obese individuals. ---------- Design and Setting: We conducted a longitudinal study in a university research center. ---------- Participants and Intervention: Twenty-two sedentary overweight/obese individuals (age, 36.9 ± 8.3 yr; body mass index, 31.3 ± 3.3 kg/m2) took part in a 12-wk supervised exercise programme (five times per week, 75% maximal heart rate) and were requested not to change their food intake during the study. ---------- Main Outcome Measures: We measured changes in body weight and fasting/postprandial plasma levels of glucose, insulin, total ghrelin, acylated ghrelin (AG), peptide YY, and glucagon-like peptide-1 and feelings of appetite. ---------- Results: Exercise resulted in a significant reduction in body weight and fasting insulin and an increase in AG plasma levels and fasting hunger sensations. A significant reduction in postprandial insulin plasma levels and a tendency toward an increase in the delayed release of glucagon-like peptide-1 (90–180 min) were also observed after exercise, as well as a significant increase (127%) in the suppression of AG postprandially. ---------- Conclusions: Exercise-induced weight loss is associated with physiological and biopsychological changes toward an increased drive to eat in the fasting state. However, this seems to be balanced by an improved Satiety Response to a meal and improved sensitivity of the appetite control system.
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sub clinical binge eating tendency associated with increased bmi weakened Satiety Response increased liking for high fat sweet food and enhanced explicit but not implicit wanting for food
Appetite, 2007Co-Authors: Graham Finlayson, A Arlotti, Neil A King, John E BlundellAbstract:Tendency to binge eat is a known risk factor for weight gain and obesity. The present study examined hedonic and homeostatic processes of appetite regulation in normal weight women with a range of binge eating scores. Thirty-five subjects (24.1±1.0 years, BMI: 21.9±0.5 kg/m 2 ) completed the Binge Eating Scale (BES), Three-Factor Eating Questionnaire (TFEQ), Food Craving Scale (FCS) and attended two test-meal sessions comprising a fixed preload followed by an ad libitum buffet. Energy intake, food selection, subjective sensations of appetite and hedonic Response were measured. Novel procedures to measure food liking, wanting and preference (Finlayson et al. 2007) were employed. BES scores correlated with BMI ( p p p p p N =12) and high (>10; N =12) tertile scores on the BES, higher scores were associated with differences in sensory perception, greater preference for high-fat sweet foods ( p p p p
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resistance and susceptibility to weight gain individual variability in Response to a high fat diet
Physiology & Behavior, 2005Co-Authors: John E Blundell, R J Stubbs, C Golding, Fiona Croden, Rahul Alam, S Whybrow, Le J Noury, Clare L LawtonAbstract:Abstract An obesigenic environment is a potent force for promoting weight gain. However, not all people exposed to such an environment become obese; some remain lean. This means that some people are susceptible to weight gain (in a weight-promoting environment) and others are resistant. Identifying the characteristics of appetite control and food motivation in these two groups could throw light on the causes of weight gain and how this can be either treated or prevented. We have investigated the issue experimentally by identifying people who habitually consume a high-fat diet (greater than 43% fat energy). These individuals have been termed high-fat phenotypes. We have compared individuals, of the same age (mean = 37 years old) and gender (male), who have gained weight (BMI = 34) or who have remained lean (BMI = 22). The susceptible individuals are characterised by a cluster of characteristics including a weak Satiety Response to fatty meals, a maintained preference for high-fat over low-energy foods in the post-ingestive Satiety period, a strong hedonic attraction to palatable foods and to eating, and high scores on the TFEQ factors of Disinhibition and Hunger. The analysis of large databases suggests that this profile of factors contributes to an average daily positive energy balance from food of approximately 0.5 MJ. This profile of characteristics helps to define the symptomatology of a thrifty phenotype.
Michael W. Schwartz - One of the best experts on this subject based on the ideXlab platform.
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a new oxytocin saporin cytotoxin for lesioning oxytocin receptive neurons in the rat hindbrain
Endocrinology, 2010Co-Authors: Denis G Baskin, Michael W. Schwartz, Gregory J Morton, Francis Kim, Richard W Gelling, Brian J Russell, Hyagriv N Simhan, Daniel H Moralejo, James E BlevinsAbstract:Evidence suggests that release of oxytocin in the nucleus tractus solitarius (NTS) of the hindbrain from descending projections that originate in the paraventricular nucleus can inhibit food intake by amplifying the Satiety Response to cholecystokinin (CCK). To further evaluate this mechanism in rats, we used a novel cytotoxin, saporin conjugated to oxytocin (OXY-SAP), a compound designed to destroy cells that express oxytocin receptors (OXYr). OXY-SAP was injected directly into the NTS to lesion neurons that express OXYr and that are implicated in potentiating CCK's Satiety effects. The control consisted of injection of saporin conjugated to a nonsense peptide. We found that OXY-SAP was cytotoxic to human uterine smooth muscle cells in vitro, demonstrating that OXY-SAP can lesion cells that express OXYr. Using laser capture microdissection and real-time quantitative PCR, we demonstrated that OXYr mRNA levels were reduced in the NTS after OXY-SAP administration. Moreover, we found that OXY-SAP attenuated the efficacy of CCK-8 to reduce food intake and blocked the actions of an OXYr antagonist to stimulate food intake. The findings suggest that OXY-SAP is an effective neurotoxin for in vivo elimination of cells that express OXYr and is potentially useful for studies to analyze central nervous system mechanisms that involve the action of oxytocin on food intake and other physiological processes.
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forebrain melanocortin signaling enhances the hindbrain Satiety Response to cck 8
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2009Co-Authors: James E Blevins, Michael W. Schwartz, Gregory J Morton, D J L Williams, David W Caldwell, Lloyd S Bastian, Brent E Wisse, Denis G BaskinAbstract:Melanocortin 4 receptors (MC4R) are hypothesized to mediate the central nervous system actions of leptin to enhance the Satiety effects of cholecystokinin (CCK). To further elucidate this mechanism, we confirmed that peripheral administration of CCK-8 is less effective in producing this effect in MC4R-deficient mice (MC4R−/−). Whereas intraperitoneal (ip) CCK-8 at 0.75 nmol/kg lean body mass (lbm) suppressed food intake in wild-type mice, CCK-8 doses of 7.5 nmol/kg lbm were required to attenuate food intake in MC4R−/− mice. To determine whether melanocortin signaling in the hypothalamic paraventricular nucleus (PVN) participates in regulating this CCK Satiety Response, we administered the MC3/MC4R antagonist, SHU9119, into the PVN of rats before ip CCK-8 administration. PVN administration of SHU9119 attenuated the ability of CCK-8 to reduce 30-min food intake by 20%. To determine whether MC4R are expressed by PVN neurons that project directly to hindbrain nuclei involved in the Satiety Response to ip CCK-8, the retrograde tracer fluorescent cholera toxin subunit B was injected into the nucleus tractus solitarius (NTS) of the hindbrain. After 4 days, labeled PVN neurons were collected by laser capture microdissection and found to express MC4R mRNA by quantitative RT-PCR analysis. These data provide evidence for a neuroanatomical link between hypothalamic melanocortin signaling in the PVN and NTS neurons that regulate food intake. These findings highlight the contribution of melanocortin signaling in the PVN toward regulating the Satiety effects of CCK-8 while acknowledging that melanocortin-dependent pathways in other brain regions and/or melanocortin-independent mechanisms are also important in this mechanism.
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Leptin deficiency induced by fasting impairs the Satiety Response to cholecystokinin.
Endocrinology, 2000Co-Authors: Julie E. Mcminn, Dana K. Sindelar, Peter J. Havel, Michael W. SchwartzAbstract:Leptin administration potentiates the Satiety Response to signals such as cholecystokinin (CCK), that are released from the gut during a meal. To investigate the physiological relevance of this observation, we hypothesized that leptin deficiency, induced by fasting, attenuates the Satiety Response to CCK. To test this hypothesis, 48-h-fasted or fed rats were injected with i.p. saline or CCK. Fasting blunted the Satiety Response to 3.0 microg/kg CCK, such that 30-min food intake was suppressed by 65.1% (relative to saline-treated controls) in fasted rats vs. 85.9% in the fed state (P < 0.05). In a subsequent experiment, rats were divided into three groups: 1) vehicle/fed; 2) vehicle/fasted; and 3) leptin-replaced/fasted; and each group received 3.0 microg/kg i.p. CCK. As expected, the Satiety Response to CCK was attenuated by fasting in vehicle-treated rats (30-min food intake: vehicle/fed, 0.3 +/- 0.1 g; vehicle/fasted, 1.7 +/- 0.4 g; P < 0.01), and this effect was prevented by leptin replacement (0.7 +/- 0.2 g, P < 0.05 vs. vehicle/fasted; P = not significant vs. vehicle/fed). To investigate whether elevated neuropeptide Y (NPY) signaling plays a role in the effect of leptin deficiency to impair the Response to CCK, we measured the Response to 3.0 microg/kg i.p. CCK after treatment with 7.5 microg intracerebroventricular NPY. We found that both CCK-induced Satiety and its ability to increase c-Fos-like-immunoreactivity in key brainstem-feeding centers were attenuated by NPY pretreatment. We conclude that an attenuated Response to meal-related Satiety signals is triggered by leptin deficiency and may contribute to increased food intake.
