The effects of weight loss strategies on gastric emptying and appetite control

Horner, Katy; Byrne, Nuala M.; Cleghorn, Geoffrey J.; Näslund, Erik; King, Neil

doi:10.1111/j.1467-789x.2011.00901.x

Cited by 47 publications

(33 citation statements)

References 187 publications

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“…Mice with Glp2r deletion in POMC neurons not only show hyperphagic behavior but also have accelerated gastric emptying. It is conceivable that the overall impact of faster gastric emptying results in a shorter satiety period, increasing meal frequency and energy intake (23). Thus, our evidence that Glp2r deletion in POMC neurons accelerated rates of gastric emptying not only explains the hyperphagic behavior but also points to the physiological role of CNS GLP-2 in the regulation of satiety.…”

Section: E861mentioning

confidence: 68%

“…Gastric emptying may serve as a key factor in the control of energy homeostasis. As a quantitative determinator of food intake (16,23), gastric emptying is fine-tuned by metabolic, neuronal, and hormonal signals. Gastric emptying is positively associated with overeating (16) and is enhanced in obese subjects (8,52).…”

Section: E861mentioning

confidence: 99%

“…GE is a key mediator of hunger, satiation, and satiety (25). Faster GE results in shorter satiety period and overeating (23) and is considered a major cause of obesity (16). GE is enhanced in obese subjects (8,52).…”

mentioning

confidence: 99%

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GLP-2 receptor in POMC neurons suppresses feeding behavior and gastric motility

Guan

Shi

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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receptor in POMC neurons suppresses feeding behavior and gastric motility. Am J Physiol Endocrinol Metab 303: E853-E864, 2012. First published July 24, 2012; doi:10.1152/ajpendo.00245.2012.-Glucagon-like peptides (GLP-1/2) are cosecreted from endocrine L cells in the gut and preproglucagonergic neurons in the brain. Peripheral GLP-2 action is essential for maintaining intestinal homeostasis, improving absorption efficiency and blood flow, promoting immune defense, and producing efficacy in treatment of gastrointestinal diseases. However, it is unknown if CNS GLP-2 plays a physiological role in the control of energy homeostasis. Since GLP-1/2 are cotranslated from preproglucagongene and coproduced by prohormone convertase-1, it is challenging to knockout GLP-2 only. Instead, our laboratory has generated a Glp2r-floxed mouse line to dissect cellspecific GLP-2 receptor GLP-2R) action in the regulation of energy balance. Our objective was to determine if GLP-2R in the hypothalamus modulates feeding behavior and gastric emptying. We show that Glp2r mRNA and protein are highly expressed in the arcuate nucleus and dorsomedial nucleus of the mouse hypothalamus. Using the Cre-LoxP system, we generated mice that lack Glp2r expression in POMC neurons (KO; mainly in the hypothalamus). The KO mice showed hyperphagic behavior (such as increases in food intake and meal frequency), accelerated gastric emptying (assessed by [ 13 C]octanoic acid breath test), and late-onset obesity, yet there was no decrease in basal metabolic rate. Infusion of GLP-2 (2.5 nmol into the 4th ventricle) suppressed food intake and gastric emptying, while GLP-2-mediated effects were abolished in the melanocortin receptor-4 (MC4R) KO mice. We conclude that Glp2r deletion in POMC neurons enhances feeding behavior and gastric motility, whereas icv GLP-2R activation suppresses food intake and gastric emptying through the MC4R signaling pathway. This study indicates that CNS GLP-2R plays a physiological role in the control of feeding behavior and gastric emptying and that this is mediated probably through the melanocortin system. glucagon-like peptides; proopiomelanocortin; energy homeostasis; food intake; gastric emptying OBESITY AND TYPE 2 DIABETES affect millions of people and are major health problems in the United States. The hypothalamus, a primary site of convergence and integration in the brain for hormonal and nutritional signals, plays pivotal roles in the regulation of energy balance (42). In the arcuate nucleus (ARC) of the hypothalamus, neurons expressing proopiomelanocortin (POMC neurons) are perfectly positioned to integrate long-term adiposity and short-term satiety signals for energy homeostasis (12). POMC neuronal activation enhances energy expenditure and suppresses food intake, yet neuroendocrine mechanisms are not fully established. Notably, the gastrointestinal (GI) tract has a crucial role in digestion, absorption, and assimilation of nutrients (15), thus controlling energy intake at the first pass. Through the gut-brain axis, gut ho...

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Section: E861mentioning

confidence: 68%

Section: E861mentioning

confidence: 99%

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GLP-2 receptor in POMC neurons suppresses feeding behavior and gastric motility

Guan

Shi

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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“…Signals related to gastric mechanoreception, motility, volume, and emptying contribute to the control of eating (166,167,339,360). Although there are sex differences in gastric emptying, there is no direct evidence that these underlie sex differences in the control of eating.…”

Section: Sex Differences In Peripheral Controls Of Eatingmentioning

confidence: 98%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

387

332

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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“…• GI transit time: Literatures reported an acceleration in gastric emptying after gastric bypass [11,22,23] ;others found that the gastric emptying time after RYGB is reduced [24] and some concluded that these changes are variable [25]. Therefore, no changes were made for the gastric emptying.…”

Section: Post Rygb Groupmentioning

confidence: 99%