Effects of surgical manipulation of the intestine on peptide YY and its physiology

Imamura, Mikio

doi:10.1016/s0196-9781(01)00618-0

Cited by 44 publications

(24 citation statements)

References 30 publications

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“…A study of the PYY profile in humans has shown that in response to the ingestion of nutrients, plasma PYY levels increase within 15 min, peak at around 60 min, and remain elevated for up to 6 h (Adrian et al 1985). The initial increase is thought to be induced via neural or endocrine mechanisms (Batterham et al 2003), and the sustained release is thought to be due to the direct effects of the gut contents on PYY-producing cells mainly located in the lower intestine (Imamura 2002). Together, PYY levels of SP and CP rats after 240 min may increase more.…”

Section: Discussionmentioning

confidence: 99%

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Bae

Hasegawa

Akieda-Asai

et al. 2014

Journal of Endocrinology

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Food texture is known to affect energy metabolism. Although feeding with soft pellets (SP) or via a tube is known to cause increases in body weight, it is unclear how different food textures influence energy metabolism. In this study, we investigated the effects of two different food textures on energy balance and glucose and lipid metabolism in male Wistar rats. The rats were fed SP or control pellets (CP) on a 3-h restricted feeding schedule for 14 weeks and their energy intake, body weight, and energy expenditure were examined. The levels of gastrointestinal hormones, glucose and insulin, were investigated at pre-, mid, and post-feeding. Glucose tolerance and insulin tolerance tests were conducted, and the expressions of molecules involved in the insulin signaling system or lipogenesis in the liver were examined. Histological investigation of pancreatic islets was carried out using anti-insulin and anti-Ki-67 antibodies. Furthermore, the expression in the liver and circulating blood of microRNA-33 (miR-33), which regulates insulin receptor substance 2, was examined. There were no significant differences in energy intake, body weight, or gastrointestinal hormone levels between the SP and CP rats; however, the SP rats showed glucose intolerance and insulin resistance with disruption of insulin signaling. Increases in lipogenic factors and miR-33 expression were also found in the SP rats. The numbers of insulin-positive areas and Ki-67-positive cells of SP rats were significantly increased. This study shows that a soft food texture causes diabetes without obesity, so differences in food texture may be an important factor in type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Bae

Hasegawa

Akieda-Asai

et al. 2014

Journal of Endocrinology

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“…Cholecystokinin, 17 ghrelin 18 and PYY peptide 19 levels are related to the fasting-eating cycle and to the motor function of the gastrointestinal tract. Duodenal infusion of lipids, like triglycerides 20 or fatty acids, 21 induces early satiety and causes both gastric relaxation and reduction of gastric emptying at least by the release of cholecystokinin.…”

Section: Discussionmentioning

confidence: 99%

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study

et al. 2006

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Objective: The stomach is the main target organ for bariatric surgery, but no medical treatment has been developed to increase satiety and decrease food intake via gastric pathways. The aim of our study was to investigate whether or not the intraparietogastric administration of botulinum toxin A (BTX), able to modify the motility patterns of the stomach, could be useful for treatment of obesity. Design: Double blind controlled study. Subjects: Twenty-four morbidly obese patients (mean weight (s.e.m.) 116.174.89 kg, mean body mass index (BMI) 43.671.09 kg/m 2 ) were blindly randomized to receive 200 IU BTX or placebo into the antrum and fundus of the stomach by intraparietal endoscopic administration. Measurements: We evaluated weight loss, BMI changes, satiety score, the maximal gastric capacity for liquids and the gastric emptying time (octanoic acid breath test). Results: The two groups were homogeneous for anthropometric characteristics. Eight weeks after treatment, BTX patients had significantly higher weight loss (1171.09 vs 5.771.1 kg, Po0.001) and BMI reduction (470.36 vs 270.58 kg/m 2 , Po0.001) and a higher satiety score on a visual analogic scale (7.6370.38 vs 4.7270.44, Po0.001) than controls. Furthermore, BTX patients showed a significantly greater reduction in maximal gastric capacity for liquids (266.6748 vs 139731, Po0.001) and a greater prolongation in gastric emptying time ( þ 18.9378 vs À2.276.9 min, Po0.05). No significant side effects or neurophysiologic changes were found. Conclusions: Topical intragastric BTX was effective in reducing food intake and body weight in morbidly obese patients.

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“…This is most likely mediated via increased circulating concentrations of leptin and the gut peptide peptide YY3-36, release of which is strongly increased by dietary fat ( 38,39), subsequently acting on leptin or Y2 receptors in the arcuate nucleus to reduce neuropeptide Y expression levels and thereby reducing feeding (1,40,41). Expression of POMC in the arcuate nucleus of wild-type and Y1 receptor knockout mice fed a high-fat diet was also reduced, a change that may contribute to the diet-induced obesity observed in these mice by decreasing secretion of α-melanocyte stimulating hormone.…”

Section: Discussionmentioning

confidence: 99%

Y2Y4 Receptor Double Knockout Protects Against Obesity Due to a High-Fat Diet or Y1 Receptor Deficiency in Mice

et al. 2006

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Sainsbury et al.: Y2Y4 receptor double knockout protects against obesity due to a high--fat diet or Y1 receptor deficiency in mice Diabetes, 55(1): 19--26, 2006 Y2Y4 receptor double knockout protects against obesity due to a high-fat diet or Y1 receptor deficiency in mice Remarkably, the antiobesity effect of Y2Y4 deficiency was stronger than the obesogenic effect of Y1 deficiency, since Y1Y2Y4 triple knockouts did not develop obesity on the high-fat diet. Resistance to diet-induced obesity in Y2Y4 knockouts was associated with reduced food intake and improved glucose tolerance in the absence of changes in total physical activity. Fecal concentration of free fatty acids was significantly increased in Y2Y4 knockouts in association with a significantly reduced bile acid pool and marked alterations in intestinal morphology. In addition, hypothalamic proopiomelanocortin expression was decreased in diet-induced obesity (in both wild-type and Y1 receptor knockout mice) but not in obesity-resistant Y2Y4 receptor knockout mice fed a high-fat diet. Therefore, deletion of Y2 and Y4 receptors synergistically protects against diet-induced obesity, at least partially via changes in food intake and hypothalamic proopiomelanocortin expression.Members of the Y receptor family, notably Y1, Y2, Y4, and Y5 receptors, are implicated in energy homeostasis and the development of obesity and insulin resistance. These receptors are activated by three endogenous ligands: neuropeptide Y, the gut-derived hormones peptide YY, and pancreatic polypeptide. Recently, there has been renewed speculation that ligands for Y receptors, such as peptide YY3-36 and pancreatic polypeptide, may be of benefit for the treatment of obesity (1). There is considerable conflict in the literature about the role of Y receptors in the regulation of body weight. For instance, pharmacological studies suggested that Y1 receptors contribute to hyperphagia induced by increased hypothalamic neuropeptide Y secretion ( 2). Fasting-induced refeeding is reduced in Y1 knockout mice ( 3). Moreover, food intake and body weight of genetically obese ob/ob mice, in which hypothalamic neuropeptide Y-ergic activity is chronically increased, are significantly reduced by Y1 knockout ( 4). In contrast, Y1 knockouts develop significant increases in body weight, fat mass, and insulinemia in the absence of hyperphagia (3,5).Similar controversies prevail regarding the role of Y2 receptors in energy homeostasis. Hypothalamus-specific or germ-line deletion of Y2 receptors resulted in significant reductions in the body weight of lean mice (6) and significant reductions in adiposity or body weight and the type 2 diabetic syndrome of ob/ob mice in the absence of reductions in food intake (7,8). In contrast, another germline Y2 receptor knockout model was shown to develop increased body weight, fat deposition, and hyperphagia (9). Furthermore, intrahypothalamic administration of the Y2 agonist neuropeptide Y[13-36] to rats significantly decreased food intake (10). Moreover, circulating pep...

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Effects of surgical manipulation of the intestine on peptide YY and its physiology

Cited by 44 publications

References 30 publications

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study

Y2Y4 Receptor Double Knockout Protects Against Obesity Due to a High-Fat Diet or Y1 Receptor Deficiency in Mice

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