GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents. - Wikidata - wikimedia - TriplyDB

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

http://www.wikidata.org/entity/Q37629291

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The Use of Rat and Mouse Models in Bariatric Surgery Experiments How do patients' clinical phenotype and the physiological mechanisms of the operations impact the choice of bariatric procedure?Increasing GLP-1 Circulating Levels by Bariatric Surgery or by GLP-1 Receptor Agonists Therapy: Why Are the Clinical Consequences so Different?Contribution of the distal small intestine to metabolic improvement after bariatric/metabolic surgery: Lessons from ileal transposition surgery Bile Acids, FXR, and Metabolic Effects of Bariatric Surgery Mechanism Underlying the Weight Loss and Complications of Roux-en-Y Gastric Bypass. Review Multiple Factors Related to the Secretion of Glucagon-Like Peptide-1 The Obese Brain--Effects of Bariatric Surgery on Energy Balance Neurocircuitry Regulation of energy balance by inflammation: common theme in physiology and pathology Roux-en-Y gastric bypass: effects on feeding behavior and underlying mechanisms Physiology of proglucagon peptides: role of glucagon and GLP-1 in health and disease Remodeling of the residual gastric mucosa after roux-en-y gastric bypass or vertical sleeve gastrectomy in diet-induced obese rats The role of gut adaptation in the potent effects of multiple bariatric surgeries on obesity and diabetes Surgical models of Roux-en-Y gastric bypass surgery and sleeve gastrectomy in rats and mice.Bariatric surgery and obesity: influence on the incretins Does gastric bypass surgery change body weight set point?Roux-en-Y gastric bypass does not affect daily water intake or the drinking response to dipsogenic stimuli in rats The CNS glucagon-like peptide-2 receptor in the control of energy balance and glucose homeostasis MGAT2 deficiency and vertical sleeve gastrectomy have independent metabolic effects in the mouse.Vertical sleeve gastrectomy restores glucose homeostasis in apolipoprotein A-IV KO mice.The physiology underlying Roux-en-Y gastric bypass: a status report.Gastric inhibitory polypeptide (GIP) is selectively decreased in the roux-limb of dietary obese mice after RYGB surgery.Leptin deficient ob/ob mice and diet-induced obese mice responded differently to Roux-en-Y bypass surgery.RYGB progressively increases avidity for a low-energy, artificially sweetened diet in female rats.Reprogramming of defended body weight after Roux-En-Y gastric bypass surgery in diet-induced obese mice Appetite and body weight regulation after bariatric surgery.Link Between Increased Satiety Gut Hormones and Reduced Food Reward After Gastric Bypass Surgery for Obesity.Peripheral, but not central, GLP-1 receptor signaling is required for improvement in glucose tolerance after Roux-en-Y gastric bypass in mice Eating in mice with gastric bypass surgery causes exaggerated activation of brainstem anorexia circuit.Roux-en-Y gastric bypass surgery is effective in fibroblast growth factor-21 deficient mice.PYY-Dependent Restoration of Impaired Insulin and Glucagon Secretion in Type 2 Diabetes following Roux-En-Y Gastric Bypass Surgery.The endocrinology of taste receptors.GLP-1: a mediator of the beneficial metabolic effects of bariatric surgery?Metabolic Mechanisms in Obesity and Type 2 Diabetes: Insights from Bariatric/Metabolic Surgery.The gut in the brain: the effects of bariatric surgery on alcohol consumption.Physiological and molecular responses to bariatric surgery: markers or mechanisms underlying T2DM resolution?Ghrelin, CCK, GLP-1, and PYY(3-36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB.Endocrine Function after Bariatric Surgery.β-Cell Glucagon-Like Peptide-1 Receptor Contributes to Improved Glucose Tolerance After Vertical Sleeve Gastrectomy.Potential Hormone Mechanisms of Bariatric Surgery.

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GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

http://www.wikidata.org/entity/Q37629291

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 15 January 2014

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@en

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@nl

type

label

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@en

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@nl

prefLabel

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@en

GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@nl

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AJPREGU.00491.2013

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American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

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GLP-1 receptor signaling is not required for reduced body weight after RYGB in rodents.

@en

P2093

Christopher D Morrison

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Hans-Rudolf Berthoud

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Heike Münzberg

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Jianping Ye

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Laurel M Patterson

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Michael B Mumphrey

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Nicholas Stylopoulos

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R Leigh Townsend

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Zheng Hao

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P2860

Metabolic and behavioral compensations in response to caloric restriction: implications for the maintenance of weight loss

Prototypic G protein-coupled receptor for the intestinotrophic factor glucagon-like peptide 2

Glucagon-like peptide (GLP)-2 action in the murine central nervous system is enhanced by elimination of GLP-1 receptor signaling

Quantitative body composition analysis in awake mice and rats by magnetic resonance relaxometry.

The effect of glucagon-like peptide-1 receptor agonist therapy on body mass index in adolescents with severe obesity: a randomized, placebo-controlled, clinical trial

Selective and brain penetrant neuropeptide y y2 receptor antagonists discovered by whole-cell high-throughput screening

Meal-induced hormone responses in a rat model of Roux-en-Y gastric bypass surgery.

High-fat intake induced by mu-opioid activation of the nucleus accumbens is inhibited by Y1R-blockade and MC3/4R- stimulation.

Gut hormone PYY(3-36) physiologically inhibits food intake.

Intravenous peptide YY3-36 and Y2 receptor antagonism in the rat: effects on feeding behaviour.

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R352-62

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scholarly article

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10.1152/AJPREGU.00491.2013

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5

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306

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Daniel J. Drucker

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2014-01-15T00:00:00Z

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259767339

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