ArticleMolecular metabolism2019
Combined loss of GLP-1R and Y2R does not alter progression of high-fat diet-induced obesity or response to RYGB surgery in mice.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 37 citations in OpenAlex.
- RYGB induces vagal sensory neuropathy characterized by altered Glp1r expression and enhanced exendin-4 responsiveness in male mice.American journal of physiology. Endocrinology and metabolism · 2026Article
- The Role of the Gut Microbiome Dysbiosis in Metabolic Dysfunction: A Mini Review.Healthcare (Basel, Switzerland) · 2025Review
- The role of the gut-brain axis in bariatric surgery.Current opinion in neurobiology · 2025Review
- Insights into the neurobiology of weight loss after bariatric surgery and GLP-1R agonists.Neuropharmacology · 2025Review
- Role of short-chain fatty acids in host physiology.Animal models and experimental medicine · 2024Review
- Intestinal FFA2 promotes obesity by altering food intake in Western diet-fed mice.The Journal of endocrinology · 2024Article
- Dorothy Hodgkin lecture 2023: The enteroendocrine system-Sensors in your guts.Diabetic medicine : a journal of the British Diabetic Association · 2023Review
- The intestine as an endocrine organ and the role of gut hormones in metabolic regulation.Nature reviews. Gastroenterology & hepatology · 2023Review
- Mechanisms of bariatric surgery for weight loss and diabetes remission.Journal of diabetes · 2023Review
- A peptide triple agonist of GLP-1, neuropeptide Y1, and neuropeptide Y2 receptors promotes glycemic control and weight loss.Scientific reports · 2023Article
- Reduction of Plasma BCAAs following Roux-en-Y Gastric Bypass Surgery Is Primarily Mediated by FGF21.Nutrients · 2023Article
- Gastric bypass surgery weight loss-independently induces gut Il-22 release in association with improved glycemic control in obese Zucker fatty rats.Metabolism open · 2023Article
- Regulation of body weight: Lessons learned from bariatric surgery.Molecular metabolism · 2023Review
- Renal Function Following Bariatric Surgery: a Literature Review of Potential Mechanisms.Obesity surgery · 2022Review
- Targeting the Enteroendocrine System for Treatment of Obesity.Handbook of experimental pharmacology · 2022Article
- Gastrointestinal peptides in eating-related disorders.Physiology & behavior · 2021 · on this mapReview
- Anorexia and Fat Aversion Induced by Vertical Sleeve Gastrectomy Is Attenuated in Neurotensin Receptor 1-Deficient Mice.Endocrinology · 2021Article
- Intravital imaging of islet CaNature communications · 2021Article
- Gut-brain communication and obesity: understanding functions of the vagus nerve.The Journal of clinical investigation · 2021Review
- IGFBP-2 partly mediates the early metabolic improvements caused by bariatric surgery.Cell reports. Medicine · 2021Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
objectiveUnderstanding the mechanisms underlying the remarkable beneficial effects of gastric bypass surgery is important for the development of non-surgical therapies or less invasive surgeries in the fight against obesity and metabolic disease. Although the intestinal L-cell hormones glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY) have attracted the most attention, direct tests in humans and rodents with pharmacological blockade or genetic deletion of either the GLP1-receptor (GLP1R) or the Y2-receptor (Y2R) were unable to confirm their critical roles in the beneficial effects gastric bypass surgery on body weight and glucose homeostasis. However, new awareness of the power of combinatorial therapies in the treatment of metabolic disease would suggest that combined blockade of more than one signaling pathway may be necessary to reverse the beneficial effects of bariatric surgery.
methodsThe metabolic effects of high-fat diet and the ability of Roux-en-Y gastric bypass surgery to lower food intake and body weight, as well as improve glucose handling, was tested in GLP1R and Y2R-double knockout (GLP1RKO/Y2RKO) and C57BL6J wildtype (WT) mice.
resultsGLP1RKO/Y2RKO and WT mice responded similarly for up to 20 weeks on high-fat diet and 16 weeks after RYGB. There were no significant differences in loss of body and liver weight, fat mass, reduced food intake, relative increase in energy expenditure, improved fasting insulin, glucose tolerance, and insulin tolerance between WT and GLP1RKO/Y2RKO mice after RYGB.
conclusionsCombined loss of GLP1R and Y2R-signaling was not able to negate or attenuate the beneficial effects of RYGB on body weight and glucose homeostasis in mice, suggesting that a larger number of signaling pathways is involved or that the critical pathway has not yet been identified.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.