ArticleGut2020
Suppression of enteroendocrine cell glucagon-like peptide (GLP)-1 release by fat-induced small intestinal ketogenesis: a mechanism targeted by Roux-en-Y gastric bypass surgery but not by preoperative very-low-calorie diet.
Article in Gut, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
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- The Effect of Standard Versus Longer Intestinal Bypass on GLP-1 Regulation and Glucose Metabolism in Patients With Type 2 Diabetes Undergoing Roux-en-Y Gastric Bypass: The Long-Limb Study.Diabetes care · 2021 · on this mapTrial
- β‑hydroxybutyric acid as a potential therapeutic metabolite for type 2 diabetes mellitus (Review).International journal of molecular medicine · 2026Review
- Effects of Maternal Clofibrate Supplementation During Gestation and Lactation on Intestinal Fatty Acid Oxidation of Suckling Piglets.International journal of molecular sciences · 2025Article
- Ketone Supplements and Alcohol-Related Responses in Rodents.Addiction biology · 2025Article
- Novel insights on remnant stomach following Roux-en-Y gastric bypass surgery based on histological evaluation and quantitative proteomics analysis.Scientific reports · 2025Article
- Not Just an Alternative Energy Source: Diverse Biological Functions of Ketone Bodies and Relevance of HMGCS2 to Health and Disease.Biomolecules · 2025Review
- β-cell heterogeneity and molecular plasticity in type 2 diabetes: multi-omics perspectives and the role of gut microbiota.Frontiers in cell and developmental biology · 2025Review
- Role of FFAR3 in ketone body regulated glucagon-like peptide 1 secretion.Biochemistry and biophysics reports · 2024Article
- Intestinal Ketogenesis and Permeability.International journal of molecular sciences · 2024Article
- Cellular mechanisms of incretin hormone secretion.Journal of molecular endocrinology · 2024Review
- RNA sequencing unravels novel L cell constituents and mechanisms of GLP-1 secretion in human gastric bypass-operated intestine.Diabetologia · 2024Article
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- Gut adaptation after gastric bypass in humans reveals metabolically significant shift in fuel metabolism.Obesity (Silver Spring, Md.) · 2023Article
- The therapeutic potential of glucagon-like peptide-1 for persons with addictions based on findings from preclinical and clinical studies.Frontiers in pharmacology · 2023Review
- Insight into the role of the gut-brain axis in alcohol-related responses: Emphasis on GLP-1, amylin, and ghrelin.Frontiers in psychiatry · 2022Review
- Circadian secretion rhythm of GLP-1 and its influencing factors.Frontiers in endocrinology · 2022Review
- Roux-en-Y gastric bypass-induced perturbative changes in microbial communities and metabolic pathways in rats.Frontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveFood intake normally stimulates release of satiety and insulin-stimulating intestinal hormones, such as glucagon-like peptide (GLP)-1. This response is blunted in obese insulin resistant subjects, but is rapidly restored following Roux-en-Y gastric bypass (RYGB) surgery. We hypothesised this to be a result of the metabolic changes taking place in the small intestinal mucosa following the anatomical rearrangement after RYGB surgery, and aimed at identifying such mechanisms.
designJejunal mucosa biopsies from patients undergoing RYGB surgery were retrieved before and after very-low calorie diet, at time of surgery and 6 months postoperatively. Samples were analysed by global protein expression analysis and Western blotting. Biological functionality of these findings was explored in mice and enteroendocrine cells (EECs) primary mouse jejunal cell cultures.
resultsThe most prominent change found after RYGB was decreased jejunal expression of the rate-limiting ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (mHMGCS), corroborated by decreased ketone body levels. In mice, prolonged high-fat feeding induced the expression of mHMGCS and functional ketogenesis in jejunum. The effect of ketone bodies on gut peptide secretion in EECs showed a ∼40% inhibition of GLP-1 release compared with baseline.
conclusionIntestinal ketogenesis is induced by high-fat diet and inhibited by RYGB surgery. In cell culture, ketone bodies inhibited GLP-1 release from EECs. Thus, we suggest that this may be a mechanism by which RYGB can remove the inhibitory effect of ketone bodies on EECs, thereby restituting the responsiveness of EECs resulting in increased meal-stimulated levels of GLP-1 after surgery.
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