ArticleCell metabolism2013
Central GLP-2 enhances hepatic insulin sensitivity via activating PI3K signaling in POMC neurons.
Article in Cell metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
58 citing papers in PubMed, 98 citations in OpenAlex.
- Hypothalamic Control of Liver Health and Disease: From Circuits to Pathophysiology and Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- TOX3 in hypothalamic POMC-lineage cells regulates energy balance via the PTEN-AKT signaling axis.Nature communications · 2026Article
- Liver fibrosis and type 2 diabetes modulate postprandial incretin and glucagon responses in fatty liver disease.Journal of physiology and biochemistry · 2026Article
- GLP-2 alleviates postmenopausal osteoporosis by acting on osteoblasts through the PI3K/AKT/FOXO1 signalling pathway to downregulate FGF23 expression.Journal of orthopaedic surgery and research · 2026Article
- The central signaling pathways related to metabolism-regulating hormones of the gut-brain axis: a review.Journal of translational medicine · 2025Review
- Glucagon-like Peptide-2 Acts Partially Through Central GLP-2R and MC4R in Mobilizing Stored Lipids from the Intestine.Nutrients · 2025Article
- GLP-2 attenuates antipsychotics' adverse metabolic effects.Nature metabolism · 2025Article
- Causal Relationship between Gut Microbiota and Endometrial Cancer: A Two-Sample Mendelian Randomization Study.International journal of medical sciences · 2025Article
- Glucagon-Like Peptide-2 as a Potential Biomarker for Nonalcoholic Fatty Liver Disease in Children with Obesity: Preliminary Assessment of Metabolic Associations and Underlying Mechanisms.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Treatment of Hypothalamic Obesity With GLP-1 Analogs.Journal of the Endocrine Society · 2024Review
- The Possible Involvement of Glucagon-like Peptide-2 in the Regulation of Food Intake through the Gut-Brain Axis.Nutrients · 2024Review
- Early changes of microRNAs in blood one month after bariatric surgery.Diabetology & metabolic syndrome · 2024Article
- GLP-2 regulation of intestinal lipid handling.Frontiers in physiology · 2024Review
- The real-world analysis of adverse events with teduglutide: a pharmacovigilance study based on the FAERS database.Frontiers in pharmacology · 2024Article
- Mechanisms of bariatric surgery for weight loss and diabetes remission.Journal of diabetes · 2023Review
- RISING STARS: Endocrine regulation of metabolic homeostasis via the intestine and gut microbiome.The Journal of endocrinology · 2023Review
- State of art on the mechanisms of laparoscopic sleeve gastrectomy in treating type 2 diabetes mellitus.World journal of diabetes · 2023Review
- N-terminal alterations turn the gut hormone GLP-2 into an antagonist with gradual loss of GLP-2 receptor selectivity towards more GLP-1 receptor interaction.British journal of pharmacology · 2022Article
- Supplementation with artificial sweetener and capsaicin alters metabolic flexibility and performance in heat-stressed and feed-restricted pigs.Journal of animal science · 2022Article
- Implications of peroxisome proliferator-activated receptor gamma (PPARY) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice.Journal of toxicology and environmental health. Part A · 2022Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Glucagon-like peptides (GLP-1/GLP-2) are coproduced and highlighted as key modulators to improve glucose homeostasis and insulin sensitivity after bariatric surgery. However, it is unknown if CNS GLP-2 plays any physiological role in the control of glucose homeostasis and insulin sensitivity. We show that mice lacking GLP-2 receptor (GLP-2R) in POMC neurons display glucose intolerance and hepatic insulin resistance. GLP-2R activation in POMC neurons is required for GLP-2 to enhance insulin-mediated suppression of hepatic glucose production (HGP) and gluconeogenesis. GLP-2 directly modulates excitability of POMC neurons in GLP-2R- and PI3K-dependent manners. GLP-2 initiates GLP-2R-p85α interaction and facilitates PI3K-Akt-dependent FoxO1 nuclear exclusion in POMC neurons. Central GLP-2 suppresses basal HGP and enhances insulin sensitivity, which are abolished in POMC-p110α KO mice. Thus, CNS GLP-2 plays a key physiological role in the control of HGP through activating PI3K-dependent modulation of membrane excitability and nuclear transcription of POMC neurons in the brain.
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Registered trials
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 OpenQuestion graph.