ArticleNutrition & diabetes2019
Gpr17 deficiency in POMC neurons ameliorates the metabolic derangements caused by long-term high-fat diet feeding.
Article in Nutrition & diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- G Protein-Coupled Receptor 17 (Gpr17) Enhances Leptin and Insulin Sensitivity in Lean and Obese Mouse Models.Obesity (Silver Spring, Md.) · 2026Review
- Leptin and G-protein coupled receptor (GPCR) signaling: Therapeutic potential in obesity.The Journal of biological chemistry · 2025Review
- Discovery of novel and selective GPR17 antagonists as pharmacological tools for developing new therapeutic strategies in diabetes and obesity.European journal of medicinal chemistry · 2025Article
- Microbiome affects mice metabolic homeostasis via differential regulation of gene expression in the brain and gut.Physiological reports · 2025Article
- Pro-Opiomelanocortin and Melanocortin Receptor 3 and 4 Mutations in Genetic Obesity.Biomolecules · 2025Review
- G Protein-Coupled Receptor 17 Inhibits Glucagon-like Peptide-1 Secretion via a Gi/o-Dependent Mechanism in Enteroendocrine Cells.Biomolecules · 2024Article
- G protein-coupled receptor 17 inhibits glucagon-like peptide-1 secretion via a Gi/o-dependent mechanism in enteroendocrine cells.bioRxiv : the preprint server for biology · 2024Article
- The role of oestrogen in determining sexual dimorphism in energy balance.The Journal of physiology · 2023Review
- Leptin signaling and leptin resistance.Medical review (2021) · 2022Review
- Metabolic Profiling of Mice with Deletion of the Orphan G Protein-Coupled Receptor, GPR37L1.Cells · 2022Article
- Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents.International journal of molecular sciences · 2022Review
- Hypothalamic control of energy expenditure and thermogenesis.Experimental & molecular medicine · 2022Review
- Intestinal Gpr17 deficiency improves glucose metabolism by promoting GLP-1 secretion.Cell reports · 2022Article
- Recent advances in neuropeptide-related omics and gene editing: Spotlight on NPY and somatostatin and their roles in growth and food intake of fish.Frontiers in endocrinology · 2022Review
- β-endorphin differentially contributes to food anticipatory activity in male and female mice undergoing activity-based anorexia.Physiological reports · 2021Article
- Leanness and Low Plasma Leptin in GPR17 Knockout Mice Are Dependent on Strain and Associated With Increased Energy Intake That Is Not Suppressed by Exogenous Leptin.Frontiers in endocrinology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundProopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARH) control energy homeostasis by sensing hormonal and nutrient cues and activating secondary melanocortin sensing neurons. We identified the expression of a G protein-coupled receptor, Gpr17, in the ARH and hypothesized that it contributes to the regulatory function of POMC neurons on metabolism.
methodsIn order to test this hypothesis, we generated POMC neuron-specific Gpr17 knockout (PGKO) mice and determined their energy and glucose metabolic phenotypes on normal chow diet (NCD) and high-fat diet (HFD).
resultsAdult PGKO mice on NCD displayed comparable body composition and metabolic features measured by indirect calorimetry. By contrast, PGKO mice on HFD demonstrated a sexually dimorphic phenotype with female PGKO mice displaying better metabolic homeostasis. Notably, female PGKO mice gained significantly less body weight and adiposity (p < 0.01), which was associated with increased energy expenditure, locomotor activity, and respiratory quotient, while males did not have an overt change in energy homeostasis. Though PGKO mice of both sexes had comparable glucose and insulin tolerance, detailed analyses of liver gene expression and serum metabolites indicate that PGKO mice could have reduced gluconeogenesis and increased lipid utilization on HFD. To elucidate the central-based mechanism(s) underlying the better-preserved energy and glucose homeostasis in PGKO mice on HFD, we examined the electrophysiological properties of POMC neurons and found Gpr17 deficiency led to increased spontaneous action potentials. Moreover, PGKO mice, especially female knockouts, had increased POMC-derived alpha-melanocyte stimulating hormone and beta-endorphin despite a comparable level of prohormone POMC in their hypothalamic extracts.
conclusionsGpr17 deficiency in POMC neurons protects metabolic homeostasis in a sex-dependent manner during dietary and aging challenges, suggesting that Gpr17 could be an effective anti-obesity target in specific populations with poor metabolic control.
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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 OpenQuestion graph.