ArticleThe Journal of clinical investigation2023
Suppression of food intake by Glp1r/Lepr-coexpressing neurons prevents obesity in mouse models.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- Leptin-sensitive hypothalamic Lepr+/Glp1r+ neurons limit hyperphagia and weight gain in diet-induced obesity.The EMBO journal · 2026Article
- The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026Review
- Generation of human appetite-regulating neurons and tanycytes from pluripotent stem cells.Cell stem cell · 2026Article
- Increased leptin signaling drives the response of hypothalamic LepRb neurons to diet-induced obesity.Molecular metabolism · 2026Article
- From identity to function: unveiling the cellular complexity of hypothalamic feeding circuits.Reviews in endocrine & metabolic disorders · 2026Review
- IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism.Molecular metabolism · 2026Article
- Hypothalamic regulation of sepsis-associated anorexia: cytokine and hormonal signalling through AgRP/POMC circuits.EMBO molecular medicine · 2026Review
- Article
- Inhibition of daily torpor in mice requires calories, not just feeding: a potential role for GLP-1.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2026Article
- Molecularly defined subpopulations of leptin receptor neurons dissociate the control of food intake from blood pressure.bioRxiv : the preprint server for biology · 2026Article
- GLP-1 physiology and pharmacology along the gut-brain axis.The Journal of clinical investigation · 2026Review
- Evaluation of leptin treatment on maintenance of body weight loss in diet-induced obese mice.Diabetes, obesity & metabolism · 2026Article
- Liraglutide use in congenital generalized lipodystrophy: glycemic and metabolic outcomes.Frontiers in endocrinology · 2026Article
- Tirzepatide Synergizes with Leptin on Weight Loss and Restoring Metabolic Homeostasis in Diet-induced Obesity Model.bioRxiv : the preprint server for biology · 2025Article
- Leptin as a Potential Modifier of Neuroinflammation: Contrasting Roles in Alzheimer's Disease and Multiple Sclerosis.International journal of molecular sciences · 2025Review
- Leptin and G-protein coupled receptor (GPCR) signaling: Therapeutic potential in obesity.The Journal of biological chemistry · 2025Review
- Glucagon-Like Peptide 1 (GLP-1) Action on Hypothalamic Feeding Circuits.Endocrinology · 2025Review
- Mechanisms of glucagon-like-peptide 1 in the brain beyond metabolic effects.Annals of pediatric endocrinology & metabolism · 2025Article
- Molecular mechanisms and neural mediators of leptin action.Genes & development · 2025Review
- Metabolic Improvements With Tirzepatide in Lipodystrophy: A Novel Option?Diabetes care · 2025Observational
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
The adipose-derived hormone leptin acts via its receptor (LepRb) in the brain to control energy balance. A potentially unidentified population of GABAergic hypothalamic LepRb neurons plays key roles in the restraint of food intake and body weight by leptin. To identify markers for candidate populations of LepRb neurons in an unbiased manner, we performed single-nucleus RNA-Seq of enriched mouse hypothalamic LepRb cells, identifying several previously unrecognized populations of hypothalamic LepRb neurons. Many of these populations displayed strong conservation across species, including GABAergic Glp1r-expressing LepRb (LepRbGlp1r) neurons, which expressed more Lepr than other LepRb cell populations. Ablating Lepr from LepRbGlp1r cells provoked hyperphagic obesity without impairing energy expenditure. Similarly, improvements in energy balance caused by Lepr reactivation in GABA neurons of otherwise Lepr-null mice required Lepr expression in GABAergic Glp1r-expressing neurons. Furthermore, restoration of Glp1r expression in LepRbGlp1r neurons in otherwise Glp1r-null mice enabled food intake suppression by the GLP1R agonist, liraglutide. Thus, the conserved GABAergic LepRbGlp1r neuron population plays crucial roles in the suppression of food intake by leptin and GLP1R agonists.
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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.