ArticleNutrition & metabolism2021
The deletion of glucagon-like peptide-1 receptors expressing neurons in the dorsomedial hypothalamic nucleus disrupts the diurnal feeding pattern and induces hyperphagia and obesity.
Article in Nutrition & metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Brain-Wide Connectivity and Topographic Organization of Leptin Receptor Neurons in the Dorsomedial Hypothalamus.CNS neuroscience & therapeutics · 2026Article
- Review
- A direct SCN-to-DMH output pathway organizes circadian behavioral timing.bioRxiv : the preprint server for biology · 2026Article
- Hypothalamic regulation of sepsis-associated anorexia: cytokine and hormonal signalling through AgRP/POMC circuits.EMBO molecular medicine · 2026Review
- GLP-1 Receptor Agonists at the Crossroads of Circadian Biology, Sleep, and Metabolic Disease.International journal of molecular sciences · 2026Review
- GLP-1 physiology and pharmacology along the gut-brain axis.The Journal of clinical investigation · 2026Review
- Glucagon-Like Peptide 1 (GLP-1) Action on Hypothalamic Feeding Circuits.Endocrinology · 2025Review
- Glucagon-Like Peptide-1 and Hypothalamic Regulation of Satiation: Cognitive and Neural Insights from Human and Animal Studies.Diabetes & metabolism journal · 2025Review
- Integration of Glucagon-Like Peptide 1 Receptor Actions Through the Central Amygdala.Endocrinology · 2025Review
- Novel neural pathways targeted by GLP-1R agonists and bariatric surgery.Pflugers Archiv : European journal of physiology · 2025Review
- Central and peripheral neural circuits regulating glucose homeostasis.npj biomedical innovations · 2025Review
- GLP-1 increases preingestive satiation via hypothalamic circuits in mice and humans.Science (New York, N.Y.) · 2024Article
- Progress in the contrary effects of glucagon-like peptide-1 and chemerin on obesity development.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Exercise-induced hypothalamic neuroplasticity: Implications for energy and glucose metabolism.Molecular metabolism · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFeeding rhythm disruption contributes to the development of obesity. The receptors of glucagon-like peptide-1 (GLP-1) are distributed in the wide regions of the brain. Among these regions, GLP-1 receptors (GLP-1R) are expressed in the dorsomedial hypothalamic nucleus (DMH) which are known to be associated with thermogenesis and circadian rhythm development. However, the physiological roles of GLP-1R expressing neurons in the DMH remain elusive.
methodsTo examine the physiological role of GLP-1R expressing neurons in the DMH, saporin-conjugated exenatide4 was injected into rat brain DMH to delete GLP-1R-positive neurons. Subsequently, locomotor activity, diurnal feeding pattern, amount of food intake and body weight were measured.
resultsThis deletion of GLP-1R-positive neurons in the DMH induced hyperphagia, the disruption of diurnal feeding pattern, and obesity. The deletion of GLP-1R expressing neurons also reduced glutamic acid decarboxylase 67 and cholecystokinin A receptor mRNA levels in the DMH. Also, it reduced the c-fos expression after refeeding in the suprachiasmatic nucleus (SCN). Thirty percent of DMH neurons projecting to the SCN expressed GLP-1R. Functionally, refeeding after fasting induced c-fos expression in the SCN projecting neurons in the DMH. As for the projection to the DMH, neurons in the nucleus tractus solitarius (NTS) were found to be projecting to the DMH, with 33% of those neurons being GLP-1-positive. Refeeding induced c-fos expression in the DMH projecting neurons in the NTS.
conclusionThese findings suggest that GLP-1R expressing neurons in the DMH may mediate feeding termination. In addition, this meal signal may be transmitted to SCN neurons and change the neural activities.
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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.