ArticleMolecular medicine (Cambridge, Mass.)2024
Hypothalamic POMC neuron-specific knockout of MC4R affects insulin sensitivity by regulating Kir2.1.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- The role of accessory proteins and co-factors in regulation of melanocortin-4 receptor signalling: An update.Journal of neuroendocrinology · 2026Review
- Interplay Between Enteroendocrine Hormone (Leptin) and Adipokines (Ghrelin and Adiponectin) with Gastric Expression of FTO and MC4R Genes.Scientific reports · 2025Article
- Gold Nanoparticles Disrupt Mitochondrial Activity in Hypothalamic POMC Cells: Implications for Energy Homeostasis.Nanomaterials (Basel, Switzerland) · 2025Article
- Uncovering the role of Gpr45 in obesity regulation.Molecular metabolism · 2025Article
- Neuroendocrinology and the Genetics of Obesity.Endocrinology · 2025Review
- Altered cognitive function in obese patients: relationship to gut flora.Molecular and cellular biochemistry · 2025Review
- Exploration of Appetite Regulation in Yangtze Sturgeon (International journal of molecular sciences · 2025Article
- GPCRs in hypothalamic neurons and their roles in controlling food intake and metabolism.Frontiers in molecular neuroscience · 2025Review
- Setmelanotide-mediated MC4R activation improves hypothalamic obesity via CaMKK2/AMPK pathways.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundImbalance in energy regulation is a major cause of insulin resistance and diabetes. Melanocortin-4 receptor (MC4R) signaling at specific sites in the central nervous system has synergistic but non-overlapping functions. However, the mechanism by which MC4R in the arcuate nucleus (ARC) region regulates energy balance and insulin resistance remains unclear.
methodsThe MC4R
resultsPOMC neuron-specific ablation of MC4R in the ARC region promoted food intake, impaired energy expenditure, leading to increased weight gain and impaired systemic glucose homeostasis. Additionally, MC4R ablation reduced the activation of POMC neuron, and is not tissue-specific for peripheral regulation, suggesting the importance of its central regulation. Mechanistically, sequencing analysis and Co-IP assay demonstrated a direct interaction of MC4R with Kir2.1. Knockdown of Kir2.1 in POMC neuron-specific ablation of MC4R restored the effect of MC4R ablation on energy expenditure and systemic glucose homeostasis, indicating by reduced body weight and ameliorated insulin resistance.
conclusionHypothalamic POMC neuron-specific knockout of MC4R affects energy balance and insulin sensitivity by regulating Kir2.1. Kir2.1 represents a new target and pathway that could be targeted in obesity.
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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.