ArticleCell reports2021
Hypothalamic steroid receptor coactivator-2 regulates adaptations to fasting and overnutrition.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Vestibular neurons link motion sickness, behavioural thermoregulation and metabolic balance in mice.Nature metabolism · 2025Article
- Neural circuits expressing the serotonin 2C receptor regulate memory in mice and humans.Science advances · 2024Article
- MANF in POMC Neurons Promotes Brown Adipose Tissue Thermogenesis and Protects Against Diet-Induced Obesity.Diabetes · 2022Article
- SRC2 controls the refeeding response in mice.Nature reviews. Endocrinology · 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
- Effects of the POMC System on Glucose Homeostasis and Potential Therapeutic Targets for Obesity and Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- The combination ofFrontiers in pharmacology · 2022Article
- Decidualization of human endometrial stromal cells requires steroid receptor coactivator-3.Frontiers in reproductive health · 2022Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
The neuroendocrine system coordinates metabolic and behavioral adaptations to fasting, including reducing energy expenditure, promoting counterregulation, and suppressing satiation and anxiety to engage refeeding. Here, we show that steroid receptor coactivator-2 (SRC-2) in pro-opiomelanocortin (POMC) neurons is a key regulator of all these responses to fasting. POMC-specific deletion of SRC-2 enhances the basal excitability of POMC neurons; mutant mice fail to efficiently suppress energy expenditure during food deprivation. SRC-2 deficiency blunts electric responses of POMC neurons to glucose fluctuations, causing impaired counterregulation. When food becomes available, these mutant mice show insufficient refeeding associated with enhanced satiation and discoordination of anxiety and food-seeking behavior. SRC-2 coactivates Forkhead box protein O1 (FoxO1) to suppress POMC gene expression. POMC-specific deletion of SRC-2 protects mice from weight gain induced by an obesogenic diet feeding and/or FoxO1 overexpression. Collectively, we identify SRC-2 as a key molecule that coordinates multifaceted adaptive responses to food shortage.
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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.