ArticleEMBO reports2026
POMC AMPKα1 deletion drives male-specific BAT thermogenesis and obesity resistance.
Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
27 authors.
Funding
Abstract
Proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARC) play a critical role in energy homeostasis. 5'-adenosine monophosphate-activated protein kinase (AMPK) is a serine/threonine kinase, which acts as the main energy sensor in the cell. The heterotrimeric AMPK results from the combination of a catalytic α subunit (α1, α2) with two regulatory subunits, β (β1, β2) and γ (γ1, γ2 and γ3). Hypothalamic AMPK plays a key role in the control of energy balance, but current evidence shows that the precise combination of its heterotrimeric components determines its physiological action. Our findings show that AMPKα1 ablation in POMC neurons has a sex-dependent protective effect against diet-induced obesity because of increased thermogenesis in brown adipose tissue (BAT) in males, but not in females. At the molecular level, deletion of AMPKα1 in POMC neurons disrupts the ARC phosphoproteome and is associated with ameliorated endoplasmic reticulum (ER) stress and reduced ceramide content. These findings highlight the complex function of the different AMPK subunits in the hypothalamic regulation of energy balance.
Identifiers
42680850What Socratic holds
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 Socratic graph.