ArticleInternational journal of biological sciences2026
Chronic Stress Induces Hepatic Steatosis via Brain-Hepatic Sympathetic Axis Mediated Catecholamine Resistance.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
- Daytime nap and nighttime sleep duration in relation to dyslipidemia among type 2 diabetes patients in eastern China: a cross-sectional study.Frontiers in nutrition · 2026Article
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5 authors.
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Abstract
Chronic stress is epidemiologically linked to metabolic dysfunction-associated steatotic liver disease (MASLD), yet the underlying mechanisms remain unclear. In mice exposed to chronic restraint stress (CRS), we observed weight-independent hepatic steatosis with marked degeneration of sympathetic fibers. Stress elevated circulating norepinephrine levels but blunted hepatic β-adrenergic/cyclic adenosine monophosphate (cAMP) signaling accompanied by downregulation of β3-adrenergic receptor (β3-AR), indicating hepatic catecholamine resistance. Blocking hepatic sympathetic input prevented stress-aggravated steatosis and restored β-adrenergic signaling, whereas pharmacologic activation of β3-AR with mirabegron alleviated stress-induced lipid accumulation. Pseudorabies virus retrograde tracing and neuronal circuit interrogation further showed that projection from the medial central amygdaloid nucleus (CeM) to paraventricular hypothalamic corticotropin-releasing hormone (CRH
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