ArticleMolecular metabolism2026
Liver-derived Indian hedgehog (Ihh) couples fast-feed transition to thermogenic and metabolic homeostasis.
Article in Molecular metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Unbiased plasma proteomics reveals hemolysis during ADAMTS13 relapse in patients with immune TTP.Blood advances · 2026Article
- Hepatic LGALS4 Alleviates Diet-Induced Steatosis by Promoting AMPK-Dependent Fatty Acid Oxidation.Diabetes, obesity & metabolism · 2026Article
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15 authors.
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Abstract
BACKGROUND &
aimsObesity and type 2 diabetes are global health challenges driven by genetic and environmental factors, including diet. While intermittent fasting improves metabolic health, the hepatic mechanisms linking feeding transitions to systemic metabolic regulation remain unclear. We investigated whether Indian Hedgehog (Ihh), a liver-derived hepatokine, coordinates metabolic responses to nutritional transitions.
methodsWe employed genetic and epigenetic tools, including liver-specific deletion of the PRC2 component Eed, to study Ihh regulation. In vivo metabolic phenotyping, thermogenic gene profiling, and Ihh immunoneutralization assessed its function. VLDL-associated Ihh levels were measured and their correlations with metabolic traits were analyzed in humans.
resultsIhh is induced upon feeding and promotes adipose thermogenesis, enhancing metabolic flexibility. The Ihh locus in hepatocytes resides in a bivalent chromatin state; hepatic Eed deletion derepresses Ihh, conferring resistance to diet-induced obesity and insulin resistance. Immunoneutralization of Ihh reverses this protection, confirming its necessity. Ihh circulates in complex with VLDL. Human Ihh-VLDL levels decline with age and correlate with improved metabolic parameters, including insulin sensitivity, HDL/LDL ratio, and reduced adiposity. CONCLUSIONS & IMPLICATIONS: Ihh is a liver-derived, epigenetically regulated hepatokine that links nutrient timing to systemic metabolic control by stimulating thermogenesis and promoting glucose homeostasis. These findings identify Ihh as a key inter-organ signal coupling hepatic chromatin dynamics to energy balance. The age-related decline in circulating Ihh and its strong association with metabolic health suggest that enhancing Ihh signaling may represent a novel therapeutic avenue for obesity and type 2 diabetes.
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