ArticleFrontiers in endocrinology2026
Disentangling metabolic impairment in the liver-heart axis: tissue-specific insulin sensitivity in type 2 diabetes.
Article in Frontiers in endocrinology, 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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Abstract
Aims/hypothesis: The liver-heart axis in type 2 diabetes (T2D) reflects key metabolic interactions disrupted by insulin resistance (IR). Organ-specific effects of insulin remain unclear due to challenges in measuring tissue-level IR. This study aims to define liver-heart phenotypes and their associated metabolic impairments, which relate to hepatic fat accumulation linked to metabolic dysfunction-associated steatotic liver disease (MASLD) and coronary artery calcifications (CACs) tied to cardiovascular disease (CVD). Methods: In this cross-sectional study, 41 individuals with controlled T2D underwent biochemical tests and [18F]FDG PET/CT scans before and after a hyperinsulinemic euglycemic clamp (HEC). Tissue-specific insulin-mediated glucose uptake was derived from PET imaging, while CT provided data on radiodensity, volume, fat, and calcifications. Results: A strong inverse correlation was observed between myocardial and liver ΔSUV (r=-0.74, p=2×10 Conclusions/interpretation: This study explores a potential liver-heart metabolic axis in T2D, linked to insulin-mediated dysfunction that may originate in the heart and extend to the liver. The coexistence of organ-specific phenotypes suggests three possible risk profiles, with the HepGluc[+]+mIR phenotype appearing most consistent with advanced T2D progression. Careful identification of this phenotype could support improved monitoring and more personalized treatment strategies in T2D.
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