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Allo-lithocholic acid is a secondary bile acid and a microbial metabolite derived from lithocholic acid. It is present in normal serum and feces and can be found at higher concentrations in certain disease states such as colon cancer. Allo-LCA acts as a dual agonist of the G protein-coupled bile acid receptor 1 (GPBAR1/TGR5) and an inverse agonist of the nuclear receptor RORγt. Through these mechanisms it modulates intestinal immunity by preventing M1 polarization of macrophages and Th17 polarization of CD4+ T cells. In animal models of metabolic dysfunction-associated steatohepatitis (MASH), administration of allo-LCA improved insulin sensitivity and liver lipid accumulation while restoring bile acid homeostasis and reducing pro-inflammatory adipokines. Allo-LCA also activates large-conductance calcium-activated potassium channels[1][2][7]. As a bile acid it facilitates excretion, absorption and transport of fats in the intestine[3][4].
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