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The liver is the central organ involved in lipid metabolism. Dyslipidemia and its related disorders, including non-alcoholic fatty liver disease(NAFLD), obesity and other metabolic diseases, are of increasing public health concern due to their increasing prevalence in the population. Besides their well-characterized functions in cholesterol homoeostasis and nutrient absorption, bile acids are also important metabolic regulators and function as signaling hormones by activating specific nuclear receptors, G-protein coupled receptors, and multiple signaling pathways. Recent studies identified a new signaling pathway by which conjugated bile acids(CBA) activate the extracellular regulated protein kinases(ERK1/2) and protein kinase B(AKT) signaling pathway via sphingosine-1-phosphate receptor 2(S1PR2). CBA-induced activation of S1PR2 is a key regulator of sphingosine kinase 2(Sph K2) andhepatic gene expression. This review focuses on recent findings related to the role of bile acids/S1PR2-mediated signaling pathways in regulating hepatic lipid metabolism.
The liver is the central organ involved in lipid metabolism. Dyslipidemia and its related disorders, including non-alcoholic fatty liver disease (NAFLD), obesity and other metabolic diseases, are of increasing public health concern due to their increasing prevalence in the population. their well-characterized functions in cholesterol homoeostasis and nutrient absorption, bile acids are also important metabolic regulators and function as signaling hormones by activating specific nuclear receptors, G-protein coupled receptors, and multiple signaling pathways. CBA-induced activation of S1PR2 is a key regulator of sphingosine (CBA) activate the extracellularly regulated protein kinases (ERK1 / 2) and protein kinase B (AKT) signaling pathway via sphingosine-1-phosphate receptor 2 kinase 2 (Sph K2) and hepatic gene expression. This review focuses on recent findings related to the role of bile acids / S1PR2-m ediated signaling pathways in regulating hepatic lipid metabolism.