Insights by which TUDCA is a potential therapy against adiposity. Frontiers in endocrinology Adipose tissue is an organ with metabolic and endocrine activity. White, brown and ectopic adipose tissues have different structure, location, and function. Adipose tissue regulates energy homeostasis, providing energy in nutrient-deficient conditions and storing it in high-supply conditions. To attend to the high demand for energy storage during obesity, the adipose tissue undergoes morphological, functional and molecular changes. Endoplasmic reticulum (ER) stress has been evidenced as a molecular hallmark of metabolic disorders. In this sense, the ER stress inhibitor tauroursodeoxycholic acid (TUDCA), a bile acid conjugated to taurine with chemical chaperone activity, has emerged as a therapeutic strategy to minimize adipose tissue dysfunction and metabolic alterations associated with obesity. In this review, we highlight the effects of TUDCA and receptors TGR5 and FXR on adipose tissue in the setting of obesity. TUDCA has been demonstrated to limit metabolic disturbs associated to obesity by inhibiting ER stress, inflammation, and apoptosis in adipocytes. The beneficial effect of TUDCA on perivascular adipose tissue (PVAT) function and adiponectin release may be related to cardiovascular protection in obesity, although more studies are needed to clarify the mechanisms. Therefore, TUDCA has emerged as a potential therapeutic strategy for obesity and comorbidities. 10.3389/fendo.2023.1090039

Effects of epoxy stearic acid on lipid metabolism in HepG2 cells. Liu Ying,Li Jinwei,Liu Yuanfa Journal of food science In the present study, effects of cis-9,10-epoxystearic acid (ESA) generated by the thermal oxidation of oleic acid on HepG2 cells, including intracellular lipid accumulation, fatty acid composition, and lipid metabolism, were investigated. Our results revealed that ESA increased the number and size of cellular lipid droplets. Intracellular triacylglycerol and total cholesterol content demonstrated that ESA induced lipid accumulation in HepG2 cells in a dose- and time-dependent manner. Results of fatty acid composition further indicated that ESA could lead to intracellular lipid accumulation. Our results also revealed that ESA may suppress the fatty acid oxidation in peroxisomes and mitochondria, including PPARα, Cpt1α, and Acox1, whereas the expression of genes involved in lipid synthesis, including Srebp-1c and Scd1, was enhanced. These findings provide critical information on the effects of ESA on HepG2 cells, particularly lipid accumulation and metabolism, which is important for evaluating the biosafety of the oxidative product of oleic acid. PRACTICAL APPLICATION: The administration of cis-9,10-epoxystearic acid to HepG2 cells could lead to disorder of lipid metabolism of cells by enhancing the intracellular lipid content, as well as suppressing the fatty acid oxidation in peroxisomes and mitochondria. These findings could provide information for the evaluation of the biosafety of the oxidative product of oleic acid. 10.1111/1750-3841.15405