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Butyrate attenuates lipolysis in adipocytes co-cultured with macrophages through non-prostaglandin E2–mediated and prostaglandin E2–mediated pathways

机译:丁酸盐通过非前列腺素E2介导和前列腺素E2介导的途径减弱与巨噬细胞共培养的脂肪细胞的脂解作用

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摘要

BackgroundInteractions between adipocytes and macrophages are associated with metabolic disorders. Production of pro-inflammatory mediators and the release of free fatty acids (FFAs) increase when these cells are co-cultured; butyrate significantly diminishes these effects by suppressing both the macrophage inflammatory and adipocyte lipolysis pathways. Butyrate is known to up-regulate the expression of prostaglandin E2 (PGE2). Therefore, we hypothesized that PGE2 is associated with the suppression of lipolysis by butyrate in co-culture.
机译:背景脂肪细胞和巨噬细胞之间的相互作用与代谢异常有关。当这些细胞共培养时,促炎介质的产生和游离脂肪酸(FFA)的释放增加;丁酸酯通过抑制巨噬细胞炎性和脂肪细胞脂解途径,显着降低了这些作用。已知丁酸盐会上调前列腺素E2(PGE2)的表达。因此,我们假设PGE2与共培养物中丁酸盐抑制脂解作用有关。

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