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首页> 外文期刊>Journal of cellular physiology. >Resveratrol and HIV-protease inhibitors control UCP1 expression through opposite effects on p38 MAPK phosphorylation in human adipocytes
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Resveratrol and HIV-protease inhibitors control UCP1 expression through opposite effects on p38 MAPK phosphorylation in human adipocytes

机译：白藜芦醇和艾滋病病毒蛋白酶抑制剂控制第38页UCP1表达式通过相反的影响在人类脂肪细胞MAPK磷酸化

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摘要

Brown and brown-like adipocytes (BBAs) control thermogenesis and are detected in adult humans. They express UCP1, which transforms energy into heat. They appear as promising cells to fight obesity. Deciphering the molecular mechanisms leading to the browning of human white adipocytes or the whitening of BBAs represents a goal to properly and safely control the pathways involved in these processes. Here, we analyzed how drugs endowed with therapeutic potential affect the differentiation of human adipose progenitor-cells into BBAs and/or their phenotype. We showed that HIV-protease inhibitors (PI) reduced UCP1 expression in BBAs modifying their metabolic profile and the mitochondria functionality. Lopinavir (LPV) was more potent than darunavir (DRV), a last PI generation. PPARy and PGC-1α were decreased in a PI or cell-specific manner, thus altering UCPl's constitutive expression. In addition, LPV altered p38 MAPK phosphorylation, blunting then the β-adrenergic responses. In contrast, low doses of resveratrol stimulated the activatable expression of UCP1 in a p38 MAPK-dependent manner and counteracted the LPV induced loss of UCP1. This effect was independent of the resveratrol-induced sirtuin-1 expression. Altogether our results uncover how drugs impact crucial components of the networks regulating the expression of the thermogenic signature. They provide important information to control the relevant pathways involved in energy expenditure.
机译：布朗和则脂肪细胞(bba)控制生热作用,在成年人中发现。他们表达UCP1,将能量转换成热量。肥胖。导致人类白色脂肪细胞的褐变或美白bba代表一个目标正确和安全的控制途径在这些流程。具有治疗的潜在影响人类脂肪祖细胞的分化bba和/或他们的表型。艾滋病病毒蛋白酶抑制剂(PI) UCP1减少表达bba修改他们的代谢概要文件和线粒体功能。比darunavir Lopinavir (LPV)更有效(DRV),最后一个π的一代。在π或特异性的方式,减少因此改变UCPl组成型表达。此外,LPV p38 MAPK磷酸化改变,削弱的β肾上腺素的反应。相反,低剂量的白藜芦醇刺激激活做UCP1 p38的表达MAPK-dependent方式和LPV中和诱导UCP1的损失。的resveratrol-induced sirtuin-1表达式。完全揭示药物如何影响我们的结果网络监管中的重要组成部分的表达产热的签名。控制提供重要的信息相关通路参与了能量消耗。

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