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首页> 外文期刊>Archives of Toxicology >Polychlorinated biphenyls exposure-induced insulin resistance is mediated by lipid droplet enlargement through Fsp27
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Polychlorinated biphenyls exposure-induced insulin resistance is mediated by lipid droplet enlargement through Fsp27

机译：聚氯氯联苯曝光诱导的胰岛素抗性通过脂质液滴扩大通过FSP27介导

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摘要

Although epidemiological and experimental studies demonstrated that polychlorinated biphenyls (PCBs) lead to insulin resistance, the mechanism underlying PCBs-induced insulin resistance has remained unsolved. In this study, we examined in vitro and in vivo effects of PCB-118 (dioxin-like PCB) and PCB-138 (non-dioxin-like PCB) on adipocyte differentiation, lipid droplet growth, and insulin action. 3T3-L1 adipocytes were incubated with PCB-118 or PCB-138 during adipocyte differentiation. For in vivo studies, C57BL/6 mice were administered PCB-118 or PCB-138 (37.5 mg/kg) by intraperitoneal injection and we examined adiposity and whole-body insulin action. PCB-118 and PCB-138 significantly promoted adipocyte differentiation and increased the lipid droplet (LD) size in 3T3-L1 adipocytes. In mice, both PCBs increased adipose mass and adipocyte size. Furthermore, both PCBs induced insulin resistance in vitro and in vivo. Expression of fat-specific protein 27 (Fsp27), which is localized to LD contact sites, was increased in PCB-treated 3T3-L1 adipocytes and mice. Depletion of Fsp27 by siRNA resulted in the inhibition of LD enlargement and attenuation of insulin resistance in PCB-treated 3T3-L1 adipocytes. An anti-diabetic drug, metformin, attenuated insulin resistance in PCB-treated 3T3-L1 adipocytes through the reduced expression of Fsp27 protein and LD size. This study suggests that PCB exposure-induced insulin resistance is mediated by LD enlargement through Fsp27.
机译：虽然流行病学和实验研究表明，多氯联苯（PCB）导致胰岛素抵抗，但依赖于PCBS诱导的胰岛素抗性的机制保持未解决。在这项研究中，我们在体外检查了PCB-118（二恶英PCB）和PCB-138（非二恶英样PCB）对脂肪细胞分化，脂质液滴生长和胰岛素作用的体内效应。在脂肪细胞分化期间，将3T3-L1脂肪细胞与PCB-118或PCB-138一起温育。对于体内研究，通过腹膜内注射施用C57BL / 6小鼠（PCB-118或PCB-138（37.5mg / kg），并检查肥胖和全身胰岛素作用。 PCB-118和PCB-138显着促进了脂肪细胞分化并增加了3T3-L1脂肪细胞中的脂质液滴（LD）尺寸。在小鼠中，PCB均增加脂肪瘤和脂肪细胞尺寸。此外，PCB均在体外和体内诱导胰岛素抵抗力。在PCB处理的3T3-L1脂肪细胞和小鼠中，掺入LD接触位点的脂肪特异性蛋白27（FSP27）的表达增加。通过siRNA的FSP27耗尽导致PCB处理的3T3-L1脂肪细胞中LD扩大和胰岛素抗性的抑制和衰减。通过减少FSP27蛋白和LD尺寸的表达，抗糖尿病药物，二甲双胍，在PCB处理的3T3-L1脂肪细胞中减弱胰岛素抗性。该研究表明，PCB暴露诱导的胰岛素抗性通过FSP27通过LD扩大介导。

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