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首页> 外文期刊>The Journal of Nutritional Biochemistry >Polychlorinated biphenyl 153 is a diet-dependent obesogen that worsens nonalcoholic fatty liver disease in male C57BL6/J mice.
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Polychlorinated biphenyl 153 is a diet-dependent obesogen that worsens nonalcoholic fatty liver disease in male C57BL6/J mice.

机译：多氯联苯153是一种饮食依赖性致肥胖剂，可加剧雄性C57BL6 / J小鼠的非酒精性脂肪肝疾病。

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Background. Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that are detectable in the serum of all American adults. Amongst PCB congeners, PCB 153 has the highest serum level. PCBs have been dose-dependently associated with obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD) in epidemiological studies. Objective. The purpose of this study is to determine mechanisms by which PCB 153 worsens diet-induced obesity and NAFLD in male mice fed a high-fat diet (HFD). Methods. Male C57BL6/J mice were fed either control or 42% milk fat diet for 12 weeks with or without PCB 153 coexposure (50 mg/kg ip x4). Glucose tolerance test was performed, and plasma and tissues were obtained at necropsy for measurements of adipocytokine levels, histology and gene expression. Results. In control diet-fed mice, addition of PCB 153 had minimal effects on any of the measured parameters. However, PCB 153 treatment in high-fat-fed mice was associated with increased visceral adiposity, hepatic steatosis and plasma adipokines including adiponectin, leptin, resistin and plasminogen activator inhibitor-1 levels. Likewise, coexposure reduced expression of hepatic genes implicated in beta-oxidation while increasing the expression of genes associated with lipid biosynthesis. Regardless of diet, PCB 153 had no effect on insulin resistance or tumor necrosis factor alpha levels. Conclusion. PCB 153 is an obesogen that exacerbates hepatic steatosis, alters adipocytokines and disrupts normal hepatic lipid metabolism when administered with HFD but not control diet. Because all US adults have been exposed to PCB 153, this particular nutrient-toxicant interaction potentially impacts human obesity/NAFLD
机译：背景。多氯联苯（PCB）是持久性环境污染物，可在所有美国成年人的血清中检测到。在多氯联苯同类物中，多氯联苯153具有最高的血清水平。在流行病学研究中，PCB与肥胖，代谢综合征和非酒精性脂肪肝疾病（NAFLD）呈剂量依赖性。目的。这项研究的目的是确定PCB 153加剧高脂饮食（HFD）喂养的雄性小鼠饮食引起的肥胖和NAFLD的机制。方法。给雄性C57BL6 / J小鼠喂食对照或42％乳脂饮食12周，有或无PCB 153共同暴露（50 mg / kg腹膜内x4）。进行葡萄糖耐量测试，并且在尸检时获得血浆和组织以测量脂肪细胞因子水平，组织学和基因表达。结果。在对照饮食喂养的小鼠中，添加PCB 153对任何测量参数的影响均最小。但是，高脂饮食小鼠的PCB 153治疗与内脏脂肪增多，肝脂肪变性和血浆脂肪因子（包括脂联素，瘦素，抵抗素和纤溶酶原激活物抑制剂1水平）增加有关。同样，共同暴露减少了与β-氧化有关的肝基因的表达，同时增加了与脂质生物合成相关的基因的表达。无论饮食如何，PCB 153对胰岛素抵抗或肿瘤坏死因子α水平均无影响。结论。 PCB 153是一种致肥胖剂，当与HFD一起使用但不控制饮食时，会加剧肝脂肪变性，改变脂肪细胞因子并破坏正常的肝脂质代谢。由于所有美国成年人都已经接触过PCB 153，因此这种特殊的营养物-毒物相互作用可能会影响人类肥胖/ NAFLD

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