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Perfluorooctanoic acid exposure for 28 days affects glucose homeostasis and induces insulin hypersensitivity in mice.
Scientific Reports ( IF 3.8 ) Pub Date : 2015-Jun-12 , DOI: 10.1038/srep11029
Shengmin Yan , Hongxia Zhang , Fei Zheng , Nan Sheng , Xuejiang Guo , Jiayin Dai

Perfluoroalkyl acids (PFAAs) are widely used in many applications due to their unique physical and chemical characteristics. Because of the increasing prevalence of metabolic syndromes, including obesity, dyslipidemia and insulin resistance, concern has arisen about the roles of environmental pollutants in such diseases. Earlier epidemiologic studies showed a potential association between perfluorooctanoic acid (PFOA) and glucose metabolism, but how PFOA influences glucose homeostasis is still unknown. Here, we report on the modulation of the phosphatidylinositol 3-kinase-serine/threonine protein kinase (PI3K-AKT) signaling pathway in the livers of mice after 28 d of exposure to PFOA. Compared with normal mice, PFOA exposure significantly decreased the expression of the phosphatase and tensin homologue (PTEN) protein and affected the PI3K-AKT signaling pathway in the liver. Tolerance tests further indicated that PFOA exposure induced higher insulin sensitivity and glucose tolerance in mice. Biochemical analysis revealed that PFOA exposure reduced hepatic glycogen synthesis, which might be attributed to gluconeogenesis inhibition. The levels of several circulating proteins were altered after PFOA exposure, including proteins potentially related to diabetes and liver disease. Our results suggest that PFOA affected glucose metabolism and induced insulin hypersensitivity in mice.

中文翻译:

全氟辛酸暴露28天会影响葡萄糖体内稳态,并引起小鼠胰岛素超敏反应。

全氟烷基酸(PFAA)由于其独特的物理和化学特性而被广泛用于许多应用中。由于包括肥胖,血脂异常和胰岛素抵抗在内的代谢综合症的患病率上升,因此人们开始关注环境污染物在此类疾病中的作用。早期的流行病学研究表明,全氟辛酸(PFOA)与葡萄糖代谢之间存在潜在的关联,但是PFOA如何影响葡萄糖体内稳态仍是未知的。在这里,我们报道了暴露于PFOA 28天后小鼠肝脏中磷脂酰肌醇3-激酶-丝氨酸/苏氨酸蛋白激酶(PI3K-AKT)信号通路的调节。与正常老鼠相比 PFOA暴露显着降低了肝脏中磷酸酶和张力蛋白同源物(PTEN)蛋白的表达,并影响了PI3K-AKT信号传导途径。耐受性测试进一步表明,PFOA暴露可引起小鼠更高的胰岛素敏感性和葡萄糖耐量。生化分析表明,PFOA的暴露减少了肝糖原的合成,这可能归因于糖异生作用的抑制。暴露于PFOA后,几种循环蛋白的水平发生了变化,包括可能与糖尿病和肝病相关的蛋白。我们的结果表明,PFOA会影响小鼠的葡萄糖代谢并引起胰岛素超敏反应。生化分析表明,PFOA的暴露减少了肝糖原的合成,这可能归因于糖异生作用的抑制。暴露于PFOA后,几种循环蛋白的水平发生了变化,包括可能与糖尿病和肝病相关的蛋白。我们的结果表明,PFOA会影响小鼠的葡萄糖代谢并引起胰岛素超敏反应。生化分析表明,PFOA的暴露减少了肝糖原的合成,这可能归因于糖异生作用的抑制。暴露于PFOA后,几种循环蛋白的水平发生了变化,包括可能与糖尿病和肝病相关的蛋白。我们的结果表明,PFOA会影响小鼠的葡萄糖代谢并引起胰岛素超敏反应。
更新日期:2015-06-15
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