Obesity is a critical risk factor for various diseases including type II diabetes, cerebral infarction, cardiovascular diseases, and various cancers. Acrylamide (ACR) is present in wide range of foods, including fried potato products, root vegetables, bakery products, chips, cakes, cereals, and coffee. In this study, ACR treatment dramatically increased the accumulation of lipid droplets. We also examined expression levels of peroxisome proliferator-activated receptors γ (PPARγ), CCAAT enhancer binding protein α (c/EBPα), and CCAAT enhancer binding protein β (c/EBPβ) as adipogenic transcription factors for adipocyte differentiation. They were dose-dependently increased by treatment of ACR. Moreover, effects of ACR on mitogen-activated protein kinases (MAPKs) and 5′ AMP-activated protein kinase (AMPK)-Acetyl-CoA carboxylase (ACC) activation were investigated. Results also showed that ACR induced phosphorylation of MAPKs and AMPK-ACC. ACR also induced expression of adipocyte fatty acid-binding protein (aP2), lipoprotein lipase (LPL), sterol regulatory element-binding protein (SREBP)-1c, and fatty acid synthase (FAS). Exposure of ACR to high fat diet (HFD)-fed mice significantly increased body weight, organ weight, and fat mass of mice. Collectively, these result showed that ACR can act as an enhancer of adipocyte. Therefore, we suggest that up-regulation of the adipogenesis by ACR may be related to the regulation of the MAPKs and AMPK-ACC pathway.

肥胖是各种疾病的关键危险因素，包括II型糖尿病，脑梗塞，心血管疾病和各种癌症。丙烯酰胺（ACR）存在于各种食品中，包括炸土豆产品，块根蔬菜，烘焙产品，薯片，蛋糕，谷物和咖啡。在这项研究中，ACR治疗显着增加了脂滴的积累。我们还检查了过氧化物酶体增殖物激活受体γ（PPARγ），CCAAT增强子结合蛋白α（c /EBPα）和CCAAT增强子结合蛋白β（c /EBPβ）的表达水平，作为脂肪细胞分化的成脂转录因子。通过治疗ACR，它们的剂量依赖性增加。而且，研究了ACR对有丝分裂原活化蛋白激酶（MAPKs）和5'AMP活化蛋白激酶（AMPK）-乙酰辅酶A羧化酶（ACC）活化的影响。结果还表明，ACR诱导了MAPK和AMPK-ACC的磷酸化。ACR还诱导脂肪细胞脂肪酸结合蛋白（aP2），脂蛋白脂肪酶（LPL），固醇调节元件结合蛋白（SREBP）-1c和脂肪酸合酶（FAS）的表达。高脂饮食（HFD）喂养的小鼠暴露于ACR会显着增加小鼠的体重，器官重量和脂肪量。总的来说，这些结果表明ACR可以作为脂肪细胞的增强剂。因此，我们建议ACR对脂肪生成的上调可能与MAPKs和AMPK-ACC通路的调节有关。ACR还诱导脂肪细胞脂肪酸结合蛋白（aP2），脂蛋白脂肪酶（LPL），固醇调节元件结合蛋白（SREBP）-1c和脂肪酸合酶（FAS）的表达。高脂饮食（HFD）喂养的小鼠暴露于ACR会显着增加小鼠的体重，器官重量和脂肪量。总的来说，这些结果表明ACR可以作为脂肪细胞的增强剂。因此，我们建议ACR对脂肪生成的上调可能与MAPKs和AMPK-ACC通路的调节有关。ACR还诱导脂肪细胞脂肪酸结合蛋白（aP2），脂蛋白脂肪酶（LPL），固醇调节元件结合蛋白（SREBP）-1c和脂肪酸合酶（FAS）的表达。高脂饮食（HFD）喂养的小鼠暴露于ACR会显着增加小鼠的体重，器官重量和脂肪量。总的来说，这些结果表明ACR可以作为脂肪细胞的增强剂。因此，我们建议ACR对脂肪生成的上调可能与MAPKs和AMPK-ACC通路的调节有关。这些结果表明ACR可以作为脂肪细胞的增强剂。因此，我们建议ACR对脂肪生成的上调可能与MAPKs和AMPK-ACC通路的调节有关。这些结果表明ACR可以作为脂肪细胞的增强剂。因此，我们建议ACR对脂肪生成的上调可能与MAPKs和AMPK-ACC通路的调节有关。