| First Author | Khan AS | Year | 2017 |
| Journal | Biochimie | Volume | 137 |
| Pages | 78-87 | PubMed ID | 28302472 |
| Mgi Jnum | J:271767 | Mgi Id | MGI:6282162 |
| Doi | 10.1016/j.biochi.2017.03.004 | Citation | Khan AS, et al. (2017) ERK1 and ERK2 activation modulates diet-induced obesity in mice. Biochimie 137:78-87 |
| abstractText | Obesity is a worldwide problem, and dietary lipids play an important role in its pathogenesis. Recently, Erk1 knock-out (ERK1(-/-)) mice have been shown to exhibit low preference for dietary fatty acids. Hence, we maintained Erk1(-/-) mice on a high-fat diet (HFD) to assess the implication of this mitogen-activated protein (MAP) kinase in obesity. The Erk1(-/-) mice, fed the HFD, were more obese than wild-type (WT) animals, fed the same diet. Erk1(-/-) obese mice gained more fat and liver mass than WT obese animals. No difference was observed in daily food and energy intake in HFD-fed both group of animals. However, feed efficiency was higher in Erk1(-/-) than WT animals. Blood cholesterol, triglyceride and insulin concentrations were higher in Erk1(-/-) obese mice compared to WT obese animals. Accordingly, homeostatic model assessment of insulin resistance (HOMA-IR) value was higher in Erk1(-/-) obese mice compared to WT obese animals. Interestingly, only Erk1(-/-) obese mice, but not WT-obese animals, exhibited high degree of phosphorylation of liver MEK, the upstream regulator of ERK1/2. This phenomenon was associated with high liver ERK2 phosphorylation in Erk1(-/-) obese mice which also had high liver acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase (FAS) mRNA expression, suggesting high lipogenesis in these animals. The Erk1(-/-) obese mice also had low PPAR-alpha and CPT1beta mRNA, indicating low fatty acid oxidation. Our observations suggest that ERK1 and ERK2 might play key roles in the regulation of obesity. |
