| First Author | Kant S | Year | 2013 |
| Journal | Cell Rep | Volume | 4 |
| Issue | 4 | Pages | 681-8 |
| PubMed ID | 23954791 | Mgi Jnum | J:202762 |
| Mgi Id | MGI:5521422 | Doi | 10.1016/j.celrep.2013.07.019 |
| Citation | Kant S, et al. (2013) Role of the mixed-lineage protein kinase pathway in the metabolic stress response to obesity. Cell Rep 4(4):681-8 |
| abstractText | Saturated free fatty acid (FFA) is implicated in the metabolic response to obesity. In vitro studies indicate that FFA signaling may be mediated by the mixed-lineage protein kinase (MLK) pathway that activates cJun NH2-terminal kinase (JNK). Here, we examined the role of the MLK pathway in vivo using a mouse model of diet-induced obesity. The ubiquitously expressed MLK2 and MLK3 protein kinases have partially redundant functions. We therefore compared wild-type and compound mutant mice that lack expression of MLK2 and MLK3. MLK deficiency protected mice against high-fat-diet-induced insulin resistance and obesity. Reduced JNK activation and increased energy expenditure contribute to the metabolic effects of MLK deficiency. These data confirm that the MLK pathway plays a critical role in the metabolic response to obesity. |
