| First Author | Li M | Year | 2015 |
| Journal | Diabetes | Volume | 64 |
| Issue | 12 | Pages | 4023-32 |
| PubMed ID | 26307588 | Mgi Jnum | J:246936 |
| Mgi Id | MGI:5923537 | Doi | 10.2337/db14-1891 |
| Citation | Li M, et al. (2015) Role of PKCdelta in Insulin Sensitivity and Skeletal Muscle Metabolism. Diabetes 64(12):4023-32 |
| abstractText | Protein kinase C (PKC)delta has been shown to be increased in liver in obesity and plays an important role in the development of hepatic insulin resistance in both mice and humans. In the current study, we explored the role of PKCdelta in skeletal muscle in the control of insulin sensitivity and glucose metabolism by generating mice in which PKCdelta was deleted specifically in muscle using Cre-lox recombination. Deletion of PKCdelta in muscle improved insulin signaling in young mice, especially at low insulin doses; however, this did not change glucose tolerance or insulin tolerance tests done with pharmacological levels of insulin. Likewise, in young mice, muscle-specific deletion of PKCdelta did not rescue high-fat diet-induced insulin resistance or glucose intolerance. However, with an increase in age, PKCdelta levels in muscle increased, and by 6 to 7 months of age, muscle-specific deletion of PKCdelta improved whole-body insulin sensitivity and muscle insulin resistance and by 15 months of age improved the age-related decline in whole-body glucose tolerance. At 15 months of age, M-PKCdeltaKO mice also exhibited decreased metabolic rate and lower levels of some proteins of the OXPHOS complex suggesting a role for PKCdelta in the regulation of mitochondrial mass at older age. These data indicate an important role of PKCdelta in the regulation of insulin sensitivity and mitochondrial homeostasis in skeletal muscle with aging. |
