| First Author | Wredenberg A | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 350 |
| Issue | 1 | Pages | 202-7 |
| PubMed ID | 16996481 | Mgi Jnum | J:114532 |
| Mgi Id | MGI:3689275 | Doi | 10.1016/j.bbrc.2006.09.029 |
| Citation | Wredenberg A, et al. (2006) Respiratory chain dysfunction in skeletal muscle does not cause insulin resistance. Biochem Biophys Res Commun 350(1):202-7 |
| abstractText | Insulin resistance in skeletal muscle is a characteristic feature of diabetes mellitus type 2 (DM2). Several lines of circumstantial evidence suggest that reduced mitochondrial oxidative phosphorylation capacity in skeletal muscle is a primary defect causing insulin resistance and subsequent development of DM2. We have now experimentally tested this hypothesis by characterizing glucose homeostasis in tissue-specific knockout mice with progressive respiratory chain dysfunction selectively in skeletal muscle. Surprisingly, these knockout mice are not diabetic and have an increased peripheral glucose disposal when subjected to a glucose tolerance test. Studies of isolated skeletal muscle from knockout animals show an increased basal glucose uptake and a normal increase of glucose uptake in response to insulin. In summary, our findings indicate that mitochondrial dysfunction in skeletal muscle is not a primary etiological event in DM2. |
