| First Author | Yuan H | Year | 2017 |
| Journal | FEBS Lett | Volume | 591 |
| Issue | 1 | Pages | 97-108 |
| PubMed ID | 27928820 | Mgi Jnum | J:240038 |
| Mgi Id | MGI:5882254 | Doi | 10.1002/1873-3468.12516 |
| Citation | Yuan H, et al. (2017) AMP-activated protein kinase-mediated expression of heat shock protein beta 1 enhanced insulin sensitivity in the skeletal muscle. FEBS Lett 591(1):97-108 |
| abstractText | Activation of AMP-activated protein kinase (AMPK) has been viewed as an important target for the treatment of insulin resistance. Here, by proteomic analysis, we found that expression of heat shock protein beta-1 (HSPB1) was induced by the AMP analog 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside in palmitate-induced insulin-resistant cells. Overexpression of AMPKalpha2, or activation of AMPKalpha via acute/chronic exercise training, increased HSPB1 expression in the skeletal muscle. In AMPKalpha2-/- mice, HSPB1 expression was downregulated in the quadriceps muscles. Exercise did not increase HSPB1 expression in AMPKalpha2-/- mice. Moreover, overexpression of HSPB1 enhanced insulin sensitivity in palmitate-induced insulin-resistant cells and restored metabolic phenotypes associated with defective AMPK. Finally, HSPB1 was required for AMPK-mediated activation of the class IIa histone deacetylases and glucose uptake in the skeletal muscle. Our results demonstrate that AMPK-mediated HSPB1 expression enhanced insulin sensitivity in the skeletal muscle. |
