Abstract:
: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-β-D-ribofuranoside in palmitate-induced insulin-resistant cells. Overexpression of AMPKα2, or activation of AMPKα via acute/chronic exercise training, increased HSPB1 expression in the skeletal muscle. In AMPKα2-/- mice, HSPB1 expression was downregulated in the quadriceps muscles. Exercise did not increase HSPB1 expression in AMPKα2-/- 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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Yuan H,Wang T,Niu Y,Liu X,Fu Ldoi
10.1002/1873-3468.12516subject
Has Abstractpub_date
2017-01-01 00:00:00pages
97-108issue
1eissn
0014-5793issn
1873-3468journal_volume
591pub_type
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