Abstract:
:Insulin-induced glucose uptake by skeletal muscle results from Akt2 activation and is severely impaired during insulin resistance. Recently, we and others have demonstrated that BMP9 improves glucose homeostasis in diabetic and non-diabetic rodents. However, the mechanism by which BMP9 modulates insulin action remains unknown. Here we demonstrate that Smad5, a transcription factor activated by BMP9, and Akt2, are upregulated in differentiated L6 myotubes. Smad5, rather than Smad1/8, is downregulated "in vivo" and "in vitro" by dexamethasone. Smad5 knockdown decreased Akt2 expression and serine phosphorylation and insulin-induced glucose uptake, and increased the expression of the lipid phosphatase Ship2. Additionally, binding of Smad5 to Akt2 gene is decreased in dexamethasone-treated rats and increased in L6 myotubes compared to myoblasts. The present study indicates that Smad5 regulates glucose uptake in skeletal muscle by controlling Akt2 expression and phosphorylation. These finding reveals Smad5 as a potential target for the therapeutic of type 2 diabetes.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Anhê FF,Lellis-Santos C,Leite AR,Hirabara SM,Boschero AC,Curi R,Anhê GF,Bordin Sdoi
10.1016/j.mce.2010.01.003subject
Has Abstractpub_date
2010-05-05 00:00:00pages
30-8issue
1-2eissn
0303-7207issn
1872-8057pii
S0303-7207(10)00005-5journal_volume
319pub_type
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