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• W2106171856 startingPage "199" @default.
• W2106171856 abstract "Type 1 diabetes mellitus (T1DM), or insulin dependent DM, is accompanied by decreased muscle mass. The growth factor myostatin (MSTN) is a negative regulator of muscle growth, and a loss of MSTN signaling has been shown to increase muscle mass and prevent the development of obesity, insulin resistance and lipodystrophic diabetes in mice. The effects of MSTN inhibition in a T1DM model on muscle mass and blood glucose are unknown. We asked whether MSTN inhibition would increase muscle mass and decrease hyperglycemia in mice treated with streptozotocin (STZ) to destroy pancreatic beta cells. After diabetes developed, mice were treated with a soluble MSTN/activin receptor fused to Fc (ACVR2B:Fc). ACVR2B:Fc increased body weight and muscle mass compared to vehicle treated mice. Unexpectedly, ACVR2B:Fc reproducibly exacerbated hyperglycemia within approximately one week of administration. ACVR2B:Fc treatment also elevated serum levels of the glucocorticoid corticosterone. These results suggest that although MSTN/activin inhibitors increased muscle mass, they may be counterproductive in improving health in patients with T1DM." @default.
• W2106171856 created "2016-06-24" @default.
• W2106171856 creator A5001553964 @default.
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• W2106171856 date "2015-01-01" @default.
• W2106171856 modified "2023-10-18" @default.
• W2106171856 title "A Soluble Activin Receptor Type IIB Does Not Improve Blood Glucose in Streptozotocin-Treated Mice" @default.
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• W2106171856 doi "https://doi.org/10.7150/ijbs.10430" @default.
• W2106171856 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4279095" @default.
• W2106171856 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25561902" @default.
• W2106171856 hasPublicationYear "2015" @default.
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