The Effect of Myostatin on Glucose Metabolism and Insulin Sensitivity

Date
2013-04-05
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Abstract
Aim : Myostatin (MSTN) is a negative regulator of skeletal muscle proliferation and differentiation that we previously associated with insulin resistance in humans and mice. We assessed its potential regulatory role in glucose metabolism and insulin sensitivity in vivo and in vitro. Methods: Using various approaches we assessed the following parameters: in vivo GTT and ITT and in vitro insulin-stimulated glucose uptake for insulin sensitivity, qRT-PCR for Glut1, Glut4, Gyg1, Hk2, IL-6, Western blotting for protein levels of AMPK and ACC and high-resolution respirometry for glucose-dependent mitochondrial respiration. Results: MSTN showed significant reduction of hepatic insulin-stimulated glucose uptake in vitro and reduced glycogen content in vivo without affecting glycolysis, glucose metabolism genes, AMPK signalling or mitochondrial respiration. Conclusion: This study presents evidence for the potential role of liver in MSTN-induced insulin resistance; especially glucose uptake and glycogen content, which necessitates further investigation of the role of MSTN in this metabolically critical organ.
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Biology--Molecular, Biochemistry
Citation
Ghozlan, M. (2013). The Effect of Myostatin on Glucose Metabolism and Insulin Sensitivity (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/28087