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Wednesday, October 26, 2011 — Poster Session III | |||
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10:00 a.m. – Noon |
Natcher Conference Center |
NIDDK |
ENDOC-3 |
* FARE Award Winner
Myostatin is a member of the TGF-b family, deletion of which results in increased muscle mass and decreased adipose tissue. Myostatin may also regulate metabolism. Myostatin knockout mice fed on high fat diet gain less weight and have improved glucose tolerance when compared to wild type controls. To determine if the effects of myostatin are directly related to altered muscle metabolism, we performed a metabolomic screen to identify biomolecules that may be altered when myostatin is inhibited in adult mice. Myostatin inhibited mice showed an overall decrease in serum amino acids and fatty acids, and an overall increase in sugars, likely due to an increased demand for protein synthesis, beta-oxidation of fatty acids and glucose utilization for increased energy production during muscle hypertrophy. Interestingly, serotonin was also found to be altered when myostatin was inhibited. There is evidence that circulating serotonin regulates bone formation, insulin secretion, and glucose uptake by skeletal muscles. We are currently examining the effects of myostatin and serotonin on metabolism using cultured cells and adult mice. We hope that this study will not only shed light on normal muscle development and metabolism, but will also suggest potential therapeutic targets for muscle wasting diseases, diabetes, and obesity.