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Background  Skeletal muscle is the most abundant tissue in the body and is a major source of total energy expenditure in mammals. Skeletal muscle consists of fast and slow fiber types, which differ in their energy usage, contractile speed, and force generation. Although skeletal muscle plays a major role in whole body metabolism, the transcription factors controlling metabolic function in muscle remain incompletely understood. Members of the myocyte enhancer factor 2 (MEF2) family of transcription factors play crucial roles in skeletal muscle development and function. MEF2C is expressed in skeletal muscle during development and postnatally and is known to play roles in sarcomeric gene expression, fiber type control, and regulation of metabolic genes.    Methods  We generated mice lacking  Mef2c  exclusively in skeletal muscle using a conditional knockout approach and conducted a detailed phenotypic analysis.    Results  Mice lacking  Mef2c  in skeletal muscle on an outbred background are viable and grow to adulthood, but they are significantly smaller in overall body size compared to control mice and have significantly fewer slow fibers. When exercised in a voluntary wheel running assay,  Mef2c  skeletal muscle knockout mice aberrantly accumulate glycogen in their muscle, suggesting an impairment in normal glucose homeostasis. Consistent with this notion,  Mef2c  skeletal muscle knockout mice exhibit accelerated blood glucose clearance compared to control mice.    Conclusions  These findings demonstrate that MEF2C function in skeletal muscle is important for metabolic homeostasis and control of overall body size.

Myocyte enhancer factor 2C function in skeletal muscle is required for normal growth and glucose metabolism in mice