title: Myocyte enhancer factor 2C function in skeletal muscle is required for normal growth and glucose metabolism in mice.
abstract: 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.
authors: Cardiovascular Research Institute, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA.
authors: Courtney M
authors: CM
authors: Anderson
authors: Cardiovascular Research Institute, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA.
authors: Jianxin
authors: J
authors: Hu
authors: Cardiovascular Research Institute, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA.
authors: Ralston M
authors: RM
authors: Barnes
authors: Cardiovascular Research Institute, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA.
authors: Analeah B
authors: AB
authors: Heidt
authors: Cardiovascular Research Institute, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA.
authors: Ivo
authors: I
authors: Cornelissen
authors: Cardiovascular Research Institute, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA ; Department of Biochemistry and Biophysics, University of California San Francisco, 555 Mission Bay Blvd, South, MC 3120, San Francisco, CA 94158-2517 USA.
authors: Brian L
authors: BL
authors: Black
keywords: Body size; Fiber type; Glucose metabolism; Glycogen; Knockout mouse; MEF2C; Skeletal muscle