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Transcriptome and proteome analysis of soleus muscle of hormone-sensitive lipase-null mice

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Author

Summary, in English

Hormone-sensitive lipase (HSL), a key enzyme in fatty acid mobilization in adipocytes, has been demonstrated also in skeletal muscle. To gain further insight into the role and importance of HSL in skeletal muscle, a transcriptome analysis of soleus muscle of HSL-null mice was performed. A total of 161 transcripts were found to be differentially expressed. Increased mRNA levels of fructose-1,6-bisphosphatase, fructose-2,6-bisphosphatase, and phosphorylase kinase gamma 1A suggest a higher glycogen flux in soleus muscle of HSL-null mice. An observed increase in the utilization of glycogen stores supports this finding. Moreover, an increased amount of intramyocellular lipid droplets, observed by transmission electron microscopy, suggests decreased mobilization of lipid stores in HSL-null mice. To complement the transcriptome data, protein expression analysis was performed. Five spots were found to be differentially expressed: pyruvate dehydrogenase E1 alpha, creatine kinase (CK), ankyrin-repeat domain 2, glyceraldehyde-3-phosphate dehydrogenase, and one protein yet to be identified. The increased protein level of CK indicates creatine phosphate degradation to be of increased importance in HSL-null mice. The results of this study suggest that in the absence of HSL, a metabolic switch from reliance on lipid to carbohydrate energy substrates takes place, supporting an important role of HSL in soleus muscle lipid metabolism.

Publishing year

2005

Language

English

Pages

2614-2623

Publication/Series

Journal of Lipid Research

Volume

46

Issue

12

Document type

Journal article

Publisher

American Society for Biochemistry and Molecular Biology

Topic

  • Basic Medicine
  • Radiology, Nuclear Medicine and Medical Imaging
  • Clinical Medicine

Keywords

  • glycogen
  • proteomics
  • metabolic switch
  • skeletal muscle

Status

Published

Research group

  • Genomics, Diabetes and Endocrinology
  • Diabetes - Epigenetics
  • Molecular Endocrinology

ISBN/ISSN/Other

  • ISSN: 1539-7262