Journal article
The CDP-Ethanolamine Pathway Regulates Skeletal Muscle Diacylglycerol Content and Mitochondrial Biogenesis without Altering Insulin Sensitivity
A Selathurai, GM Kowalski, ML Burch, P Sepulveda, S Risis, RS Lee-Young, S Lamon, PJ Meikle, AJ Genders, SL McGee, MJ Watt, AP Russell, M Frank, S Jackowski, MA Febbraio, CR Bruce
Cell Metabolism | CELL PRESS | Published : 2015
Abstract
Accumulation of diacylglycerol (DG) in muscle is thought to cause insulin resistance. DG is a precursor for phospholipids, thus phospholipid synthesis could be involved in regulating muscle DG. Little is known about the interaction between phospholipid and DG in muscle; therefore, we examined whether disrupting muscle phospholipid synthesis, specifically phosphatidylethanolamine (PtdEtn), would influence muscle DG content and insulin sensitivity. Muscle PtdEtn synthesis was disrupted by deleting CTP:phosphoethanolamine cytidylyltransferase (ECT), the rate-limiting enzyme in the CDP-ethanolamine pathway, a major route for PtdEtn production. While PtdEtn was reduced in muscle-specific ECT knoc..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
We thank C. Yang and R. Kanojia for technical assistance. The MHC antibodies were obtained from the Developmental Studies Hybridoma Bank, created by the NICHD of the NIH, and maintained at The University of Iowa, Department of Biology. The authors acknowledge the facilities and scientific and technical assistance of Monash Micro Imaging, Monash University. These studies were supported by grants from the NHMRC (APP1004239 to C.R.B. and M.A.F.), NIH (GM0457370), and the American Lebanese Syrian Associated Charities (to S.J.). C.R.B. (586698), R.S.L.-Y. (APP1052573), P.J.M. (APP1042095), S.L.M. (APP1030474), M.J.W. (606460), and M.A.F. (APP1021168) have been supported by fellowships from the NHMRC.