Hepatic expression of malonyl-CoA decarboxylase reverses muscle, liver and whole-animal insulin resistance View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-03

AUTHORS

Jie An, Deborah M Muoio, Masakazu Shiota, Yuka Fujimoto, Gary W Cline, Gerald I Shulman, Timothy R Koves, Robert Stevens, David Millington, Christopher B Newgard

ABSTRACT

Lipid infusion or ingestion of a high-fat diet results in insulin resistance, but the mechanism underlying this phenomenon remains unclear. Here we show that, in rats fed a high-fat diet, whole-animal, muscle and liver insulin resistance is ameliorated following hepatic overexpression of malonyl-coenzyme A (CoA) decarboxylase (MCD), an enzyme that affects lipid partitioning. MCD overexpression decreased circulating free fatty acid (FFA) and liver triglyceride content. In skeletal muscle, levels of triglyceride and long-chain acyl-CoA (LC-CoA)-two candidate mediators of insulin resistance-were either increased or unchanged. Metabolic profiling of 36 acylcarnitine species by tandem mass spectrometry revealed a unique decrease in the concentration of one lipid-derived metabolite, beta-OH-butyrate, in muscle of MCD-overexpressing animals. The best explanation for our findings is that hepatic expression of MCD lowered circulating FFA levels, which led to lowering of muscle beta-OH-butyrate levels and improvement of insulin sensitivity. More... »

PAGES

268-274

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm995

DOI

http://dx.doi.org/10.1038/nm995

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1000733180

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14770177


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