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Updating the effects of fatty acids on skeletal muscle
Author(s) -
Silveira Leonardo R.,
Fiamoncini Jarlei,
Hirabara Sandro M.,
Procópio Joaquim,
Cambiaghi Tavane D.,
Pinheiro Carlos Hermano J.,
Lopes Lúcia R.,
Curi Rui
Publication year - 2008
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21514
Subject(s) - insulin resistance , insulin receptor , diacylglycerol kinase , endocrinology , skeletal muscle , insulin , medicine , biology , proinflammatory cytokine , kinase , lipid metabolism , oxidative stress , signal transduction , phosphatidylinositol , microbiology and biotechnology , protein kinase c , inflammation
In this review we updated the fatty acid (FA) effects on skeletal muscle metabolism. Abnormal FA availability induces insulin resistance and accounts for several of its symptoms and complications. Efforts to understand the pathogenesis of insulin resistance are focused on disordered lipid metabolism and consequently its effect on insulin signaling pathway. We reviewed herein the FA effects on metabolism, signaling, regulation of gene expression and oxidative stress in insulin resistance. The elevated IMTG content has been associated with increased intracellular content of diacylglycerol (DAG), ceramides and long‐chain acyl‐coenzyme A (LCA‐CoA). This condition has been shown to promote insulin resistance by interfering with phosphorylation of proteins of the insulin pathway including insulin receptor substrate‐1/2 (IRS), phosphatidylinositol‐3‐kinase, (PI3‐kinase) and protein kinase C. Although the molecular mechanism is not completely understood, elevated reactive oxygen (ROS) and nitrogen species (RNS) are involved in this process. Elevated ROS/RNS activates nuclear factor‐kappaB (NFkB), which promotes the transcription of proinflammatory tumoral necrosis factor alpha (TNFα), decreasing the insulin response. Therefore, oxidative stress induced by elevated FA availability may constitute one of the major causes of insulin resistance in skeletal muscle. J. Cell. Physiol. 217: 1–12, 2008. © 2008 Wiley‐Liss, Inc.