NDLI: Inhibited insulin signaling in mouse hepatocytes is associated with increased phosphatidic acid but not diacylglycerol.

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Inhibited insulin signaling in mouse hepatocytes is associated with increased phosphatidic acid but not diacylglycerol.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Chongben Harris, Thurl E. Grevengoed, Trisha J. Eaton, James M. Natarajan, Viswanathan Coleman, Rosalind A. Hwarng, Gwen Cooper, Daniel E.
Description	Author Affiliation: Zhang C ( From the Department of Nutrition, University of North Carolina, Chapel Hill, North Carolina 27599.); Hwarng G ( From the Department of Nutrition, University of North Carolina, Chapel Hill, North Carolina 27599.); Cooper DE ( From the Department of Nutrition, University of North Carolina, Chapel Hill, North Carolina 27599.); Grevengoed TJ ( From the Department of Nutrition, University of North Carolina, Chapel Hill, North Carolina 27599.); Eaton JM ( the Department of Pharmacology, University of Virginia Health System, Charlottesville, Virginia 22908, and.); Natarajan V ( the Departments of Pharmacology & Medicine, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612.); Harris TE ( the Department of Pharmacology, University of Virginia Health System, Charlottesville, Virginia 22908, and.); Coleman RA ( From the Department of Nutrition, University of North Carolina, Chapel Hill, North Carolina 27599, rcoleman@unc.edu.)
Abstract	Although an elevated triacylglycerol content in non-adipose tissues is often associated with insulin resistance, the mechanistic relationship remains unclear. The data support roles for intermediates in the glycerol-3-phosphate pathway of triacylglycerol synthesis: diacylglycerol (DAG), which may cause insulin resistance in liver by activating PKCÏµ, and phosphatidic acid (PA), which inhibits insulin action in hepatocytes by disrupting the assembly of mTOR and rictor. To determine whether increases in DAG and PA impair insulin signaling when produced by pathways other than that of de novo synthesis, we examined primary mouse hepatocytes after enzymatically manipulating the cellular content of DAG or PA. Overexpressing phospholipase D1 or phospholipase D2 inhibited insulin signaling and was accompanied by an elevated cellular content of total PA, without a change in total DAG. Overexpression of diacylglycerol kinase-Î¸ inhibited insulin signaling and was accompanied by an elevated cellular content of total PA and a decreased cellular content of total DAG. Overexpressing glycerol-3-phosphate acyltransferase-1 or -4 inhibited insulin signaling and increased the cellular content of both PA and DAG. Insulin signaling impairment caused by overexpression of phospholipase D1/D2 or diacylglycerol kinase-Î¸ was always accompanied by disassociation of mTOR/rictor and reduction of mTORC2 kinase activity. However, although the protein ratio of membrane to cytosolic PKCÏµ increased, PKC activity itself was unaltered. These data suggest that PA, but not DAG, is associated with impaired insulin action in mouse hepatocytes.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	6
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-02-06
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Diglycerides Metabolism Hepatocytes Insulin Phosphatidic Acids Signal Transduction Animals Carrier Proteins Cells, Cultured Diacylglycerol Kinase Genetics Glycerol-3-Phosphate O-Acyltransferase Mice Mice, Inbred C57BL Phospholipase D Protein Kinase C TOR Serine-Threonine Kinases Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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