NDLI: Deletion of ELOVL6 blocks the synthesis of oleic acid but does not prevent the development of fatty liver or insulin resistance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Moon, Young-Ah Ochoa, Courtney R. Mitsche, Matthew A. Hammer, Robert E. Horton, Jay D.
Description	Author Affiliation: Moon YA ( Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046.); Ochoa CR ( Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046.); Mitsche MA ( Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046.); Hammer RE ( Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046.); Horton JD ( Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046.)
Abstract	Elongation of very long chain fatty acid-like family member 6 (ELOVL6) is a fatty acyl elongase that performs the initial and rate-limiting condensing reaction required for microsomal elongation of long-chain fatty acids. Our previous in vitro studies suggested that ELOVL6 elongated long-chain saturated fatty acids and monounsaturated fatty acids with chain lengths of 12 to 16 carbons. Here, we describe the generation and phenotypic characterization of Elovl6(-/-) mice. As predicted from the in vitro studies, livers from Elovl6(-/-) mice accumulated palmitic (C16:0) and palmitoleic (C16:1, n-7) fatty acids and contained significantly less stearic (C18:0) and oleic (C18:1, n-9) acids, confirming that ELOVL6 is the only enzyme capable of elongating palmitate (C16:0). Unexpectedly, Elovl6(-/-) mice produced vaccenic acid (C18:1, n-7), the elongated product of palmitoleate (C16:1, n-7), suggesting that palmitoleate (C16:1, n-7) to vaccenate (C18:1, n-7) elongation was not specific to ELOVL6. The only detected consequence of deleting Elovl6(-/-) in mice was that their livers accumulated significantly more triglycerides than wild-type mice when fed a fat-free/high-carbohydrate diet. When mice were fed a high-fat diet or ELOVL6 was deleted in ob/ob mice, the absence of ELOVL6 did not alter the development of obesity, fatty liver, hyperglycemia, or hyperinsulinemia. Combined, these results suggest that palmitoleic (C16:1, n-7) and vaccenic (C18:1, n-7) acids can largely replace the roles of oleic acid (C18:1, n-9) in vivo and that the deletion of ELOVL6 does not protect mice from the development of hepatic steatosis or insulin resistance.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M054353
Journal	The Journal of Lipid Research
Issue Number	12
Volume Number	55
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2014-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Acetyltransferases Metabolism Diabetes Mellitus, Experimental Insulin Resistance Liver Non-alcoholic Fatty Liver Disease Obesity Oleic Acid Antagonists & Inhibitors Genetics Animals Chimera Clone Cells Crosses, Genetic Complications Etiology Diet, Fat-restricted Adverse Effects Diet, High-fat Dietary Carbohydrates Embryonic Stem Cells Cytology Enzymology Gene Knockout Techniques Mice, Inbred C57bl Mice, Knockout Mice, Mutant Strains Oleic Acids Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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Deletion of ELOVL6 blocks the synthesis of oleic acid but does not prevent the development of fatty liver or insulin resistance[S]

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Deletion of ELOVL6 blocks the synthesis of oleic acid but does not prevent the development of fatty liver or insulin resistance.

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