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Elovl6: a new player in fatty acid metabolism and insulin sensitivity.

Abstract
Obesity is a major health problem in industrialized societies often associated with diabetes, insulin resistance, and hepatic steatosis. This review addresses the hypothesis that elongation of long-chain fatty acids family member 6 (Elovl6) has an important role in energy metabolism and insulin sensitivity. Elovl6 is a microsomal enzyme involved in the elongation of saturated and monounsaturated fatty acids with 12, 14, and 16 carbons. Mice with targeted disruption in the gene for Elovl6 (Elovl6 (-/-)) are resistant to diet-induced insulin resistance despite their hepatosteatosis and obesity being similar to that of the wild-type mice. Protection against diet-induced insulin resistance in Elovl6 (-/-) mice is partially due to restoration of hepatic insulin receptor substrate-2 and suppression of hepatic protein kinase C epsilon, resulting in restoration of Akt phosphorylation. We suggest that inhibition of this elongase could be a new therapeutic approach for the treatment of insulin resistance, diabetes, cardiovascular disease, and other metabolic diseases.
AuthorsTakashi Matsuzaka, Hitoshi Shimano
JournalJournal of molecular medicine (Berlin, Germany) (J Mol Med (Berl)) Vol. 87 Issue 4 Pg. 379-84 (Apr 2009) ISSN: 1432-1440 [Electronic] Germany
PMID19259639 (Publication Type: Journal Article, Review)
Chemical References
  • ELOVL6 protein, human
  • Elovl6 protein, mouse
  • Fatty Acids
  • Acetyltransferases
  • Fatty Acid Elongases
Topics
  • Acetyltransferases (genetics, metabolism)
  • Animals
  • Fatty Acid Elongases
  • Fatty Acids (metabolism)
  • Humans
  • Insulin Resistance (physiology)
  • Liver (metabolism)
  • Mice
  • Mice, Knockout
  • Models, Biological

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