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

J Mol Med (Berl). 2009 Apr;87(4):379-84. doi: 10.1007/s00109-009-0449-0. Epub 2009 Mar 4.


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.

Publication types

  • Review

MeSH terms

  • Acetyltransferases / genetics
  • Acetyltransferases / metabolism*
  • Animals
  • Fatty Acid Elongases
  • Fatty Acids / metabolism*
  • Humans
  • Insulin Resistance / physiology*
  • Liver / metabolism
  • Mice
  • Mice, Knockout
  • Models, Biological


  • ELOVL6 protein, human
  • Elovl6 protein, mouse
  • Fatty Acids
  • Acetyltransferases
  • Fatty Acid Elongases