The absence of ABCD2 sensitizes mice to disruptions in lipid metabolism by dietary erucic acid

Jingjing Liu, Shuang Liang, Xiaoxi Liu, J. Andrew Brown, Kylie E. Newman, Manjula Sunkara, Andrew J. Morris, Saloni Bhatnagar, Xiangan Li, Aurora Pujol, Gregory A. Graf

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


ABCD2 (D2) is a peroxisomal transporter that is highly abundant in adipose tissue and promotes the oxidation of long-chain MUFA. Erucic acid (EA, 22:1ω9) reduces very long chain saturated fatty acids in patients with X-linked adrenoleukodystrophy but promotes dyslipidemia and dilated cardiomyopathy in rats. To determine the role of D2 in the metabolism of EA, we challenged wild-type and D2 defi- cient mice (D2 KO) with an enriched EA diet. In D2 KO mice, dietary EA resulted in the rapid expansion of adipose tissue, adipocyte hypertrophy, hepatic steatosis, and the loss of glycemic control. However, D2 had no impact on the development of obesity phenotypes in two models of diet-induced obesity. Although there was a significant increase in EA in liver of D2 KO mice, it constituted less than 2% of all fatty acids. Metabolites of EA (20:1, 18:1, and 16:1) were elevated, particularly 18:1, which accounted for 50% of all fatty acids. These data indicate that the failure to metabolize EA in adipose results in hepatic metabolism of EA, disruption of the fatty acid profile, and the development of obesity and reveal an essential role for D2 in the protection from dietary EA.

Original languageEnglish
Pages (from-to)1071-1079
Number of pages9
JournalJournal of Lipid Research
Issue number6
StatePublished - Jun 2012


  • Adipocyte
  • Adipose
  • Adrenoleukodystrophy
  • Fatty liver
  • Insulin resistance
  • Lorenzo's oil
  • Peroxisome

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Cell Biology


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