Dietary fatty acids modulate antigen presentation to hepatic NKT cells in nonalcoholic fatty liver disease

Jing Hua, Xiong Ma, Tonya Webb, James J. Potter, Mathias Oelke, Zhiping Li

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Dietary fatty acids are major contributors to the development and progression of insulin resistance and non-alcoholic fatty liver disease (NAFLD). Dietary fatty acids also alter hepatic NKT cells that are activated by antigens presented by CD1d. In the current study, we examine the mechanism of dietary fatty acid induced hepatic NKT cell deficiency and its causal relationship to insulin resistance and NAFLD. We discover that dietary saturated fatty acids (SFA) or monounsaturated fatty acids (MUFA), but not polyunsaturated fatty acids (PUFA), cause hepatic NKT cell depletion with increased apoptosis. Dietary SFA or MUFA also impair hepatocyte presentation of endogenous, but not exogenous, antigen to NKT cells, indicating alterations of the endogenous antigen processing or presenting pathway. In vitro treatment of normal hepatocytes with fatty acids also demonstrates impaired ability of CD1d to present endogenous antigen by dietary fatty acids. Furthermore, dietary SFA and MUFA activate the NFκB signaling pathway and lead to insulin resistance and hepatic steatosis.jlr In conclusion, both dietary SFA and MUFA alter endogenous antigen presentation to hepatic NKT cells and contribute to NKT cell depletion, leading to further activation of inammatory signaling, insulin resistance, and hepatic steatosis.

Original languageEnglish (US)
Pages (from-to)1696-1703
Number of pages8
JournalJournal of Lipid Research
Issue number7
StatePublished - Jul 1 2010
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Cell Biology


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