Summary

Original source:
http://www.sciencedaily.com/releases/2005/10/051005080007.htm

Details

• NKT cells originate in the thymus but accumulate in the liver where they regulate the production of cytokines (cell proteins).
• A previous study of leptin-deficient obese mice noted depleted levels of NKT cells.
• However, since obese humans have increased leptin levels, the researchers were not sure if their findings in mice were relevant to human fatty liver disease.
• The researchers, led by Zhiping Li of Johns Hopkins University in Baltimore, obtained wild-type mice and fed them commercial diets with different nutritional contents for four to twelve weeks.
• The researchers isolated hepatic mononuclear cells, which they then incubated and evaluated by flow cytometry.
• Finally, they measured levels of serum alanine aminotransferases (ALT), a marker of liver injury.
• The mice on high fat diets gained significantly more weight than the mice on normal diets, and they also developed fatty livers.
• Subsequent tests revealed doubled production of IL-12, a cytokine that reduces NKT cell viability, as well as increased NKT cell death.
• "Preliminary studies suggest that hepatic NKT cell numbers remain constant before high fat-fed mice develop significant steatosis after consuming the high fat diet for one week," the authors report.
• When the researchers induced liver injury in mice on the varying diets, they found that high fat-diet mice experienced more inflammation and necrosis than normal-diet mice.
• The researchers suggest a potential mechanism for this outcome: diet-induced depletion of the hepatic NKT cells that balance local production of pro- and anti-inflammatory cytokines.
• "Further evaluation of other mouse strains, different age groups and genders will be necessary to clarify if any of these factors modulate susceptibility to diet-related changes in hepatic NKT cells," the authors say.
• "Nevertheless," they conclude, "our findings are important because they clearly demonstrate significant dietary effects on 'classic' NKT cells and cytokine production by other liver mononuclear cells."

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