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Dietary Walnut Attenuates Adipose Tissue Inflammation and Apoptosis: Implications of Its Role in Non-alcoholic Fatty Liver

Thursday, September 17, 2015 — Poster Session III

3:30 p.m. – 5:00 p.m.
FAES Terrace
NIAAA
CELLBIO-4

Authors

  • Y Choi
  • MA Abdelmegeed
  • M Akbar
  • BJ Song

Abstract

Walnuts have been reported to show several health benefits. However, the underlying mechanisms for the beneficial effects of walnuts on metabolic disorders associated with obesity are still unknown. Therefore, we evaluated the protective effects of dietary walnuts on high fat diet (HFD)-induced steatohepatitis and potential mechanisms. Young male C57BL/6J mice (n=6/group) were fed either a regular chow diet or HFD (45% energy-derived) with or without physiologically relevant amounts of walnuts (20% energy-derived) for up to 20 weeks (wk). Walnut supplementation did not affect HFD-associated increase in body weight, visceral fat mass. However, there was a marked decrease in the levels of hepatic steatosis in the walnut-fed mice compared to those in mice fed HFD alone. In addition, TUNEL assay revealed that the hepatic apoptosis rates were significantly suppressed in mice fed HFD+walnuts, compared to the corresponding HFD-fed mice. We also examined whether the addition of walnuts ameliorates HFD-induced adipocytes inflammation and apoptosis. Indeed, adipose tissue from mice fed the HFD+walnuts showed decreased levels of macrophage infiltration with suppressed expression of inflammatory genes compared to those in HFD-fed mice. These improvements also coincided with reduced HFD-induced apoptosis of adipocytes when walnuts were supplemented. These results suggest that the protective effects of walnuts against HFD-induced steatohepatitis in mice were mediated, at least in part, by the regulation of adipose tissue macrophage recruitment and apoptosis. Collectively, these data provide new results of the protective effects of walnuts on preventing HFD obesity-related hepatic and adipose tissue injuries via mechanisms independent of insulin resistance.

Category: Cell Biology