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J Nutr Metab. 2014;2014:980547. doi: 10.1155/2014/980547. Epub 2014 Sep 9.

HO-1 Upregulation Attenuates Adipocyte Dysfunction, Obesity, and Isoprostane Levels in Mice Fed High Fructose Diets.

Author information

1
Department of Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, WV 25701, USA.
2
Department of Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, WV 25701, USA ; Departments of Medicine and Pharmacology, New York Medical College, Valhalla, NY 10595, USA.

Abstract

BACKGROUND:

Fructose metabolism is an unregulated metabolic pathway and excessive fructose consumption is known to activate ROS. HO-1 is a potent antioxidant gene that plays a key role in decreasing ROS and isoprostanes. We examined whether the fructose-mediated increase in adipocyte dysfunction involves an increase in isoprostanes and that pharmacological induction of HO-1 would decrease both isoprostane levels and adipogenesis.

METHODS AND RESULTS:

We examined the effect of fructose, on adipogenesis in human MSCs in the presence and absence of CoPP, an inducer of HO-1. Fructose increased adipogenesis and the number of large lipid droplets while decreasing the number of small lipid droplets (P < 0.05). Levels of heme and isoprostane in fructose treated MSC-derived adipocytes were increased. CoPP reversed these effects and markedly increased HO-1 and the Wnt signaling pathway. The high fructose diet increased heme levels in adipose tissue and increased circulating isoprostane levels (P < 0.05 versus control). Fructose diets decreased HO-1 and adiponectin levels in adipose tissue. Induction of HO-1 by CoPP decreased isoprostane synthesis (P < 0.05 versus fructose).

CONCLUSION:

Fructose treatment resulted in increased isoprostane production and adipocyte dysfunction, which was reversed by the increased expression of HO-1.

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