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Increased serum adiponectin by heme oxygenase‐1 in obese diabetic zucker rats increases insulin sensitivity and glucose tolerance
Author(s) -
Kim Dong Hyun,
Burgess Angela P.,
Peterson Stephen J.,
Li Ming,
Asprinio David,
Abraham Nader G.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.912.27
Subject(s) - medicine , endocrinology , adiponectin , copp , insulin , heme oxygenase , type 2 diabetes , diabetes mellitus , insulin tolerance test , insulin resistance , chemistry , heme , insulin sensitivity , enzyme , biochemistry
We hypothesized that heme oxygenase‐1 (HO‐1) attenuates diabetic complications via stimulation of a potent vascular protector including adiponectin in rodent with type 2 diabetes. We examined the effect of cobalt protoporphyrin (CoPP) on serum levels of adiponectin in obese and obsess‐diabetic Zucker rats. The onset of diabetes or obesity coincided with a decrease in HO activity, which was restored by administration of CoPP. Upregulation of HO‐1 expression in diabetic rats produced an increase in adiponectin (p<0.003), decreased superoxide (p<0.05) and reduced blood pressure (p<0.01). Increased HO activity was associated with an increase in insulin sensitivity, glucose tolerance and significant reduction in body weight and fat content. The increases in HO‐1‐adiponectin resulted in a decrease within TNF, IL‐1 and IL‐6. The effect of HO‐1 on human MSC show similar results, increases in HO‐1 and decreased adipogenesis. The administration of an inhibitor of HO activity decreased adiponectin. This study suggests that the anti‐diabetic/anti‐obesity effect of HO‐1 is due to regulation of adipogenesis, increases adiponectin secretion, decreases TNF, IL‐1 and IL‐6. HO‐1 treatment was associated with the restoration of insulin sensitivity, preserve pancreatic insulin response to glucose, reduction in weight gains and the amelioration vascular diseases. This work is supported by NIH grants HL55601 and HL34300.