Uric Acid-Induced Adipocyte Dysfunction Is Attenuated by HO-1 Upregulation: Potential Role of Antioxidant Therapy to Target Obesity

Figure 8

Proposed mechanism demonstrating the beneficial role of heme oxygenase 1 (HO-1) in the attenuation of adipocyte dysfunction in mesenchymal stem cell- (MSC-) derived adipocytes. Excessive fructose consumption is accompanied by an increase in xanthine oxidase and uric acid and a concurrent increase in cellular ROS levels. HO-1 suppresses adipocyte differentiation by increasing expression of key regulators including Wnt10b and adiponectin and decreasing expression of adipogenic transcription factors CCAAT/enhancer binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), Mest, and FAS. These effects led to decrease in lipid accumulation and increase of preadipocytes and healthy adipocytes that improve adipocyte function.