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Systemic upregulation of NADPH oxidase in diet-induced obesity in rats
Fan Jiang1, Han K Lim, Margaret J Morris
1O'Brien Institute and Department of Surgery, University of Melbourne, Melbourne, Victoria, Australia. fjiang@sdu.edu.cn
Abstract:
Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is upregulated in a variety of tissues in obesity. It is still unclear as to whether NADPH oxidase upregulation in a specific tissue is part of a systemic response. Here we analyzed the expression pattern of NADPH oxidase in vascular, adipose, and kidney tissues in a rat model of diet-induced obesity. After weaning, rats were fed either a normal or high-fat diet for 12 weeks. The high-fat diet resulted in 20% increased body weight. In the aorta, Nox4 expression was increased by three-fold in obese rats. Upregulations of p22phox and p47phox in adipose, and Nox4, p22phox, and p47phox in kidney were observed in obesity. Marked increases in plasma leptin and insulin were observed, with more modest changes in adiponectin in obese rats. The average systolic blood pressure in the obese group was 11 mmHg higher than that of lean rats (P < 0.005). There was a significant correlation between blood pressure and aortic Nox4 expression (P < 0.01). In cultured vascular smooth muscle cells, adiponectin reduced the expression of Nox4 in a protein kinase A-dependent manner. Our results suggest that upregulation of NADPH oxidase in multiple tissues during obesity appears to be a systemic response. At least in vitro, adiponectin may have a protective antioxidant role by suppressing vascular NADPH oxidase expression. The association between NADPH oxidase Nox4 expression in the vasculature and the elevated blood pressure in obesity requires further investigation.
Insights
Obesity upregulates Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in multiple tissues, indicating a systemic response. Adiponectin may protect against this by reducing vascular NADPH oxidase expression.
Area of Science:
- Biochemistry
- Physiology
- Molecular Biology
Background:
- Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is implicated in various tissues during obesity.
- The systemic nature of NADPH oxidase upregulation in obesity remains unclear.
Purpose of the Study:
- To investigate the expression pattern of NADPH oxidase in vascular, adipose, and kidney tissues in a rat model of diet-induced obesity.
- To explore the relationship between obesity, NADPH oxidase expression, and blood pressure.
Main Methods:
- Rats were fed a high-fat diet for 12 weeks to induce obesity.
- NADPH oxidase component expression (Nox4, p22phox, p47phox) was analyzed in aorta, adipose, and kidney tissues.
- Plasma leptin, insulin, and adiponectin levels were measured.
- Systolic blood pressure was recorded.
- In vitro studies examined the effect of adiponectin on vascular smooth muscle cells.
Main Results:
- High-fat diet increased body weight by 20% and elevated systolic blood pressure by 11 mmHg.
- Obese rats showed increased Nox4 expression in the aorta and upregulation of p22phox and p47phox in adipose and kidney tissues.
- Plasma leptin and insulin were significantly increased, while adiponectin showed modest changes.
- Aortic Nox4 expression correlated significantly with elevated blood pressure.
- Adiponectin reduced Nox4 expression in cultured vascular smooth muscle cells via protein kinase A.
Conclusions:
- NADPH oxidase upregulation in obesity appears to be a systemic response affecting multiple tissues.
- Adiponectin may exert a protective antioxidant effect by suppressing vascular NADPH oxidase.
- Further research is needed to clarify the link between vascular NADPH oxidase (Nox4) and hypertension in obesity.
