Increase in glucose-6-phosphate dehydrogenase in adipocytes stimulates oxidative stress and inflammatory signals
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- Increase in glucose-6-phosphate dehydrogenase in adipocytes stimulates oxidative stress and inflammatory signals
- Park, Jiyoung; Choe, Sung Sik; Choi, A. Hyun; Kim, Kang Ho; Yoon, Myeong Jin; Suganami, Takayoshi; Ogawa, Yoshihiro; Kim, Jae Bum
- INDUCED INSULIN-RESISTANCE; NF-KAPPA-B; IKK-BETA; TARGETED DISRUPTION; ADIPOSE-TISSUE; PROTEIN-KINASE; NITRIC-OXIDE; OBESITY; ACTIVATION; PATHWAYS
- Issue Date
- AMER DIABETES ASSOC
- DIABETES, v.55, no.11, pp.2939 - 2949
- In adipocytes, oxidative stress and chronic inflammation are closely associated with metabolic disorders, including insulin resistance, obesity, cardiovascular disease, and type 2 diabetes. However, the molecular mechanisms underlying these metabolic disorders have not been thoroughly elucidated. In this report, we demonstrate that overexpression of glucose-6-phosphate dehydrogenase (G6PD) in adipocytes stimulates oxidative stress and in-flammatory responses, thus affecting the neighboring macrophages. Adipogenic G6PD overexpression promotes the expression of pro-oxidative enzymes, including inducible nitric oxide synthase and NADPH oxidase, and the activation of nuclear factor-κB (NF-κB) signaling, which eventually leads to the dysregulation of adipocytokines and inflammatory signals. Furthermore, secretory factors from G6PD-overexpressing adipocytes stimulate macrophages to express more proinflammatory cytokines and to be recruited to the adipocytes; this would cause chronic inflammatory conditions in the adipose tissue of obesity. These effects of G6PD overexpression in adipocytes were abolished by pretreatment with NF-κB inhibitors or antioxidant drugs. Thus, we propose that a high level of G6PD in adipocytes may mediate the onset of metabolic disorders in obesity by increasing the oxidative stress and inflammatory signals.
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