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首页> 外文期刊>American Journal of Physiology >NOX2 deficiency attenuates markers of adiposopathy and brain injury induced by high-fat diet
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NOX2 deficiency attenuates markers of adiposopathy and brain injury induced by high-fat diet

机译：NOX2缺乏症减轻高脂饮食诱发的脂肪病和脑损伤的标志物

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The consumption of high-fat/ calorie diets in modern societies is likely a major contributor to the obesity epidemic, which can increase the prevalence of cancer, cardiovascular disease, and neurological impairment. Obesity may precipitate decline via inflammatory and oxidative signaling, and one factor linking inflammation to oxidative stress is the proinflammatory, pro-oxidant enzyme NADPH oxidase. To reveal the role of NADPH oxidase in the metabolic and neurological consequences of obesity, the effects of high-fat diet were compared in wild-type C57B1/6 (WT) mice and in mice deficient in the NAPDH oxidase subunit NOX2 (NOX2KO). While diet-induced weight gains in WT and NOX2KO mice were similar, N0X2K0 mice had smaller visceral adipose deposits, attenuated visceral adipocyte hypertrophy, and diminished visceral adipose macrophage infiltration. Moreover, the detrimental effects of HFD on markers of adipocyte function and injury were attenuated in NOX2KO mice; NOX2KO mice had improved glucose regulation, and evaluation of NOX2 expression identified macro-phages as the primary population of NOX2-positive cells in visceral adipose. Finally, brain injury was assessed using markers of cerebro-vascular integrity, synaptic density, and reactive gliosis, and data show that high-fat diet disrupted marker expression in WT but not N0X2K0 mice. Collectively, these data indicate that NOX2 is a significant contributor to the pathogenic effects of high-fat diet and reinforce a key role for visceral adipose inflammation in metabolic and neurological decline. Development of NOX-based therapies could accordingly preserve metabolic and neurological function in the context of metabolic syndrome.
机译：在现代社会中，高脂/卡路里饮食的消费可能是肥胖病流行的主要原因，肥胖病流行会增加癌症，心血管疾病和神经系统疾病的患病率。肥胖可能通过炎症和氧化信号沉淀而下降，并且将炎症与氧化应激相关的一个因素是促炎性促氧化剂NADPH氧化酶。为了揭示NADPH氧化酶在肥胖的代谢和神经系统后果中的作用，在野生型C57B1 / 6（WT）小鼠和N​​APDH氧化酶亚基NOX2（NOX2KO）缺乏的小鼠中比较了高脂饮食的影响。尽管饮食引起的WT和NOX2KO小鼠体重增加相似，但N0X2K0小鼠的内脏脂肪沉积较小，内脏脂肪细胞肥大减弱，内脏脂肪巨噬细胞浸润减少。此外，在NOX2KO小鼠中，HFD对脂肪细胞功能和损伤标志物的有害作用减弱。 NOX2KO小鼠的葡萄糖调节性得到改善，对NOX2表达的评估确定巨噬细胞是内脏脂肪中NOX2阳性细胞的主要种群。最后，使用脑血管完整性，突触密度和反应性胶质增生的标记物评估了脑损伤，数据表明高脂饮食破坏了WT小鼠的标记表达，但没有破坏N0X2K0小鼠。总的来说，这些数据表明，NOX2是高脂饮食致病作用的重要贡献者，并增强了内脏脂肪炎症在代谢和神经功能下降中的关键作用。基于NOX的疗法的发展可以相应地在代谢综合征的背景下保留代谢和神经功能。

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