Manna Prasenjit, Jain Sushil K
Department of Pediatrics, LSU Health Sciences Center , Shreveport, Louisiana.
Metab Syndr Relat Disord. 2015 Dec;13(10):423-44. doi: 10.1089/met.2015.0095.
Obesity is gaining acceptance as a serious primary health burden that impairs the quality of life because of its associated complications, including diabetes, cardiovascular diseases, cancer, asthma, sleep disorders, hepatic dysfunction, renal dysfunction, and infertility. It is a complex metabolic disorder with a multifactorial origin. Growing evidence suggests that oxidative stress plays a role as the critical factor linking obesity with its associated complications. Obesity per se can induce systemic oxidative stress through various biochemical mechanisms, such as superoxide generation from NADPH oxidases, oxidative phosphorylation, glyceraldehyde auto-oxidation, protein kinase C activation, and polyol and hexosamine pathways. Other factors that also contribute to oxidative stress in obesity include hyperleptinemia, low antioxidant defense, chronic inflammation, and postprandial reactive oxygen species generation. In addition, recent studies suggest that adipose tissue plays a critical role in regulating the pathophysiological mechanisms of obesity and its related co-morbidities. To establish an adequate platform for the prevention of obesity and its associated health risks, understanding the factors that contribute to the cause of obesity is necessary. The most current list of obesity determinants includes genetic factors, dietary intake, physical activity, environmental and socioeconomic factors, eating disorders, and societal influences. On the basis of the currently identified predominant determinants of obesity, a broad range of strategies have been recommended to reduce the prevalence of obesity, such as regular physical activity, ad libitum food intake limiting to certain micronutrients, increased dietary intake of fruits and vegetables, and meal replacements. This review aims to highlight recent findings regarding the role of oxidative stress in the pathogenesis of obesity and its associated risk factors, the role of dysfunctional adipose tissue in development of these risk factors, and potential strategies to regulate body weight loss/gain for better health benefits.
肥胖正逐渐被视为一种严重的原发性健康负担，因其相关并发症（包括糖尿病、心血管疾病、癌症、哮喘、睡眠障碍、肝功能障碍、肾功能障碍和不孕症）而损害生活质量。它是一种起源多因素的复杂代谢紊乱。越来越多的证据表明，氧化应激作为将肥胖与其相关并发症联系起来的关键因素发挥作用。肥胖本身可通过多种生化机制诱导全身氧化应激，如NADPH氧化酶产生超氧化物、氧化磷酸化、甘油醛自氧化、蛋白激酶C激活以及多元醇和己糖胺途径。肥胖中也导致氧化应激的其他因素包括高瘦素血症、低抗氧化防御、慢性炎症和餐后活性氧生成。此外，最近的研究表明，脂肪组织在调节肥胖及其相关合并症的病理生理机制中起关键作用。为建立预防肥胖及其相关健康风险的适当平台，了解导致肥胖的因素是必要的。目前最新的肥胖决定因素清单包括遗传因素、饮食摄入、身体活动、环境和社会经济因素、饮食失调以及社会影响。基于目前确定的肥胖主要决定因素，已推荐了广泛的策略来降低肥胖患病率，如定期体育活动、随意限制某些微量营养素的食物摄入、增加水果和蔬菜的饮食摄入量以及代餐。本综述旨在强调关于氧化应激在肥胖发病机制及其相关危险因素中的作用、功能失调的脂肪组织在这些危险因素发展中的作用以及调节体重减轻/增加以获得更好健康益处的潜在策略的最新发现。
