Rani Vibha, Deep Gagan, Singh Rakesh K, Palle Komaraiah, Yadav Umesh C S
Department of Biotechnology, JayPee Institute of Information Technology, A-10, Sector-62, Noida 201 307, UP, India.
Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Denver, 12850 E. Montview Blvd, Aurora, CO 80045, USA.
Life Sci. 2016 Mar 1;148:183-93. doi: 10.1016/j.lfs.2016.02.002. Epub 2016 Feb 3.
Increased body weight and metabolic disorder including insulin resistance, type 2 diabetes and cardiovascular complications together constitute metabolic syndrome. The pathogenesis of metabolic syndrome involves multitude of factors. A number of studies however indicate, with some conformity, that oxidative stress along with chronic inflammatory condition pave the way for the development of metabolic diseases. Oxidative stress, a state of lost balance between the oxidative and anti-oxidative systems of the cells and tissues, results in the over production of oxidative free radicals and reactive oxygen species (ROS). Excessive ROS generated could attack the cellular proteins, lipids and nucleic acids leading to cellular dysfunction including loss of energy metabolism, altered cell signalling and cell cycle control, genetic mutations, altered cellular transport mechanisms and overall decreased biological activity, immune activation and inflammation. In addition, nutritional stress such as that caused by high fat high carbohydrate diet also promotes oxidative stress as evident by increased lipid peroxidation products, protein carbonylation, and decreased antioxidant system and reduced glutathione (GSH) levels. These changes lead to initiation of pathogenic milieu and development of several chronic diseases. Studies suggest that in obese person oxidative stress and chronic inflammation are the important underlying factors that lead to development of pathologies such as carcinogenesis, obesity, diabetes, and cardiovascular diseases through altered cellular and nuclear mechanisms, including impaired DNA damage repair and cell cycle regulation. Here we discuss the aspects of metabolic disorders-induced oxidative stress in major pathological conditions and strategies for their prevention and therapy.
体重增加和包括胰岛素抵抗、2型糖尿病及心血管并发症在内的代谢紊乱共同构成代谢综合征。代谢综合征的发病机制涉及多种因素。然而,许多研究在一定程度上一致表明,氧化应激以及慢性炎症状态为代谢性疾病的发展铺平了道路。氧化应激是细胞和组织的氧化与抗氧化系统之间失衡的一种状态,会导致氧化自由基和活性氧(ROS)的过度产生。产生的过量ROS会攻击细胞蛋白质、脂质和核酸,导致细胞功能障碍,包括能量代谢丧失、细胞信号传导和细胞周期控制改变、基因突变、细胞转运机制改变以及整体生物活性降低、免疫激活和炎症。此外,高脂肪高碳水化合物饮食等营养应激也会促进氧化应激,脂质过氧化产物增加、蛋白质羰基化以及抗氧化系统和还原型谷胱甘肽(GSH)水平降低就证明了这一点。这些变化会引发致病环境并导致多种慢性疾病的发展。研究表明,在肥胖人群中,氧化应激和慢性炎症是重要的潜在因素,它们通过改变细胞和核机制,包括受损的DNA损伤修复和细胞周期调控,导致诸如致癌、肥胖、糖尿病和心血管疾病等病理状况的发展。在此,我们讨论主要病理状况下代谢紊乱诱导的氧化应激的各个方面及其预防和治疗策略。
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