Oguntibeju Oluwafemi Omoniyi
Phytomedicine and Phytochemistry Group, Department of Biomedical Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology Bellville 7535, South Africa.
Int J Physiol Pathophysiol Pharmacol. 2019 Jun 15;11(3):45-63. eCollection 2019.
Diabetes mellitus has been recognised as one of the four major non-communicable diseases that demands urgent attention from all key shareholders globally in an effort to address its prevalence and associated complications. It is considered as a top 10 cause of death globally, killing about 1.6 million people worldwide and is seen as the third highest risk factor for worldwide premature mortality due to hyperglycaemia and hyperglycaemic-induced oxidative stress and inflammation. There is a strong link between hyperglycaemia, hyperglycaemic-induced oxidative stress, inflammation and the development and progression of type 2 diabetes mellitus. Various reports have shown that chronic low-grade inflammation is associated with the risk of developing type 2 diabetes and that sub-clinical inflammation contributes to insulin resistance and is linked to the characteristics of metabolic syndrome which include hyperglycaemia. Oxidative stress stimulates the generation of inflammatory mediators and inflammation in turn enhances the production of reactive oxygen species. This interaction between diabetes, oxidative stress and inflammation is the primary motivation for the compilation of this review. Based on previous studies, the review examines the interaction between diabetes, oxidative stress and inflammation, factors promoting prevalence of diabetes mellitus, mechanisms involved in hyperglycaemia-induced oxidative stress with particular focus on type 2 diabetes and selected diabetic complications.
糖尿病已被公认为四大主要非传染性疾病之一，全球所有关键利益相关方都迫切需要关注这一疾病，以应对其流行情况及相关并发症。它被视为全球十大死因之一，在全球导致约160万人死亡，并且被视为全球因高血糖及高血糖诱导的氧化应激和炎症导致过早死亡的第三大风险因素。高血糖、高血糖诱导的氧化应激、炎症与2型糖尿病的发生和发展之间存在密切联系。各种报告表明，慢性低度炎症与2型糖尿病的发病风险相关，亚临床炎症会导致胰岛素抵抗，并与包括高血糖在内的代谢综合征特征有关。氧化应激刺激炎症介质的产生，而炎症反过来又会增强活性氧的生成。糖尿病、氧化应激和炎症之间的这种相互作用是撰写本综述的主要动机。基于以往的研究，本综述探讨了糖尿病、氧化应激和炎症之间的相互作用、促进糖尿病流行的因素、高血糖诱导氧化应激的机制，特别关注2型糖尿病和选定的糖尿病并发症。
