Post Graduate Department of Biochemistry, Cell and Molecular Therapeutics Laboratory, Oriental Institute of Science and Technology, Rangamati, Midnapore, WB, 721102, India.
Endocr Metab Immune Disord Drug Targets. 2020;20(6):869-877. doi: 10.2174/1871530320666200217123901.
The present review critically discusses the high occurrence rate, insulin resistance and type-2 diabetes in tobacco exposed individuals. Tobacco extracts and smoke contain a large number of toxic materials and a significant number of those are metabolic disintegrators.
Glucose and lipid homeostasis is severely impaired by this compound. Tobacco exposure contributes to adverse effects by impairing the physical, biochemical and molecular mechanisms in the tissues. The immunological components are damaged by tobacco with high production of proinflammatory cytokines (IL-6, TNF-∞) and augmentation of inflammatory responses. These events result in damages to cytoskeletal structures of different tissues. Degradation of matrix structure (by activation of different types of MMPs) results in the permanent damages to the tissues and their metabolic functions. Cellular antioxidant defense system mostly cannot or hardly nullify CS-induced ROS production that activates polymorphonuclear neutrophils (PMNs), which are a major source of cytokines and chemokines (TNFα, IL6, IL8, INFγ). Additive effects of these immediately promote the low energy-metabolism as well as inflammation. Oxidative stress, mitochondrial dysfunction, and inflammation contribute to the direct nicotine toxicity via nAChRs in diabetes. The investigator identified that skeletal muscle insulin-resistance occurs in smokers due to phosphorylation of insulin receptor substrate1 (IRS1) at Ser-636 position.
Tobacco exposure initiates free radical related immunological impairment, DNA damage, and inflammation. So, the present analysis is of importance to figure out the mechanistic layout of tobacco-induced tissue damage and its possible therapeutic interventions.
目前的综述批判性地讨论了烟草暴露个体中高发生率、胰岛素抵抗和 2 型糖尿病。烟草提取物和烟雾中含有大量有毒物质，其中相当一部分是代谢分解物。
这种化合物严重损害了葡萄糖和脂质的动态平衡。烟草暴露通过损害组织中的物理、生化和分子机制来导致不良影响。烟草会损害免疫成分，导致促炎细胞因子（IL-6、TNF-∞）的高产生和炎症反应的增强。这些事件导致不同组织的细胞骨架结构受损。基质结构的降解（通过不同类型的 MMP 激活）导致组织及其代谢功能的永久性损伤。细胞抗氧化防御系统大多不能或难以消除 CS 诱导的 ROS 产生，从而激活多形核粒细胞（PMNs），PMNs 是细胞因子和趋化因子（TNFα、IL6、IL8、INFγ）的主要来源。这些立即产生的附加效应促进了低能量代谢和炎症。氧化应激、线粒体功能障碍和炎症通过糖尿病中的 nAChR 导致直接的尼古丁毒性。研究人员发现，由于胰岛素受体底物 1（IRS1）在 Ser-636 位置的磷酸化，吸烟者的骨骼肌胰岛素抵抗发生。
烟草暴露会引发与自由基相关的免疫损伤、DNA 损伤和炎症。因此，目前的分析对于了解烟草引起的组织损伤的机制布局及其可能的治疗干预措施非常重要。
