Chronic Tobacco Exposure by Smoking Develops Insulin Resistance

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.