Background and Objectives: 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.
Discussion: 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.
Conclusion: 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.