Evaluation of the Relationship Between Smoking and Insulin Resistance: A Case-Control Study

Abstract

Introduction: In recent years, there has been a surge in research focusing on the link between smoking and insulin resistance in the context of obesity and diabetes. In this study, our objective was to investigate the relationship between smoking and insulin resistance. Materials and Methods: This is a case-control study. The case and control groups were formed using the hospital patient information database and clinically randomized using data obtained, including age, gender, height, and weight. The case group for this study consisted of smokers, whereas the control group consisted of non-smokers. Chi-square tests were used to compare numbers and rates, and independent sample t-tests were used for the averages. Binary logistic regression analysis was performed between the case and control groups. Results: According to logistic regression analysis, the odds ratio for non-smokers was 0.59 (0.31-1.14). The risk of insulin resistance is decreased by 41% non-significantly in non-smokers. The odds ratio for age was 1.03 (1.01-1.05). When the age variable increases by one unit, the risk of insulin resistance increase by 1.03 times. Conclusion: Our study found no significant relationship between smoking and insulin resistance in healthy individuals. The relationship between smoking and insulin resistance, as reported in the scientific literature, may be suggestive of an association in which smoking exacerbates insulin resistance as a result of other contributing factors rather than serving as a direct causal factor. Further studies are warranted to elucidate the potential mechanisms underlying this association fully.

Deciphering the complex interplay of risk factors in type 2 diabetes mellitus: A comprehensive review

“…The relationship between smoking and insulin resistance is frequently reported but the underlying mechanisms are not fully understood. However, studies show that nicotine stimulates catecholamine-mediated glucagon release from the adrenal medulla, which further increases gluconeogenesis thus causing hyperglycemia [ 187 ]. In another cell culture study, it was recapitulated that nicotine stimulated p44/p42 MAPK and mTOR signaling pathway thereby causing insulin resistance and glucose intolerance.…”

“…Additionally, it was found that smokers had greater IRS-1 ser636 phosphorylation as compared to non-smokers which may be implicated in the insulin resistance of smoking [ 188 ]. On the contrary, some studies have found no notable association between smoking and insulin resistance in healthy individuals suggesting that smoking may result in transitory stimulation of these pathways or are both the outcomes of underlying pathophysiological mechanisms that are not entirely elucidated thus challenging the prevailing notion of smoking as a key risk factor for insulin resistance [ 187 , 188 ].…”

Genetic CYP2A6 Polymorphism May Worsen Glycohemoglobin Levels: Study among Javanese Indonesian Smokers

“…HbA1c levels are normal if <5.7%, prediabetes 5.7 to 6.4%, and diabetes ≥6.5% 10 . Nicotine, the main compound in cigarettes, was considered most responsible for increasing blood sugar levels due to insulin resistance 11 . Nicotine is primarily metabolized by the CYP2A6 enzyme to cotinine and excreted in the urine 12 .…”