This study investigated the interaction of smoking with insulin resistance and β-cell function and their relation to the incidence of type 2 diabetes in a homogenous Asian population. A total of 10 038 subjects were followed for 4 years and the analysis was limited to 4041 men due to the low smoking rates in women. The incidence of diabetes was 7.9% in never-smokers, 12.5% in ex-smokers, 10.7% in current smokers and 11% in heavy smokers. The highest rate of type 2 diabetes was observed among ex- and current smokers with the lowest homeostasis model assessment for β-cell function (HOMA-β) and the highest homeostasis model assessment for insulin resistance (HOMA-IR). Thus, these results suggest a synergistic contribution of insulin resistance additive to β-cell impairment to the development of type 2 diabetes among smokers of this cohort. The degree of deterioration of HOMA-IR was significantly related to a higher rate of type 2 diabetes across groups with different smoking status. In conclusion, smoking confers a risk of developing 2 diabetes independent of all confounding factors and this risk is further increased in the presence of impaired glucose tolerance, low β-cell function and insulin resistance.
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