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Insulin resistance and β‐cell function in smokers: results from the EGIR ‐ RISC European multicentre study
Author(s) -
Gottsäter M.,
Balkau B.,
Hatunic M.,
Gabriel R.,
Anderwald C.H.,
Dekker J.,
Lalic N.,
Nilsson P. M.
Publication year - 2017
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/dme.13172
Subject(s) - medicine , insulin resistance , diabetes mellitus , insulin , population , homeostatic model assessment , glucose tolerance test , glucose clamp technique , type 2 diabetes , impaired glucose tolerance , cohort , area under the curve , endocrinology , insulin sensitivity , environmental health
Aims Tobacco smoking is known to increase the long‐term risk of developing Type 2 diabetes mellitus, but the mechanisms involved are poorly understood. This observational, cross‐sectional study aims to compare measures of insulin sensitivity and β‐cell function in current, ex‐ and never‐smokers. Methods The study population included 1246 people without diabetes (mean age 44 years, 55% women) from the EGIR‐RISC population, a large European multicentre cohort. Insulin sensitivity was measured using a hyperinsulinaemic, euglycaemic clamp and the homeostatic model assessment – insulin resistance (HOMA‐IR) index. Two β‐cell function parameters were derived from measures during an oral glucose tolerance test: the early insulin response index and β‐cell glucose sensitivity. Additionally, the areas under the curve during the oral glucose tolerance test were calculated for glucose, insulin and C‐peptide. Results According to smoking habits, there were differences in insulin sensitivity, which was lower in women who smoked, and in β‐cell glucose sensitivity, which was lower in men who smoked, but these associations lost significance after adjustment. However, after adjustment, the areas under the glucose and the C‐peptide curves during the oral glucose tolerance test were significantly higher in men who smoked. Conclusions Smoking habits were not independently associated with insulin sensitivity or β‐cell function in a healthy middle‐aged European population. Health‐selection bias, methodological shortcomings or a true lack of causal links between smoking and impaired insulin sensitivity/secretion are possible explanations. The mechanisms behind the observed increased glucose and C‐peptide areas under the curve during the oral glucose tolerance test in male smokers need to be further evaluated.