Gottsäter M, Balkau B, Hatunic M, Gabriel R, Anderwald C-H, Dekker J, Lalic N, Nilsson P M
Department of Clinical Sciences, Lund University, Skåne University Hospital, Malmö, Sweden.
INSERM U-1018, CESP, Team5 (EpReC, Renal and Cardiovascular Epidemiology), Villejuif, France.
Diabet Med. 2017 Feb;34(2):223-228. doi: 10.1111/dme.13172. Epub 2016 Jul 28.
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.
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.
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.
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.
已知吸烟会增加患2型糖尿病的长期风险，但其中涉及的机制尚不清楚。这项观察性横断面研究旨在比较当前吸烟者、既往吸烟者和从不吸烟者的胰岛素敏感性和β细胞功能指标。
研究人群包括来自欧洲大型多中心队列EGIR-RISC人群的1246名无糖尿病患者（平均年龄44岁，55%为女性）。使用高胰岛素正葡萄糖钳夹技术和稳态模型评估-胰岛素抵抗（HOMA-IR）指数测量胰岛素敏感性。从口服葡萄糖耐量试验期间的测量值中得出两个β细胞功能参数：早期胰岛素反应指数和β细胞葡萄糖敏感性。此外，还计算了口服葡萄糖耐量试验期间葡萄糖、胰岛素和C肽的曲线下面积。
根据吸烟习惯，胰岛素敏感性存在差异，吸烟女性的胰岛素敏感性较低，β细胞葡萄糖敏感性也存在差异，吸烟男性的β细胞葡萄糖敏感性较低，但调整后这些关联失去了显著性。然而，调整后，吸烟男性口服葡萄糖耐量试验期间葡萄糖和C肽曲线下面积显著更高。
在健康的欧洲中年人群中，吸烟习惯与胰岛素敏感性或β细胞功能无独立关联。健康选择偏倚、方法学缺陷或吸烟与胰岛素敏感性/分泌受损之间确实缺乏因果联系可能是解释原因。男性吸烟者口服葡萄糖耐量试验期间观察到的曲线下葡萄糖和C肽面积增加背后的机制需要进一步评估。
