Nielsen Nina O, Bjerregaard Peter, Rønn Pernille F, Friis Henrik, Andersen Stig, Melbye Mads, Lundqvist Marika, Cohen Arieh S, Hougaard David M, Jørgensen Marit E
National Institute of Public Health, University of Southern Denmark, Copenhagen, Denmark.
Greeenland Centre for Health Research, University of Greenland, Nuuk, Greenland.
PLoS One. 2016 Apr 13;11(4):e0152763. doi: 10.1371/journal.pone.0152763. eCollection 2016.
Epidemiological studies have provided evidence of an association between vitamin D insufficiency and type 2 diabetes. Vitamin D levels have decreased among Inuit in Greenland, and type 2 diabetes is increasing. We hypothesized that the decline in vitamin D could have contributed to the increase in type 2 diabetes, and therefore investigated associations between serum 25(OH)D3 as a measure of vitamin D status and glucose homeostasis and glucose intolerance in an adult Inuit population.
2877 Inuit (≥18 years) randomly selected for participation in the Inuit Health in Transition study were included. Fasting- and 2hour plasma glucose and insulin, C-peptide and HbA1c were measured, and associations with serum 25(OH)D3 were analysed using linear and logistic regression. A subsample of 330 individuals who also donated a blood sample in 1987, were furthermore included.
After adjustment, increasing serum 25(OH)D3 (per 10 nmol/L) was associated with higher fasting plasma glucose (0.02 mmol/L, p = 0.004), 2hour plasma glucose (0.05 nmol/L, p = 0.002) and HbA1c (0.39%, p<0.001), and with lower beta-cell function (-1.00 mmol/L, p<0.001). Serum 25(OH)D3 was positively associated with impaired fasting glycaemia (OR: 1.08, p = 0.001), but not with IGT or type 2 diabetes.
Our results did not support an association between low vitamin D levels and risk of type 2 diabetes. Instead, we found weak positive associations between vitamin D levels and fasting- and 2hour plasma glucose levels, HbA1c and impaired fasting glycaemia, and a negative association with beta-cell function, underlining the need for determination of the causal relationship.
流行病学研究已提供证据表明维生素D不足与2型糖尿病之间存在关联。格陵兰因纽特人的维生素D水平有所下降,且2型糖尿病的发病率正在上升。我们推测维生素D水平的下降可能导致了2型糖尿病发病率的增加,因此研究了作为维生素D状态指标的血清25(OH)D3与成年因纽特人群的葡萄糖稳态及葡萄糖不耐受之间的关联。
纳入了随机选取的2877名年龄≥18岁参与因纽特人健康转型研究的因纽特人。测量了空腹及餐后2小时的血浆葡萄糖、胰岛素、C肽和糖化血红蛋白(HbA1c),并使用线性和逻辑回归分析了与血清25(OH)D3的关联。此外,还纳入了1987年也捐献了血样的330名个体的子样本。
调整后,血清25(OH)D3每增加10 nmol/L,与更高的空腹血糖(0.02 mmol/L,p = 0.004)、餐后2小时血糖(0.05 nmol/L,p = 0.002)和HbA1c(0.39%,p<0.001)相关,且与更低的β细胞功能(-1.00 mmol/L,p<0.001)相关。血清25(OH)D3与空腹血糖受损呈正相关(比值比:1.08,p = 0.001),但与糖耐量受损或2型糖尿病无关。
我们的结果不支持低维生素D水平与2型糖尿病风险之间存在关联。相反,我们发现维生素D水平与空腹及餐后2小时血浆葡萄糖水平、HbA1c和空腹血糖受损之间存在微弱的正相关,与β细胞功能呈负相关,这突出了确定因果关系的必要性。