Associations between vitamin D status and type 2 diabetes measures among Inuit in Greenland may be affected by other factors

TY - JOUR

T1 - Associations between vitamin D status and type 2 diabetes measures among Inuit in Greenland may be affected by other factors

AU - Nielsen, Nina O

AU - Bjerregaard, Peter

AU - Rønn, Pernille F

AU - Friis, Henrik

AU - Andersen, Stig

AU - Melbye, Mads

AU - Lundqvist, Marika

AU - Cohen, Arieh S

AU - Hougaard, David M

AU - Jørgensen, Marit E

N1 - CURIS 2016 NEXS 123

PY - 2016/4

Y1 - 2016/4

N2 - Objective 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. Methods 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. Results 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. Conclusions 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.

AB - Objective 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. Methods 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. Results 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. Conclusions 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.

U2 - 10.1371/journal.pone.0152763

DO - 10.1371/journal.pone.0152763

M3 - Journal article

C2 - 27073876

SN - 1932-6203

VL - 11

JO - PLoS Computational Biology

JF - PLoS Computational Biology

IS - 4

M1 - e0152763

ER -