Objective: There is growing evidence suggesting that low vitamin D may be related to type 2 diabetes and cardiovascular disease. It has been suggested that this relationship is mediated via chronic low-grade inflammation. The aim of the present study was to examine the relationship between vitamin D and glucose homeostasis, cardiovascular risk factors and markers of inflammation in healthy normoglycaemic individuals.
Methods: We measured circulating 1,25-hydroxyvitamin D3, waist to hip ratio (WHR), body mass index (BMI), adiposity (dual energy x-ray absorptiometry), fasting and 2 hour glucose (OGTT), insulin sensitivity (M, hyperinsulinemic-euglycemic clamp), blood pressure, lipid profile, white blood cell count, circulating CRP, IL6, MCP-1, TNF alpha levels (ELISA), and NF-KB activity in peripheral mononuclear cells (PBMC, DNA-binding assay) in 49 healthy, non-diabetic adults [28F/21M, age 31±10y and BMI 28.4±4.6kg (mean ± SD)].
Results: Mean vitamin D level was 48±24.5nmol/l with no significant gender difference (p=0.2). Vitamin D levels were significantly related to fasting glucose (r=-0.31, p=0.03) but not 2-hour glucose (r=0.15, p=0.3) or insulin sensitivity (r=0.02, p=0.9). Vitamin D was not related to measures of obesity nor to cardiovascular risk factors including blood pressure and lipid profiles (all p>0.1). Vitamin D was related to NF-ΚB in PBMC (r=0.33, p=0.03) but not to plasma inflammation markers (all p>0.1). After adjusting for age, gender, BMI and WHR, vitamin D remained significantly related to both fasting glucose (p=0.0001), and NF-ΚB (p=0.006).
Conclusions: These cross-sectional data from a metabolically well-characterized cohort of healthy normoglycaemic individuals suggest a role for vitamin D in glucose homeostasis and chronic low-grade inflammation. Large-scale intervention studies are needed to further investigate the role of vitamin D in the pathophysiology and prevention of type 2 diabetes and cardiovascular disease.