Lipid accumulation product and 25-OH-vitamin D deficiency in type 2 diabetes.

Emerging data suggest a link between vitamin D (25(OH)D) deficiency, type 2 diabetes (T2D), and visceral adiposity. The lipid accumulation product (LAP), strictly correlated with abdominal fat depots, is proposed as marker of dysfunctional adiposity.To verify the association between 25(OH)D levels and LAP in T2D.Body mass index (BMI), waist circumference (WC), glucose, HbA1c, lipids, and 25(OH)D were assessed in 420 T2D outpatients and in 150 non-diabetic obese with similar anthropometric characteristics. LAP was computed as the product of sex-specific enlarged WC and triglycerides (TG).In T2D patients, 63.0% showed 25(OH)D deficiency (<20 ng/ml) vs. 71.3% in the obese control group. Overweight males showed a higher prevalence of 25(OH)D deficiency (60.3%) than women (48.8%, p < 0.001), while in obese patients this prevalence was not significant. In both genders, 25(OH)D was not significantly associated with HbA1c and fasting glucose. Age-adjusted 25(OH)D levels were inversely correlated with BMI (p < 0.001), WC (p < 0.001), and LAP (p < 0.001) in both genders. Metabolic syndrome presented an odds ratio (OR) for 25(OH)D deficiency of 1.6 (1.1-2.5, p = 0.048) in females and 1.7 (1.2-2.7, p = 0.016) in males, while the highest quartile of LAP showed an OR of 2.1 (1.2-3.6, p = 0.019) in females and 3.2 (1.6-6.5, p = 0.02) in males. A similar trend was observed in the obese control group.In the presence of excess weight, subjects with and without T2D frequently feature low 25(OH)D levels. Subjects with higher LAP exhibit a high risk of 25(OH)D deficiency, suggesting that dysfunctional adiposity is a worsening factor for vitamin D hypovitaminosis.