Secondary aims were to evaluate the effects of vitamin D 3 on: fasting- and OGTT-derived indices of insulin sensitivity, insulin secretion, β-cell function, metabolic markers, blood pressure and anthropometric measurements. The primary aim of this 6-month trial was to determine whether vitamin D 3 supplementation improves peripheral insulin sensitivity (M-value) in individuals at high risk for type 2 diabetes or with newly diagnosed type 2 diabetes, using the gold-standard hyperinsulinemic–euglycemic clamp. Despite adequate sample size ( n = 62–65) and robust methodology, the two other studies failed to show benefits of vitamin D in metabolically healthy overweight or obese subjects ( 10) and in individuals with long-standing type 2 diabetes ( 9). However, three of these trials were limited by small sample size ( n = 12–18) ( 6, 7, 8). Yet, the five studies that used the gold-standard method to assess insulin sensitivity, the hyperinsulinemic-euglycemic clamp, found no effect of vitamin D supplementation on insulin sensitivity ( 6, 7, 8, 9, 10). A meta-analysis concluded that variable results among RCTs could be explained by heterogeneous study populations in terms of ethnicity, glucose tolerance and vitamin D status, by variations in vitamin D dosage and duration of treatment and by use of surrogate measures of insulin sensitivity ( 4, 5). However, randomised controlled trials (RCTs) of vitamin D supplementation have shown inconstant effects on measures of insulin sensitivity, insulin secretion and β-cell function.
Since low vitamin D status is highly prevalent worldwide ( 3), the potential role of vitamin D supplementation in improving glucose homeostasis generated great enthusiasm among scientists and clinicians.
Low serum 25-hydroxyvitamin D (25(OH)D) has been associated with an increased risk of developing insulin resistance and type 2 diabetes in prospective observational studies ( 1, 2).
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