Animal studies have demonstrated lower levels of 1,25(OH)2D3 in a type 2 diabetes model compared with controls (1). Alterations in circulating vitamin D3 metabolites, such as decreased 1α-hydroxylase activity and enhanced renal 25-hydroxylase activity, have been found in both experimental and human diabetes. These alterations in vitamin D metabolism may be associated with the deranged mineral homeostasis and skeletal morphology observed in rats and people with chronic insulin deficiency (2). Experimentally, vitamin D deficiency progressively reduces insulin secretion, and this reduction soon becomes irreversible (3). It was also shown that insulin deficiency may be associated with lower vitamin D–binding protein and 1,25(OH)2D3 serum levels in rats. These decreases are somewhat dependent on androgen concentration, but they are counteracted by estrogens (4).

Several studies have demonstrated abnormalities in calcium, phosphate, and vitamin D metabolism in diabetic patients. In particular, Pietschmann et al. (5) evaluated 25(OH)D levels in type 1 and type 2 diabetic patients and found no difference in 25(OH)D levels between type 1 diabetic patients and control subjects, whereas 25(OH)D levels were significantly decreased in type 2 diabetic patients (5).

We conducted an observational study in 799 ambulatory postmenopausal Italian women in order to assess the prevalence of hypovitaminosis D and dietary calcium insufficiency. In all patients, the levels of 25(OH)D3 (obtained by radioimmunoassay method with double antibody provided by DiaSorin), calcium intake (obtained by a questionnaire filled in by a general practitioner), and several Activity Daily Living (ADL) criteria were assessed. The samples were collected in February and March 2000.

We identified 66 type 2 diabetic patients based on medical history. Female patients and control subjects were comparable for age and years since menopause, but BMI was significantly higher in diabetic patients. The ADL score was significantly worse in diabetic patients than in control subjects (P < 0.01). The 25(OH)D levels (means ± SD) were significantly lower in diabetic patients than in control subjects (11 ± 9.8 vs. 9 ± 11.3 ng/ml, P < 0.008), and the prevalence of 25(OH) deficiency (<5 ng/ml) was significantly higher in diabetic patients than in control subjects (39 vs. 25%). Dietary calcium intake was significantly lower in diabetic patients than in control subjects (792.9 ± 400.9 vs. 679 ± 316.9 mg/day, P < 0.020).

The significance of these findings remains unclear. The general recommendation for overweight diabetic patients to lower fat dairy product consumption may explain the lower calcium intake. We have no data that might explain the higher prevalence of hypovitaminosis D among diabetic patients. We believe our results will lead to additional studies on the hypothetical circular relationship among diabetes, vitamin D repletion, and calcium intake and absorption. We believe this relationship leads to both a worsening of diabetes and an increased risk of fractures (6), despite higher bone mineral density levels being found in diabetic subjects (6,7).

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Address correspondence to Giancarlo Isaia, Department of Internal Medicine, University of Torino, Corso Dogliotti 14, 10126 Torino, Italy. E-mail: giancarlo.isaia@unito.it.