High Prevalence of Hypovitaminosis D in Postmenopausal Women with Type 2 Diabetes Mellitus.

The link between vitamin D and type 2 diabetes mellitus (T2DM) is intensively studied. This study aims to define the serum concentration of 25-hydroxyvitamin D (25-OH D) and to investigate the relationship between 25-OH D status, glycated hemoglobin (HbA1c) and body composition in postmenopausal women with T2DM and in non-diabetic controls. In this cross-sectional study, 75 women with T2DM and 32 control subjects were selected. Serum 25-OH D, intact parathyroid hormone (PTH), calcium, fasting glucose and HbA1c, were measured. The mean 25-OH D level was 21.4±11.4 ng/ml (range 4.1-50.7 ng/ml) in diabetic women and 30.3±9.4 ng/ml (range 10.8-54.2 ng/ml) in control group (p<0.001). The prevalence of hypovitaminosis D (<30 ng/ml) was higher in vitamin D3 non-supplemented T2DM women (89% vs. 63% controls); the difference diminished in vitamin D3 (500-1000 IU per day) supplemented subgroups (45% diabetics vs. 42% controls). In T2DM women, 25-OH D levels were not associated to HbA1c, duration of diabetes, fasting glucose and PTH levels, however, 25-OH D levels negatively associated with body mass index (p=0.011), total body fat mass (p=0.005) and total body lean mass (p=0.004). The prevalence of hypovitaminosis D is higher in non-supplemented postmenopausal women with T2DM than in non-diabetic controls (89% vs. 63%). Obesity is a risk factor for vitamin D insufficiency in T2DM postmenopausal women. Further studies evaluating relationships between fat, muscle, bone and vitamin D metabolism in T2DM patients are warranted.

Marked reduction of bone turnover by alendronate attenuates the acute response of bone resorption marker to endogenous parathyroid hormone.

The aim of this study was to assess the effects of the antiresorptive treatments of alendronate (ALN), risedronate (RIS) and raloxifene (RLX) on the response of bone to endogenous parathyroid hormone (PTH) induced by acute hypocalcemia. Forty women (age, 55-80 years) with postmenopausal osteoporosis (treated with ALN, RIS and RLX or untreated-control group) were given infusions of sodium ethylenediaminetetraacetic acid (EDTA; 10 mg/kg of body weight). Serum ionized calcium (iCa), plasma intact PTH and marker of bone resorption, serum beta C-terminal telopeptide of type I collagen (beta-CTX; beta CrossLaps) were followed for 180 min. In all women, decrease in serum iCa following the EDTA load resulted in an acute increase in serum PTH. Between 60 and 180 min, plasma PTH in the ALN and RIS treated women remained significantly higher than in the control group. The integrated beta-CTX responses (area under curves, AUCs) to peaks of PTH were significantly lower in the ALN treated women than in those treated with RIS, RLX or control group. There was no significant difference in beta-CTX AUC response to PTH between RIS, RLX and control women. Taken together, these findings suggest that in women with postmenopausal osteoporosis treated with ALN, a substantial reduction of bone turnover blunts the acute bone resorbing effect of endogenous PTH.