Effects of insulin on altered mineral and vitamin D metabolism in streptozotocin-induced diabetes

Abstract

In order to ascertain whether or not abnormal mineral and vitamin D metabolism in diabetes can be reversed by insulin therapy, plasma calcium, ionized calcium, phosphorus, parathyroid hormone (PTH) and vitamin D metabolites were measured in control, streptozotocin (STZ) diabetic and insulin-treated diabetic rats. Blood glucose levels in diabetic rats treated with insulin decreased to normal. The low plasma calcium and ionized calcium levels in diabetic rats were found to be normal in insulin-treated diabetic rats. An elevated PTH level was observed in the diabetic group, but it was at normal levels in the insulin-treated diabetic group.Plasma 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)2D) in the diabetic group were decreased compared to those in control rats, but these were also fully restored to control levels by insulin therapy. However, plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) levels in the untreated diabetic group tended to be lower than in controls, and the values in insulin-treated rats were significantly decreased compared to the control group. The ratio of 1,25(OH)2D to 25(OH)D in diabetic rats was higher than in controls, but it was decreased after insulin therapy and was significantly lower than in the control group. It is suggested, therefore, that the negative calcium balance and decreased 25(OH)D and 24,25(OH)2D levels are derived from the metabolic derangement due to the insulin deficiency. Furthermore, insulin seems to suppress the conversion of 25(OH)D to 1,25(OH)2D in experimental diabetes in vivo. Some investigators have reported that mineral and bone metabolism is altered both in human (McNair et al. 1979) and experimental (Hough et al. 1981) diabetes. We have previously studied the serial changes of mineral and vitamin D metabolism in streptozotocin (STZ) diabetic rat and have found that plasma calcium, 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25 (OH)2D) levels are decreased at the later stage of diabetes (Ishida et al. 1983a). McNair et al. (1983) have also demonstrated that serum ionized calcium concentrations are decreased in insulin-dependent diabetic patients. On the other hand, it has been shown that hypercalciuria in diabetic patients is ameliorated with insulin therapy (Raskin et al. 1978). Furthermore, intestinal calcium malabsorp¬ tion (Schneider et al. 1977;Petith & Schedi 1978) and hypercalciuria (Hough et al. 1981) in STZ diabetic rats have been demonstrated to be im¬ proved after insulin administration. The present study was designed, accordingly, to investigate

Vitamin D and diabetes mellitus

“…In streptozotocin-induced diabetic rats with b cell destruction, plasma calcium levels, DBP, circulating vitamin D, and bone mass were reduced [76][77][78]. After insulin therapy, plasma 25(OH)D3 was fully restored [77].…”

Morphological Study of the Palatal Gingiva of the Maxillary First Molar in the Type 2 Diabetes Mellitus Model Rat

“…In this model, STZ destroyed the β cells of the pancreas islet, and this results in the induction of type 1 DM. However, STZ might also influence the kidney and liver 7,8) . It was of note that these rats showed extremely high fasting blood glucose levels, on the order of 421-573 mg/dL 9,10) .…”

Tetracycline administration restores osteoblast structure and function during experimental diabetes

“…These osteoblastic functions are regulated by la,25-dihydroxyvitamin D, (1,25(OH),D,), and acute and chronic streptozotocin (STZI-induced diabetes has been shown to decrease plasma 1,25(OH),D3 levels (Schneider et al, 1977;Schedl et al, 1978;Hough et al, 1981;Shires et al, 1981;Ishida et al, 1985). Schedl et al (1978) suggested that a primary result of insulin deficiency in diabetes is a n abnormality in vitamin D, metabolism leading to impaired 1,25(OH),D, production.…”