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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperparathyroidism is associated with abnormalities in glucose tolerance and insulin secretion. To assess the effects of hyperparathyroidism on the control of diabetes mellitus, 56 patients with concomitant hyperparathyroidism and diabetes mellitus were studied before and after parathyroidectomy. Fifty patients (89.3%) had hypercalcemia, and six patients (10.7%) had normocalcemia associated with inappropriately elevated parathyroid hormone. After surgery, three of five patients with insulin-dependent diabetes mellitus showed more than a 50% reduction in insulin requirement. Thirty-nine of 49 patients with noninsulin-dependent diabetes mellitus were followed. Of these, three patients had restoration of normal blood glucose levels without any diabetic treatment including diet restriction. Diabetes control improved in eight parents, remained stable in 18, and deteriorated in 10 patients. In the remaining two patients, impaired glucose tolerance disappeared in one patient and progressed to frank diabetes in the other. Overall 60.7% of the patients improved or remained stable in their diabetes control after parathyroidectomy. We conclude that in patients with hyperparathyroidism, the coexistence of diabetes mellitus might be a further indication for parathyroidectomy. Physicians should be alerted to the possible change in diabetic regimen and the risk of hypoglycemia in patients with diabetes after parathyroidectomy.
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PMID:Effect of hyperparathyroidism on the control of diabetes mellitus. 353 62

In eight normal pregnant women and in eighteen women with a family history of diabetes, plasma calcitonin (CT), parathyroid hormone (PTH), insulin and glucagon variations and total plasma calcium levels were investigated. Calcitonin, parathyroid hormone and glucagon were all increased during the 2nd and 3rd trimester of pregnancy in normal women (N.W.) and in women with a family history of diabetes (W.F.H.D.). Plasma calcitonin levels were statistically significantly different between the two groups only in the 3rd trimester (118 +/- 4.9 vs 139 +/- 3.6 pg/ml p less than 0.01 in N.W. and W.F.H.D. respectively). Total plasma calcium levels were decreased significantly in the 3rd trimester in both groups: 3rd vs 1st trimester p less than 0.005 and p less than 0.001 in N.W. and W.F.H.D. respectively. Statistically significant difference between the two groups in total insulinemic area (p less than 0.001), in the rapid phase area (p less than 0.01) and insulinogenic index (p less than 0.05) were observed in the 3rd trimester.
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PMID:Plasma calcitonin variations in normal women and in women with family history of diabetes during pregnancy. 354 28

This study reports a 22% prevalence of significant cortical osteopenia in 206 patients, aged 7-20 years, with established insulin-dependent diabetes mellitus (IDDM). A parallel decrease in trabecular bone mass was also noted. Bone loss was more evident in males (16%) than in females (6%) and was rare before 10 years of age (3%). No relationship between bone loss and the duration of diabetes, degree of metabolic control or diabetic complications was apparent. Delayed skeletal maturation did not account for cortical thinning, and the mean bone age of osteopenic diabetics was similar to that of non-osteopenic diabetics. There was no significant correlation between HLA-antigen frequency and the predisposition to diabetic osteopenia. Metabolic alterations comparable with previous findings in the chronically diabetic rat were documented in IDDM. The data documented are consistent with the conclusion that IDDM results in intestinal hyperabsorption of calcium, absorptive hypercalciuria, phosphaturia, hypomagnesaemia, hyperphosphatasaemia, and decreased circulating parathyroid hormone levels. These alterations in mineral metabolism may relate to the decrease in cortical and trabecular bone mass observed in patients with IDDM.
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PMID:Alterations of bone and mineral metabolism in diabetes mellitus. Part II. Clinical studies in 206 patients with type I diabetes mellitus. 361 83

Forty patients with diabetes mellitus and a reference group of forty-five healthy controls have been studied. Significantly increased serum concentrations of parathyroid hormone and calcitonin were found in the diabetics as well as increased levels of alkaline phosphatase activity and phosphate independent of the duration of the diabetic state. No difference was found in serum calcium levels when compared with the healthy controls. Since these results cannot be explained by diabetes nephropathy an altered balance between parathyroid hormone and calcitonin in diabetes mellitus is postulated.
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PMID:Parathyroid hormone and calcitonin in diabetes mellitus. 371 26

To determine the significance of serum aluminum levels in dialysis patients, the authors retrospectively analyzed a series of patients on maintenance hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD). All patients had always been treated with a dialysate containing negligible amounts of aluminum. The serum aluminum levels of hemodialysis and CAPD patients were not significantly different, not related to age or sex, and not affected by the presence of diabetes or vitamin D intake. The most important determinant of serum aluminum level in the hemodialysis patients was the current dose of aluminum-containing phosphate-binding medication. This relationship was most striking in the compliant patients. In hemodialysis patients, after an increase during the first one to two years, the aluminum levels plateaued. Aluminum levels remained stable more than five years in CAPD patients. Red blood cell mean corpuscular volume was negatively correlated with serum aluminum level. In 28 dialysis patients who had bone biopsy, aluminum levels were positively correlated to histochemical aluminum staining and bone aluminum content. A level greater than 100 ng/mL was a reliable indicator of aluminum-associated osteomalacia, although a lower level did not exclude the presence of low turnover bone disease or mixed uremic osteodystrophy--two disorders possibly related to aluminum. In the presence of a high serum aluminum, elevated levels of immunoreactive parathyroid hormone (iPTH) were useful in detecting the presence of hyperparathyroidism; low levels of iPTH did not allow the authors to distinguish between other subtypes of uremic osteodystrophy.
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PMID:Interpretation of serum aluminum values in dialysis patients. 377 14

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.
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PMID:Effects of insulin on altered mineral and vitamin D metabolism in streptozotocin-induced diabetes. 388 88

Previous studies have shown that there is an impairment in renal production of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the major biologically active metabolite of vitamin D3, in diabetes. This impairment is not due to a deficiency in the parathyroid hormone (PTH), a major stimulator of renal 1,25(OH)2D3 production. Therefore, we have investigated the capacity of PTH to stimulate 1,25(OH)2D3 production in insulin deficiency and with insulin replacement. Experiments were performed in rats fed a 0.6% calcium, vitamin D sufficient diet for 2 weeks. Thyroparathyroidectomy was performed on all rats. Rats to be rendered diabetic were injected with streptozotocin immediately after surgery. In non-diabetic rats, PTH administration significantly increased renal 1,25(OH)2D3 production (11 +/- 2 vs 46 +/- 5 pg/min/g; P less than 0.05). In diabetic rats, however, PTH caused only a modest increase in 1,25(OH)2D3 production (11 +/- 1 vs 19 +/- 4 pg/min/g; P less than 0.05). With insulin replacement, PTH stimulation of 1,25(OH)2D3 production was markedly increased over that seen in diabetic rats (48 +/- 12 vs 19 +/- 4 pg/min/g; P less than 0.05). PTH was equally effective in raising serum calcium, depressing serum phosphorus and tubular reabsorption of phosphate in non-diabetic as well as in diabetic rats. These results demonstrate that insulin is necessary for the maximal stimulation of renal 1,25(OH)2D3 production by PTH. However, insulin is not necessary for PTH action in terms of renal handling of phosphate and inducing hypercalcaemia. These results suggest multiple pathways for the action of PTH, only some of which are insulin requiring.
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PMID:Insulin modulates the stimulation of renal 1,25-dihydroxyvitamin D3 production by parathyroid hormone. 389 9

The parathyroid gland responsiveness to hypocalcemia induced by short-term calcium-free hemodialysis in patients with insulin-dependent diabetes mellitus was investigated in comparison with 10 nondiabetic uremic patients and compared with test results from the autonomic nervous system. Diabetic patients had lower C-terminal parathyroid hormone (cPTH) levels before hemodialysis than uremic control patients and showed a significantly smaller increase in cPTH during hypocalcemia. The neurological tests revealed severe disturbances of the autonomic functions in the diabetic group. In conclusion, the disturbances observed in the parathyroid secretory pattern are probably caused by gland dysfunction; it is hypothesized that the defective autonomic nervous system has an additional effect on the development of this hormonal dysfunction.
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PMID:Diminished parathyroid gland responsiveness to hypocalcemia in diabetic patients with uremia. 396 Feb 40

The effect of mild, non-insulin-dependent diabetes (NIDDM) on bone calcification and calcium (Ca) homeostasis was studied in growing rats (males and females). The diabetic state was characterized by mild insulin deficiency, plasma levels being 73% of controls, and mild hyperglycemia, with nonfasting plasma glucose levels of 1.5 times normal. There was no difference in plasma levels of Ca, phosphate (Pi), magnesium (Mg), alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), calcitonin, 25-(OH)vitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]2D), and 24,25-dihydroxyvitamin D (24,25[OH]2D) between the NIDDM rats and their controls of either sex. Metabolic Ca and Pi balance studies revealed that the experimental animals of both sexes were in positive Ca and Pi balance similar to that of their controls. Histologic studies of the kidney and intestinal slices from the experimental group were normal. Ca and Pi bone content calculated per gram bone ash of the femur, mandible, and second and fourth caudal vertebrae, and the organic content in the bones of the NIDDM animals showed no difference from their controls. Femur bone density and tibial epiphyseal growth plate width and morphology were similar histologically in the experimental and control rats. No decreased osteoid content in the tibial bone was found in the diabetic rats compared with controls. Physiologic sex differences, consisting of lower plasma Pi, higher plasma calcitonin levels, increased ratio of femur dry bone weight to total body weight, and increased percentage of mineralized and total bone volume at the tibial metaphysis seen in female compared with male control rats were also seen in the diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Apr
PMID:Bone calcification and calcium homeostasis in rats with non-insulin-dependent diabetes induced by streptozocin. 397 85

Calcium homeostasis was studied in freely fed control, streptozotocin diabetic, long-term and short-term insulin-treated diabetic rats 7 wk after the induction of diabetes. In contrast to the short-term (5-12 day) diabetic rat model, intestinal absorption of calcium was markedly enhanced in chronically insulin-deficient animals. Moreover, conventional balance studies showed that these animals were in positive calcium balance despite severe hypercalciuria. Intestinal hyperabsorption of calcium in long-standing diabetic rats occurred despite low levels of circulating 1,25-dihydroxyvitamin D and hypercorticosteronism and was attended by hypercalcemia and suppression of both plasma parathyroid hormone (PTH) and urinary cyclic 3',5'-AMP (cAMP). Long-term insulin replacement completely normalized the intestinal hyperabsorption of calcium, corrected the plasma calcium, and significantly increased circulating PTH and urinary cAMP excretion. Insulin therapy also corrected the decreased plasma 1,25-dihydroxyvitamin D observed in untreated diabetic animals. Intestinal hyperabsorption of calcium appeared to be only partially corrected by short-term insulin therapy. The accumulated results reveal decided differences in calcium homeostasis and hormonal response between the rats with long-standing diabetes and those with diabetes of short duration.
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PMID:Calcium homeostasis in chronic streptozotocin-induced diabetes mellitus in the rat. 628 97


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