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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of insulin on plasma and bone mineral homeostasis was studied in the BB rat model, which develops an autoimmune form of diabetes at the age of about 100 days. Untreated diabetes of short duration resulted in hypercalciuria and intestinal calcium malabsorption despite increased free concentrations of serum 1,25-dihydroxyvitamin D. The concentrations of two vitamin D-dependent calcium-binding proteins were also decreased: a low duodenal calbindin-D 9K concentration corresponding to the low intestinal active calcium absorption and a low serum osteocalcin concentration, corresponding to a low bone formation and highly correlated with serum IGF-I concentration. Indeed, on bone histology a very low number of osteoblasts and low osteoblast activity (osteoid formation and mineral apposition rate) were observed. Similar abnormalities persisted in rats with long-standing diabetes resulting in markedly decreased bone mass and increased brittleness of bone. Diabetes therefore resulted in low-turnover osteoporosis. Several hormones (testosterone, growth hormone and 1,25-dihydroxyvitamin D) and growth factors (IGF-I and its binding proteins) with known effects on bone were markedly decreased in diabetic rats. A continuous infusion of testosterone, GH or 1,25-(OH)2D3 for 14 d by miniosmotic pumps could not improve the biochemical or histomorphometric abnormalities. Insulin infusion for 2 weeks, however, rapidly increased and overcorrected the number of osteoblasts, normalized serum osteocalcin and IGF-I concentrations but could not yet normalize bone mineralization. Continuous infusion of IGF-I alone did not improve the osteoblast number of osteocalcin but markedly stimulated bone mineralization. From these data we can conclude that both insulin and IGF-I are potent bone growth factors but with different mode of action. In human type 1 diabetes, a similar decrease in serum osteocalcin and IGF-I was observed. A reduction of regional bone mass, both in long and trabecular bones, is frequently observed in human diabetes. Cumulative data from case control studies indicate that the life-time fracture risk is increased in diabetes.
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PMID:Diabetic bone disease. Low turnover osteoporosis related to decreased IGF-I production. 146 60

To investigate the frequency and etiology of diabetic osteopenia, we measured spinal bone mineral density (SBMD), total body bone mineral density (TBBMD), total body fat and lean body mass in 69 female diabetic patients (14 IDDMs and 55 NIDDMs). SBMD decreased with age in both IDDM and NIDDM, but when expressed as a percentage of age-matched normal Japanese females, some had lower SEMD, but others had normal or increased SBMD. Postmenopausal IDDM patients had lower SBMD than postmenopausal NIDDM patients. Thirteen out of 69 (18.8%) had an SBMD lower than 90% of age-matched controls. SBMD correlated positively with TBBMD. Those with lower SBMD had poor glycemic control, but there was no relation between SBMD and either duration of diabetes or presence of retinopathy and/or nephropathy. IDDM patients had lower 1.25 (OH)2D, osteocalcin than NIDDMs. SBMD correlated negatively with urinary pyridinoline and deoxypyridinoline excretion. SBMD correlated positively with body weight, and those with lower SBMD had significantly lower body mass index, body weight, fat weight and lean body mass than those with normal or increased SBMD. These results suggest that IDDM patients may be at higher risk of losing bone postmenopausally, and diabetic patients with lower SBMD have characteristics of poor diabetic control, lean habitus, low serum 1.25 (OH)2D.
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PMID:[Spinal bone mineral density in the female diabetic patients]. 149 83

The goal of this study was to evaluate in 98 diabetic patients the serum levels of osteocalcin (OC) and their relationship with glycosylated hemoglobin levels and with the duration, calculated in years, of the disease. Patients were divided in 3 groups: 17 IDDM patients, 62 NIDDM patients treated with oral hypoglycaemic agents, and 19 NIDDM patients treated with insulin. Results were compared to 2 different control groups. In IDDM patients OC serum levels were significantly lower if compared either to control group and to NIDDM patients. The 2 groups of NIDDM patients showed significantly higher OC values than controls. No significant relationship resulted between OC levels, the duration of diabetes and the glycosylated hemoglobin values. The results of the study indicate a direct correlation between pancreatic function and osteoblastic activity: insulin lack is associated with reduced OC serum levels.
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PMID:[Serum osteocalcin and diabetes mellitus. A study of 98 patients]. 155 61

Insulin-dependent diabetes mellitus (IDDM) is a chronic metabolic disorder which can induce alterations in bone metabolism (osteopenia) and/or in mineral homeostasis, mainly during growth. Some data suggest that these alterations may be related to low serum magnesium values found in IDDM that induce a functional hypoparathyroid state. In this paper, some aspects are revised relating to altered magnesium and mineral homeostasis in children with IDDM and their possible relationships. The role of osteocalcin, a specific osteoblast protein product, as a biochemical marker of diabetic osteopenia is also discussed. In addition, on the basis of personal experience, it is shown that the deranged parathyroid hormone-vitamin D axis in IDDM is reversed after normalization of magnesium serum levels by oral magnesium. Thus available data suggest that hypomagnesaemia is involved in the genesis of the altered mineral metabolism in children with IDDM.
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PMID:The parathyroid hormone- 1,25-dihydroxyvitamin D endocrine system and magnesium status in insulin-dependent diabetes mellitus: current concepts. 159 Nov 43

To determinate which type of bone is damaged in IDDM, we assessed the bone mineral content (BMC) in both cortical and trabecular bones, in a group of 48 IDDM patients without hepatic or kidney diseases, or any other pathology with implications in the mineral metabolism. For the evaluation techniques of single photon absorptiometry (SPA) and double photon absorptiometry (DPA) were used. All the patients controlled their disease with insulin. The results showed the presence of osteopenia in both types of bone. It was more evident in male group. In the patients group the mean value of serum osteocalcin (BGP) was significantly decreased (2.34 +/- 1.05) in comparison with the controls (p less than 0.001). The deficient of BMC is neither related with the parameters of new bone formation nor with the time of disease evolution.
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PMID:[Cortical and trabecular bone lesions in insulin-dependent diabetes mellitus]. 179 68

Osteocalcin, non-collagenous vitamin K dependent bone protein is as a biochemical indicator of osteoblastic activity and metabolic turnover in bone, valuable in the diagnosis of several diseases and in investigations of the dynamics of osseous changes (processes) during treatment of osteopathies. Elevated osteocalcin levels are normal in childhood and adolescence. In the diurnal rhythm the peak is recorded in the early hours. Pathologically elevated values are associated with primary hyperparathyroidism, Paget's disease, chronic renal failure, acromegaly and some malignities. A rise in women during the early postmenopausal period signalizes an enhanced metabolic turnover of bone in those women who are candidates of postmenopausal osteoporosis. Low levels are as a rule recorded in advanced age, in nanism, hypoparathyroidism, type 1 diabetes, rheumatoid arthritis, vitamin D deficiency, vitamin K deficiency, hypercorticalism and glucocorticoid treatment.
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PMID:[Osteocalcin]. 227 72

While people with type 1 diabetes mellitus (DM) often have bone deficiency, the relation between this deficiency and the duration or control of diabetes remains controversial. To assess the possibility of such an interrelationship, we studied parameters relating to mineral metabolism (Ca, P, alkaline phosphatase, Mg, PTH, and hydroxyproline (OHP)); bone remodeling (osteocalcin); diabetic control (HbA1c); and radiological study of the second metacarpal of the left hand and of bone age in 87 children with type 1 DM. The mineral parameters were not abnormal among the diabetics. Diabetic children had similar levels of fasting osteocalcin as normals (10.05 +/- 4.9 vs. 9.79 +/- 3.34 ng/ml, mean +/- SD); this did not differ by sex. The bone age fell within two standard deviations of the mean, and 9.5% of the diabetics had a bone mass deficit (less than the mean cortical thickness) greater than 2 SD. There was no correlation between osteocalcin and Ca, P, glycemia, HbA1c, PTH, Mg, or OHP. Our results do not support any association between bone mass loss and the severity or duration of type 1 diabetes. Bone turnover, measured by serum osteocalcin, was normal. Therefore the pathogenesis of osteopenia in type 1 DM remains unclear, and requires further investigation.
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PMID:Study of bone loss in diabetes mellitus type 1. 278 8

Recent studies indicate that serum levels of osteocalcin, a 49-aminoacid bone matrix protein, are a biochemical marker of bone formation. In order to study bone metabolism in diabetes mellitus, in 28 patients with Type 1 (insulin-dependent) diabetes mellitus, in 38 patients with Type 2 (non-insulin-dependent) diabetes mellitus and two control groups, matched for Type 1 and Type 2 diabetic patients, respectively, serum levels of osteocalcin, parathyroid hormone and 25 hydroxy vitamin D were measured by radioimmunoassay. Whereas in Type 1 diabetic patients and control subjects serum levels of osteocalcin and 25 hydroxy vitamin D were not statistically different, serum osteocalcin and 25 hydroxy vitamin D levels were significantly decreased in Type 2 diabetic patients when compared with corresponding control subjects (p less than 0.03 and p less than 0.001, respectively). Independent of the type of diabetes, serum parathyroid hormone levels were comparable in diabetic patients and matched control subjects. Serum osteocalcin levels were significantly lower in Type 1 diabetic patients with retinopathy and/or proteinuria than in Type 1 diabetic patients without microangiopathy (p less than 0.05). Whereas serum parathyroid hormone levels in Type 2 diabetic patients with retinopathy and/or proteinuria were significantly increased (p less than 0.02), 25 hydroxy vitamin D levels were decreased (p less than 0.02) when compared with Type 2 diabetic patients without microangiopathy. Our data give evidence of a vitamin D deficiency and a decreased bone formation in patients with Type 2 diabetes mellitus. In Type 1 diabetes mellitus bone formation as reflected by serum osteocalcin levels is influenced by the presence or absence of microangiopathic complications.
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PMID:Serum osteocalcin levels in diabetes mellitus: analysis of the type of diabetes and microvascular complications. 326 86

Amylin is normally secreted in a regulated fashion by the pancreatic beta-cells in parallel with insulin and has been reported to have bone-conserving properties. Type I diabetes mellitus results in a low-turnover osteopenia in the presence of decreased amylin, which is in contrast to type II diabetes where less bone loss, in the presence of high amylin levels, occurs. We investigated the effects of amylin on bone mineral metabolism in normal and diabetic (streptozotocin-induced) rats, in order to ascertain whether amylin would modify the streptozotocin-induced diabetic osteopenia. Ten-week-old male Sprague-Dawley rats were randomized as follows: group A (n = 18) received normal saline; group B (n = 18) received amylin; group C, diabetic rats (n = 23), received normal saline; and group D, diabetic rats (n = 23), received amylin. Amylin (100 pmol/100 g b.w.) was administered by a daily subcutaneous injection. Double calcein-labeled tibiae were removed for histomorphometric analysis followed sacrifice on day 19. Results showed no difference in blood ionized calcium between groups. Blood glucose remained above 600 mg/dl in the diabetic animals and was not affected by the administration of amylin. Serum osteocalcin, insulin-like growth factor-1 (IGF-1), parathyroid hormone (PTH), and 1,25 dihydroxyvitamin D [1,25(OH)2D] were significantly lower in the diabetic rats compared with control group A by day 19. Amylin produced higher levels of serum osteocalcin in group B on day 9 (P < 0.05) compared with controls but returned to control values (group A) by day 19; no such change occurred in the diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amylin increases bone volume but cannot ameliorate diabetic osteopenia. 779 48

Serum osteocalcin levels are a marker of bone formation. In this study, bone and mineral metabolism in type I diabetes mellitus (DM) were investigated, and the changes related to diabetic microvascular complications were examined. Serum calcium (Ca), inorganic phosphate (P), osteocalcin (OC) and parathyroid hormone (PTH) levels were measured in 42 type I diabetic subjects. Diabetics were subdivided into those with or without complications. Age and sex-matched control subjects were used for comparisons with the diabetic groups. Serum P and PTH levels were not different from those of controls. Serum Ca levels were significantly increased (p < 0.001) although the values were within the normal range. OC levels were significantly lower in the complicated (retinopathy and/or protenuria) diabetic group (p < 0.005). In Type I diabetes mellitus, the serum OC level is influenced by the presence of microvascular complications.
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PMID:Serum osteocalcin levels in type I diabetes mellitus. 856 May 99


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