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

Bone mineral density (BMD) at the lumbar spine, quantified by dual energy X-ray absorptiometry, and biochemical bone remodeling markers (serum alkaline phosphatase, osteocalcin, tartrate-resistant acid phosphatase and urinary hydroxyproline) have been studied in 94 patients with diabetes mellitus aged 18-62 years. BMD was normal (1.13 +/- 0.02 g/cm2 in patients vs. 1.16 +/- 0.12 g/cm2 in controls), although it was found to be negatively correlated with HbA1, microalbuminuria, age and the duration of the disease. Serum alkaline phosphatase (188 +/- 75 I.U./l vs. 168 +/- 42 I.U./1; P < 0.03), serum tartrate-resistant acid phosphatase (14.3 +/- 4.3 I.U./l vs. 11.7 +/- 3.7 I.U./l; P < 0.0001) and urinary hydroxyproline (0.018 +/- 0.016 mmol/mmol creatinine vs. 0.011 +/- 0.008 mmol/mmol creatinine; P < 0.001) were higher in diabetics than in controls. Serum osteocalcin was lower (2.5 +/- 1.3 ng/ml vs. 3.4 +/- 1.2 ng/ml; P < 0.0001). No relationship was found between bone remodeling markers and BMD. It is concluded that lumbar BMD is normal in type 1 diabetic patients, although the degree of metabolic control, age and duration of the disease may affect it. In the light of the biochemical markers, bone remodeling may be disturbed in diabetes, but such disturbance seems to be unimportant regarding BMD.
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PMID:Bone densitometry and biochemical bone remodeling markers in type 1 diabetes mellitus. 795 May 1

The accumulated data indicate that bone mineral density (BMD) is decreased in humans with insulin-dependent diabetes mellitus. The purpose of this study was to prospectively determine sequential lumbar and femoral BMD utilizing dual energy X-ray absorptiometry in rats that spontaneously become diabetic to determine if weight and blood glucose control would prevent the diabetes-related bone mass changes. BMD of the lumbar spine and femur was measured prior to the onset of diabetes and at 3-week intervals after the diagnosis of diabetes for 12 weeks in 14 diabetes-prone BB/Wor rats (DP) and eight diabetes-resistant BB/Wor control rats (DR). At 12 weeks, the lumbar (0.238 +/- 0.013 vs 0.262 +/- 0.007 g/cm2, P < 0.001) and femoral (0.313 +/- 0.013 vs 0.343 +/- 0.013 g/cm2, P < 0.001) BMD were significantly lower in the DP rats despite significantly greater body weights (387 +/- 26 vs 329 +/- 46 g, P < 0.001) and plasma glucose levels of only 178 mg/dl. There was no difference in plasma values of calcium, phosphorus, osteocalcin, or tartrate-resistant acid phosphatase between groups or differences in osteoblast numbers in histologic sections. There was a significant (P < 0.001) decrease in plasma creatinine in the diabetic animals. The results indicate that in this animal model of type I diabetes, spine and femoral BMD do not increase comparable to control despite weight and blood glucose control. This would suggest that the diabetic condition itself affects bone mass in the absence of weight loss and poor blood glucose control.
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PMID:Bone mineral density in the femur and lumbar vertebrae decreases after twelve weeks of diabetes in spontaneously diabetic-prone BB/Worcester rats. 805 73

We have evaluated changes in bone volume, bone marrow tissue, and the density of osteoclasts caused by intermittent administration of human parathyroid hormone (h-PTH) to experimental osteopenia induced in rat by ovariectomy (OVX) or by diabetes mellitus (use of streptozotocin: STZ). A bone and marrow histomorphometric study was performed on HE-stained and tartrate-resistant acid phosphatase-stained (TRAP-stain) tibial bone sections. Retired Wistar rats, 7-8 months old, were used. They were separated into the following nine groups; sham operated, base line control, vehicle administered, low or high dosage h-PTH administered OVX and STZ groups. 6.0 micrograms/kg/day of h-PTH (1-34) as a low dosage, and 60.0 micrograms/kg/day as a high dosage, was injected subcutaneously six times a week for 4 weeks from 9 weeks after ovariectomy or injection of streptozotocin. The bone volume decreased in both the OVX and STZ groups, while the fat tissue volume increased in the bone marrow in the OVX groups to compensate for this decrease, and the foamy marrow tissue volume increased in the STZ groups. The bone volume and the mean trabecular thickness in both the OVX and STZ groups increased by the intermittent administration of h-PTH, while the TRAP positive trabecular surface and the number of osteoclasts decreased. There was no significantly different bone changes between the low and high dosage groups. It is thought that the TRAP positive trabecular surface represented not only the active bone resorption surface but also the related contiguous uneroded surface.
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PMID:[Effect of h-PTH on bone and bone marrow tissue in experimental osteopenia in rat]. 855 Nov

Because of the previous controversial findings in non-insulin-dependent diabetes mellitus (NIDDM), we measured bone-mineral density (BMD) by two different methods, studied biochemical markers of bone remodeling and calciotropic hormones (parathyroid hormone and calcitonin) in women with NIDDM, and compared the results with age-matched controls. Forty-seven women with NIDDM and 252 healthy nondiabetic women as controls were recruited for this study. BMD was measured by dual X-ray absorptiometry (DEXA) and by quantitative computed tomography (QCT). Biochemical markers of bone remodeling included plasma alkaline phosphatase (AP), osteocalcin (BGP), tartrate-resistant acid phosphatase (TRAP), parathyroid hormone (PTH), calcitonin (CT), and 24-h urine calcium, hydroxyproline. Diabetic patients were more obese with a higher body-mass index (BMI) than controls. Bone mass was normal in NIDDM, both by DEXA and by QCT. Biochemical markers of bone remodeling, PTH and CT were also normal. There was no statistical correlation between bone mass and any of the other measurements studied. There is no evidence that NIDDM produces any change in bone metabolism or mass.
J Diabetes Complications
PMID:Bone mineral metabolism is normal in non-insulin-dependent diabetes mellitus. 883 19

Polymorphisms at the vitamin D receptor (VDR) gene have been reported to mediate important differences in bone mineral density (BMD) and bone metabolism. In this longitudinal study we examined the relationships between VDR genotypes and bone metabolism, changes in BMD and changes in ultrasound transmission velocity in a population of healthy unrelated German women. The study population comprised 50 physically active women (aged 43.3 to 62.8 years, 14 premenopausal, 36 postmenopausal) with a daily calcium intake of (mean +/- SD) 1045 +/- 338 mg, who had earlier participated in a longitudinal study on the association of physical activity and bone density and bone turnover. Each participant was genotyped for the BsmI polymorphism at the VDR gene locus. Markers of bone turnover (alkaline phosphatase, osteocalcin, procollagen type I C-terminal propeptide, collagen type I C-terminal telopeptide, tartrate-resistant acid phosphatase) were measured at baseline. BMD (determined by peripheral quantitative computed tomography at the distal radius) and ultrasound transmission velocity through bone (at calcaneus, patella and thumb) were analysed at baseline and 15 months later. The genotypic groups did not differ significantly (p > 0.05) in any of the parameters determined at baseline. Neither were there any differences between these groups in the changes of BMD or ultrasound transmission velocity during the study period. Thus, we conclude that in physically active German women with a relatively high calcium intake the impact of VDR genotypic polymorphisms on bone density, bone metabolism and changes in bone density may be of limited importance.
Exp Clin Endocrinol Diabetes 1997
PMID:Vitamin D receptor genotypes and changes of bone density in physically active German women with high calcium intake. 913 41

We investigated the combined effects of estrogen deficiency and diabetes on bone mineral density (BMD) and bone metabolism in rats. Ten-week-old, female rats were randomly divided into four groups: controls (C), an ovariectomized group (O), a streptozotocin-induced diabetic group (S), and a combined ovariectomy and streptozotocin-induced diabetic group (OS). The BMD of the lumbar spine and the femur were measured before grouping and at 23 weeks old. At the end of the experiment, blood samples were obtained via cardiac puncture, and bone gla protein (BGP), tartrate-resistant acid phosphatase (TRAP) and 1,25-dihydroxyvitamin D levels were measured. The rats in the C, O, S, and OS groups, in that order, had higher levels of BMD of the lumbar spine and femur at 23 weeks of age. The BGP levels in the S and OS groups were significantly lower than in C and O groups. Significantly higher 1,25-dihydroxyvitamin D was observed in the O group compared with the C, S and OS groups. No differences were obtained in TRAP among four groups. Our data suggest that the combined effects of estrogen deficiency and diabetes on BMD are not synergistic or counteractive but additive.
Diabetes Res Clin Pract 2000 Apr
PMID:Additive effects of estrogen deficiency and diabetes on bone mineral density in rats. 1070 93

Vitamin E has been shown to affect bone metabolism. In this study we determined the effects of palm vitamin E and alpha-tocopherol on bone metabolism. Sprague-Dawley female rats fed with normal rat chow were divided into 4 groups and supplemented with either palm vitamin E 30 mg/kg rat weight, palm vitamin E 60 mg/kg rat weight or alpha-tocopherol 30 mg/kg rat weight. One group was not supplemented. Half of these rats were ovariectomised before supplementation was given for 10 months. As expected, bone mineral density of the ovariectomised rats fed on normal rat chow diet was lower compared to the intact rats. However, these changes were not seen in the supplemented group of rats. Both intact and ovariectomised rats supplemented with palm vitamin E 30 mg/kg rat weight had a lower bone calcium content in both femoral and vertebral bones whilst rats fed palm vitamin E 60 mg/kg rat weight or alpha-tocopherol 30 mg/kg rat weight were able to maintain bone calcium content. Alkaline phosphatase activity was elevated in ovariectomised rats supplemented with palm vitamin E 30 mg/kg rat weight and alpha-tocopherol 30 mg/kg rat weight compared to the intact rats. Alpha-tocopherol also reduced the activity of tartrate-resistant acid phosphatase post-ovariectomy. These findings indicate that both palm vitamin E and alpha-tocopherol maintained bone mineral density in ovariectomised rats but caused conflicting effects on bone calcium content. Further study is needed in order to determine the mechanisms involved.
Exp Clin Endocrinol Diabetes 2000
PMID:Palm vitamin E is comparable to alpha-tocopherol in maintaining bone mineral density in ovariectomised female rats. 1096 63

The pathophysiological processes underlying the development of diabetic osteopenia has not hitherto been elucidated. Induction of streptozotocin diabetes leads in our experiments to decrease of bone density, ash, mineral content and to thinner cortical width compared to control male rats. In order to investigate the pathogenetic role of bone resorption by osteoclasts in streptozotocin-induced diabetes, we determined the circulating levels of tartrate-resistant acid phosphatase (TRAP), a biochemical marker for bone resorption. Plasma TRAP values in diabetic rats did not differ from their corresponding controls. Streptozotocin diabetes by itself did not have any effect on the weight of seminal vesicles which are highly testosterone-dependent. Low doses of nitric oxide cause bone resorption, but higher doses of NO inhibit bone resorbing activity. We examined the effect of L-NAME (inhibitor of nitric oxide production) after six weeks of administration to diabetic rats. There was no further significant loss of bone mineral density, ash and mineral content or tibia weight in diabetic rats treated with L-NAME. L-NAME itself did not decrease bone metabolism. In our study no evidence of an increased bone resorption was found. Our results have indicated that a predominance of bone resorption over bone formation is not involved in the pathogenesis of diabetes-associated osteopenia. Inhibition of NO neither increased osteoclastic activity (TRAP) nor induced osteopenia in L-NAME-treated rats. This suggests a possibility that NO is not involved in the pathogenesis of diabetic osteopenia.
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PMID:The influence of nitric oxide synthase inhibitor L-NAME on bones of male rats with streptozotocin-induced diabetes. 1464 Aug 94

To clarify the pathogenesis of altered bone metabolism in diabetic state and its underlying mechanisms, the bone mineral content and fasting levels of serum intact parathyroid hormone (i-PTH), intact osteocalcin (i-OC), tartrate-resistant acid phosphatase (TRAP) and osteoclastgenesis inhibitory factor/osteoprotegerin (OCIF/OPG) were measured in male type 2 diabetic patients and their age-matched controls. In addition, urine levels of osteoclastic markers, C-telopeptide of type I collagen (CTx), deoxypyridinoline (DPD), and N-telopeptide of type I collagen (NTx) were simultaneously determined. Serum levels of i-PTH and i-OC in diabetic patients were significantly lower than those in the controls. Conversely, serum concentrations of TRAP were significantly elevated in diabetic patients. However, no clear correlation was observed between serum i-OC and TRAP. It was also observed that urinary excretion of CTx, DPD, and NTx was significantly increased in the diabetics as compared with the controls. Unexpectedly, serum levels of OCIF/OPG tended to be higher in the diabetic group, and these values exhibited a significantly positive correlation with those of serum TRAP. There was found a significantly negative correlation between serum TRAP and bone mineral density (BMD) and also between serum OCIF/OPG and bone mineral density. It seems probable that OCIF/OPG has a suppressive role on the increased bone resorption to prevent further loss of the skeletal bone mass in type 2 diabetic patients.
Diabetes Res Clin Pract 2005 May
PMID:Osteoclastic function is accelerated in male patients with type 2 diabetes mellitus: the preventive role of osteoclastogenesis inhibitory factor/osteoprotegerin (OCIF/OPG) on the decrease of bone mineral density. 1586 Feb 39

Decreased bone mass, osteoporosis, and increased fracture rates are common skeletal complications in patients with insulin-dependent diabetes mellitus (IDDM; type I diabetes). IDDM develops from little or no insulin production and is marked by elevated blood glucose levels and weight loss. In this study we use a streptozotocin-induced diabetic mouse model to examine the effect of type I diabetes on bone. Histology and microcomputed tomography demonstrate that adult diabetic mice, exhibiting increased plasma glucose and osmolality, have decreased trabecular bone mineral content compared with controls. Bone resorption could not completely account for this effect, because resorption markers (tartrate-resistant acid phosphatase 5b, urinary deoxypyridinoline excretion, and tartrate-resistant acid phosphatase 5 mRNA) are unchanged or reduced at 2 and/or 4 wk after diabetes induction. However, osteocalcin mRNA (a marker of late-stage osteoblast differentiation) and dynamic parameters of bone formation were decreased in diabetic tibias, whereas osteoblast number and runx2 and alkaline phosphatase mRNA levels did not differ. These findings suggest that the final stages of osteoblast maturation and function are suppressed. We also propose a second mechanism contributing to diabetic bone loss: increased marrow adiposity. This is supported by increased expression of adipocyte markers [peroxisome proliferator-activated receptor gamma2, resistin, and adipocyte fatty acid binding protein (alphaP2)] and the appearance of lipid-dense adipocytes in diabetic tibias. In contrast to bone marrow, adipose stores at other sites are depleted in diabetic mice, as indicated by decreased body, liver, and peripheral adipose tissue weights. These findings suggest that IDDM contributes to bone loss through changes in marrow composition resulting in decreased mature osteoblasts and increased adipose accumulation.
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PMID:Increased bone adiposity and peroxisomal proliferator-activated receptor-gamma2 expression in type I diabetic mice. 1590 21


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