Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to assess skeletal status in diabetic and nondiabetic subjects with end-stage renal disease (ESRD). One hundred twenty-three patients with ESRD (57 patients with diabetes: 9 type 1 and 48 type 2) and 66 nondiabetic patients were evaluated. Control group comprised 1541 subjects (614 males and 927 females). Diabetes and/or renal insufficiency was the only reason of bone disease and, in control group, no factors known to influence bone metabolism (chronic diseases or prolonged medications) were noted. Skeletal status was evaluated by quantitative ultrasound measurements at the hand phalanges using DBM 1200 (IGEA, Carpi, Italy), which measures amplitude-dependent speed of sound (Ad-SoS [m/s]). Because of some differences in mean age in subgroups of patients and controls, comparisons were performed using values of Z-score. In all diabetic patients, Z-score was significantly higher compared with nondiabetics (p < 0.05). In all type 1 diabetes patients, Z-score was significantly lower than in all nondiabetic patients (p < 0.05) and in patients with type 2 diabetes (p < 0.001). Z-score was also significantly lower in type 2 diabetics than in nondiabetic females (p < 0.00001) but did not differ in males. Comparisons between Z-scores in controls and patients showed that Z-score in nondiabetic females was significantly lower than in female controls (p < 0.000001), and in nondiabetic males--diabetic type 2 males as well as females--Z-score did not differ vs. results in adequate control group. Z-score was significantly lower in patients with diabetes type 1 vs. all controls (p < 0.001). Correlation analysis showed in all nondiabetic patients that Z-score was negatively affected by duration time of dialysis (r = -0.37, p < 0.01) and parathyroid hormone (PTH) serum level (r = -0.35, p < 0.01). In patients with type 1 diabetes, only PTH influenced significantly Z-score (r = -0.76, p < 0.05) and, in patients with type 2 diabetes, no significant correlations were obtained. Subjects with type 1 diabetes seemed to be sensitive for skeletal disturbances in a course of renal insufficiency, whereas subjects with type 2 diabetes did not show such skeletal pathology as shown by ultrasound measurements at hand phalanges.
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PMID:Quantitative ultrasound measurements in diabetic and nondiabetic patients with end-stage renal disease. 1741 82

Abnormalities of bone mineral metabolism in patients with stage-5 chronic kidney disease may contribute to the high incidence of cardiovascular disease. Noninvasive imaging methods may help predict the simultaneous presence of vasculopathy and bone disease. Accordingly, we measured pulse wave velocity and bone mineral density (BMD), and T-scores (number of SDs below the BMD of a younger reference group) of the spine by both dual energy x-ray absorptiometry and quantitative computed tomography (QCT) in 110 maintenance hemodialysis patients. Older age, white race, diabetes mellitus, lower diastolic blood pressure, and lower albumin levels were associated with lower QCT-assessed T-scores (each P<0.05). After age and multivariable adjustment, pulse wave velocity (PWV) increased as QCT BMD decreased (the prevalence of PWV >or=9 m/s was 32.4%, 61.8%, and 76.5% for participants in the highest to the lowest tertile of QCT-assessed BMD; P<0.001). In contrast, there was no relationship between spine dual energy x-ray absorptiometry-BMD and PWV. In unadjusted models, thoracic spine QCT-assessed T-scores correlated significantly, albeit weakly, with aorta calcification (r=0.22; P=0.01) but not with coronary calcification. The odds ratio of PWV >or=9 m/s for patients taking vitamin D(3) or its analogs was 0.51 (95% CI: 0.19 to 1.39). In conclusion, low spine BMD is associated with increased PWV in stage-5 chronic kidney disease, supporting the notion of a close interaction of vascular and bone disease in this patient group. QCT and not dual energy x-ray absorptiometry should be used to assess spine BMD in dialysis patients.
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PMID:Pulse wave velocity is inversely related to vertebral bone density in hemodialysis patients. 1742 Mar 31

Cystic fibrosis (CF) is a multisystem disease. Some of this is accounted for by CF transmembrane regulator (CFTR) dysfunction in individual organs but in some cases this is compounded by the effects of systemic inflammation. The inflammation is in response to the chronic infection in the airways and is particularly important as a contributor to CF-related bone disease, CF-related diabetes mellitus, CF-related arthropathy, and vasculitis. Preventing these multisystem complications is difficult. Aggressive specific therapies to treat complications is critically important to maintain nutrition, stop the damaging effects of diabetes, and improve bone mineral density. Aggressive treatment of lung disease to reduce systemic inflammation is likely to be of benefit in preventing the development of CF-related bone disease and may be beneficial in at least delaying the onset of CF-related diabetes. Aggressive treatment of pulmonary infection and inflammation in conjunction with holistic management plans to treat specific organ diseases is an important strategy in improving morbidity and reducing mortality in people with CF.
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PMID:How can we prevent multisystem complications of cystic fibrosis? 1756

Diabetic bone disease is associated with increased oxidative damage and 2-deoxy-D: -ribose (dRib) is used to induce oxidative damage similar to that observed in diabetics. To determine if hesperetin (3',5,7-trihydroxy-4-methoxyflavanone) could influence osteoblast dysfunction induced by dRib, osteoblastic MC3T3-E1 cells were treated with dRib and hesperetin. Then, markers of osteoblast function and oxidative damage were examined. Hesperetin (10(-7)-10(-5) M) caused a significant elevation of alkaline phosphatase (ALP) activity, collagen content, and total antioxidant potential of MC3T3-E1 cells in the presence of 20 mM dRib (p < 0.05). Moreover, hesperetin (10(-7) M) decreased cellular protein carbonyl (PCO), advanced oxidation protein products (AOPP), and malondialdehyde (MDA) contents of osteoblastic MC3T3-E1 cells in the presence of 20 mM dRib. These results demonstrate that hesperetin attenuates dRib-induced damage, suggesting that hesperetin may be a useful dietary supplement for minimizing oxidative injury in diabetes related bone diseases.
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PMID:Hesperetin attenuates the highly reducing sugar-triggered inhibition of osteoblast differentiation. 1770 Oct 78

Renal osteodystrophy is a complication of chronic kidney disease (CKD) that present in low and high turnover patterns. This disorder has a key role in the disability of CKD patients in whom early diagnosis and treatment can result in better outcome. We studied hyperparathyroidism prevalence and its relationship with renal osteodystrophy in our advanced CKD population. We included 80 patients (of whom 44 (55%) were diabetic) during 6 months period. The patients answered a questionnaire about symptoms related to bone disease and blood levels of parathormone (PTH), calcium, phosphorus, and alkaline phosphatase were obtained, in addition to hand and skull radiographs in all the study patients. Prevalence of clinically evident hyperparathyroidism in our patients was 45%. Hyperparathyroidism had significant relationship with alkaline phosphatase and radiological findings, but did not have a significant relationship with dialysis duration, age, sex, familial history, diabetes mellitus, or hypertension. We conclude that secondary hyperparathyroidism is prevalent in our dialysis population and has high correlation with serum alkaline phosphatase levels and radiological changes.
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PMID:Evaluation of secondary hyperparathyroidism in patients undergoing hemodialysis. 1808 40

Type 1 diabetes mellitus is associated with a number of disorders of skeletal health, conditions that rely, in part, on dynamic bone formation. A mouse model of distraction osteogenesis was used to study the consequences of streptozotocin-induced diabetes and insulin treatment on bone formation and osteoblastogenesis. In diabetic mice compared with control mice, new bone formation was decreased, and adipogenesis was increased in and around, respectively, the distraction gaps. Although insulin treatment restored bone formation to levels observed in nondiabetic control mice, it failed to significantly decrease adipogenesis. Molecular events altered during de novo bone formation in untreated type 1 diabetes mellitus, yet restored with insulin treatment were examined so as to clarify specific osteogenic genes that may contribute to diabetic bone disease. RNA from distraction gaps was analyzed by gene microarray and quantitative RT-PCR for osteogenic genes of interest. Runt-related transcription factor 2 (RUNX2), and several RUNX2 target genes, including matrix metalloproteinase-9, Akp2, integrin binding sialoprotein, Dmp1, Col1a2, Phex, Vdr, osteocalcin, and osterix, were all significantly down-regulated in the insulin-deficient, hyperglycemic diabetic animals; however, insulin treatment of diabetic animals significantly restored their expression. Expression of bone morphogenic protein-2, transcriptional coactivator with PDZ-binding motif, and TWIST2, all important regulators of RUNX2, were not impacted by the diabetic condition, suggesting that the defect in osteogenesis resides at the level of RUNX2 expression and its activity. Together, these data demonstrate that insulin and/or glycemic status can regulate osteogenesis in vivo, and systemic insulin therapy can, in large part, rescue the diabetic bone phenotype at the tissue and molecular level.
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PMID:Runt-related transcription factor 2 (RUNX2) and RUNX2-related osteogenic genes are down-regulated throughout osteogenesis in type 1 diabetes mellitus. 1816 13

Diabetes is a chronic disease associated with hyperglycemia and altered bone metabolism that may lead to complications including osteopenia, increased risk of fracture and osteoporosis. Hyperglycemia has been implicated in the pathogenesis of diabetic bone disease; however, the biologic effect of glucose on osteoclastogenesis is unclear. In the present study, we examined the effect of high d(+)glucose (d-Glc) and l(-)glucose (l-Glc; osmotic control) on RANKL-induced osteoclastogenesis using RAW264.7 cells and Bone Marrow Macrophages (BMM) as models. Cells were exposed to sustained high glucose levels to mimic diabetic conditions. Osteoclast formation was analyzed using tartrate resistant acid phosphatase (TRACP) assay, expression of calcitonin receptor (CTR) and cathepsin K mRNAs, and cultures were examined for reactive oxygen species (ROS) using dichlorodihydrofluorescein diacetate (DCF-DA) fluorescence, caspase-3 and Nuclear Factor kappaB (NF-kappaB) activity. Cellular function was assessed using a migration assay. Results show, for the first time, that high d-Glc inhibits osteoclast formation, ROS production, caspase-3 activity and migration in response to RANKL through a metabolic pathway. Our findings also suggest that high d-Glc may alter RANKL-induced osteoclast formation by inhibiting redox-sensitive NF-kappaB activity through an anti-oxidative mechanism. This study increases our understanding of the role of glucose in diabetes-associated bone disease. Our data suggest that high glucose levels may alter bone turnover by decreasing osteoclast differentiation and function in diabetes and provide new insight into the biologic effects of glucose on osteoclastogenesis.
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PMID:High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis. 1837 5

An 82-year-old diabetic female had been aware of gradually enlarging, painless scalp depressions in the bilateral parietal regions for more than 6 years. She had no history of head injury, or inflammatory or malignant disease. Her family history was unremarkable for hereditary bone disease. She had diabetes mellitus which had been well controlled with orally administered drugs. Blood examination showed normal renal and liver functions with normal serum calcium, magnesium, and phosphorus concentrations, in addition to normal parathyroid hormone and calcitonin levels. Neuroimaging including skull radiography, head computed tomography, and magnetic resonance imaging demonstrated symmetric thinning in the bilateral parietal bones attributed to loss of diploe and thinning of the outer table. The inner table was intact without associated soft tissue mass or vascular lesions. Technetium-99m methylene diphosphate systemic bone scintigraphy showed mild hypoaccumulation in the affected calvarium on the left. No other pathological findings were found by systemic examination. She underwent open biopsy for histological verification which revealed homogeneous membranous bone tissue with regressed diploe, absence of osteoblasts, absence of osteoclastic appearance, and absence of findings of underlying malignancy. There was no markedly fibrovascular connective tissue typical of Gorham-Stout disease. Calvarial thinning in the present case may have been caused by an undetermined complex mechanism.
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PMID:Idiopathic calvarial thinning. 1857 36

Secondary hyperparathyroidism (SHPTH) can develop early in the course of chronic renal failure and becomes more prominent as kidney function declines. We studied the effect of diabetes, age, and dialysis on parathyroid function in 60 (21 women, 39 males; 44 non-diabetic, 16 diabetic) hemodialysis (HD) patients. Serum intact PTH (iPTH), calcium, phosphorus, alkaline phosphatase (ALP), and magnesium (Mg) were measured. Adequacy of HD was evaluated by calculating the urea reduction rate (URR). There were significantly lower values of serum iPTH, ALP, and dialysis adequacy among diabetic than non-diabetes HD patients. In addition, there were an inverse correlation of age and serum iPTH (r= -0.27, p=0.034) as well as age and serum phosphorus (r= -0.28, p=0.031). There was also a positive correlation between serum iPTH with the duration (r=0.001, p=0.42) and doses of dialysis treatment (r=0.38, p=0.002). We conclude that a significant negative correlation between age and serum phosphorus and lower parathyroid activity in diabetic HD patients, which implies more prevalence of bone disease in elderly diabetic HD patients. Further study of bone disease in this group of patients is required to evaluate its effect on outcome and different therapeutic interventions.
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PMID:Effects of diabetes mellitus, age, and duration of dialysis on parathormone in chronic hemodialysis patients. 1858 21

Successful kidney transplantation leads to restoration of renal function. Some metabolic disorders from chronic renal failure may persist and new metabolic abnormalities can develop (obesity, diabetes, hypertension, bone disease, and anemia). Additionally, influence of immunosuppressive drugs (corticosteroids, cyclosporine A, tacrolimus, and rapamycin) may aggravate the course of diabetes, hypertension, and dyslipidemia. Nutritional management of renal transplantation is divided into the pretransplant period, transplant surgery, and early and late posttransplant period. Patients in the pretransplant period in dialysis treatment may develop protein-energy malnutrition and negative nitrogen balance, with loss of lean body mass and fat deposits. Nutritional management in the early posttransplant period with a functioning kidney graft necessitates fluid and electrolyte balance control with protein intake of 1,2/kg BW/day and 30-35 kcal/kg BW/day. In a nonfunctioning kidney graft, dialysis treatment continues and the therapeutic dose of immunosuppressive drugs must be reduced. The principal objective in the late posttransplant period is the maintenance of optimal nutritional status. Nutrition is important in managing obesity, insulin resistance, diabetes, hyperlipidemia, and hypertension. Other posttransplant conditions for which diet and/or nutritional supplements may be beneficial include hypomagnesemia, hypophosphatemia, hyperuricemia, hyperkalemia, hyperhomocysteinemia, chronic renal allograft failure, renal anemia, and renal bone disease.
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PMID:Nutritional consequences of renal transplantation. 1912 81


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