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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the occurrence of osteopenia, as reflected by decreased cortical bone thickness, in a nonobese animal model of hereditary non-insulin-dependent diabetes with long duration, i.e., 8-month-old Goto-Kakizaki (GK) rats. In addition, motor nerve-conduction velocity was measured in the GK rats. Age- and weight-matched Wistar rats served as controls. The GK rats displayed marked glucose intolerance, as compared to control rats, in an intraperitoneal glucose tolerance test. Decreased cortical bone thickness by approximately 15%, was evident in X-ray analysis of metatarsal bones (p < 0.001) and humerus (p < 0.05) of the GK rats. Motor nerve-conduction velocity, measured in the sciatic nerve, was also decreased (by 10%) in the GK as compared with the age-matched control rats (p < 0.05). In conclusion, reduction of cortical bone thickness is present in 8-month-old GK rats, which simultaneously demonstrate signs of peripheral neuropathy. Thus, the GK rat appears to be a model of NIDDM suitable for studies of diabetic bone disease in the absence of obesity.
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PMID:Decreased cortical bone thickness in spontaneously non-insulin-dependent diabetic GK rats. 936 71

Localized lesions at the foot skeleton are a serious and well recognized complication of diabetes mellitus which may impair the clinical outcome of the patients remarkably. In contrast, the presence of a generalized bone disease or osteoporosis related to diabetes mellitus is less acknowledged and its clinical relevance is less obvious. This paper is a clinically focused review of the literature on osteoporosis related to diabetes mellitus. Due to the different pathogenesis of diabetes mellitus type 1 and type 2 it is not surprising that there is no uniform entity of diabetic osteopathy. The majority of clinical studies in subjects with diabetes mellitus type 1 showed a moderately decreased bone mass at the forearm, while bone mass at the femur or lumbar spine was either decreased or not different from non-diabetic controls. In patients with diabetes mellitus type 2 the risk of osteopenia is not as clear as in type 1 diabetes. Bone mineral density at the forearm in patients with type 2 diabetes mellitus was decreased, unchanged or even increased in comparison to controls, while bone mineral density at the vertebrae or femoral neck was either not significantly different or increased, but rarely decreased. The underlying mechanisms triggering changes in bone mass in patients with diabetes mellitus type 1 and type 2 are not well known. In most studies there was no consistent relationship between the metabolic control of diabetes and bone mineral density. Biochemical parameters of the calcium and bone metabolism showed no clear relationship to the bone mineral density measurements. From few bone histology studies in humans and experimental studies there is evidence that a decreased bone formation is one major mechanism leading to reduced bone mass in diabetics. Microangiopathy at the bone tissue was also discussed as a possible reason for diabetic osteopenia. It was shown that insulin and insulin like growth factors (IGF-1, IGF-2) have an influence on bone metabolism itself and other growth factors, cytokines and hormones may determine changes in diabetic bone metabolism. Recent findings suggest that leptin is involved in the regulation of osteoblast function and bone mass, which is of special interest in diabetes mellitus type 2. The clinical relevance of osteoporosis or osteopenia is determined by the increased risk for insufficiency fractures. Few studies found an increased fracture risk, especially in older women with type 1 diabetes mellitus, while others did not show an increased risk for fractures or even found a decreased rate of fractures in women with diabetes mellitus type 2. There is a need for further longitudinal studies, including the incidence and risk factors for osteoporotic fractures. In clinical routine the extent of diagnostic and therapeutic activities in patients with type 1 or type 2 diabetes mellitus in respect to generalized bone disease or diabetic osteopenia should be based on individual conditions and risk profile for osteoporosis.
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PMID:Diabetes mellitus a risk for osteoporosis? 1146 May 94

Osteoporosis is the most prevalent metabolic bone disease in the United States. Although the disease has historically been reported mostly in white women, it can affect individuals of both sexes and all ethnic groups. The presence of osteoporosis related to diabetes is not well acknowledged and the impact of osteoporosis in a diabetic patient is often not considered. Routine screening or initiation of preventive medications for osteoporosis in all patients with type 1 or type 2 diabetes is not recommended at the present time. However, in all patients with diabetes, besides optimal glycemic control, general recommendations regarding adequate dietary calcium intake, regular exercise, and avoidance of other potential risk factors such as smoking should be given. In patients who have positive risk factors for osteoporosis, or in those who present with fractures, evaluation of bone density should be done and respective preventive or therapeutic interventions should be applied.
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PMID:Osteoporosis and diabetes. 1264 44

Bone disease in hemodialysis (HD) patients with type 2 diabetes mellitus (DM) is characterized by low bone turnover (Inaba M, et al. Am J Kidney Dis 2002; 39:1261-1269), although their bone quality is yet to be determined. The present study was designed to examine whether the prevalence of vertebral fracture in female HD patients with type 2 DM, age 65 years and older, might be increased, and the relation of this fracture to bone mineral density (BMD) determined by dual X-ray absorptiometry (DXA), since few data are available on the effect of DM on bone strength at lumbar spine. The prevalence of vertebral fracture in type 2 DM HD patients was 32.3%, which was greater than that of non-DM HD patients (13.3%) when adjusted for age and HD duration. Logistic regression analysis elucidated the presence of DM and age as independent risk factors for an increased prevalence of vertebral fracture in HD patients. In non-DM HD patients, those with vertebral fracture showed age significantly higher and BMD in either lumbar spine or distal one third of radius significantly lower than the respective value in those without fracture. However, in DM HD patients, neither BMD in lumbar spine nor distal one third of radius was significantly lower in those with vertebral fracture than in those without. Furthermore, age did not differ significantly between DM HD patients with and without fracture. In conclusion, female type 2 DM HD patients, age 65 years and older, showed significantly higher incidence of vertebral fracture than non-DM HD patients. Although age and low BMD emerged as independent risk factors for vertebral fracture in non-DM HD patients, those factors failed to be a risk factor in DM HD patients, suggesting that BMD determined by DXA might not be reliable in assessing bone strength in DM HD patients.
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PMID:Increased incidence of vertebral fracture in older female hemodialyzed patients with type 2 diabetes mellitus. 1569 25

Diabetic osteoporosis is increasingly recognized as a significant comorbidity of type 1 diabetes mellitus. In contrast, type 2 diabetes mellitus is more commonly associated with modest increases in bone mineral density for age. Despite this dichotomy, clinical, in vivo, and in vitro data uniformly support the concept that new bone formation as well as bone microarchitectural integrity are altered in the diabetic state, leading to an increased risk for fragility fracture and inadequate bone regeneration following injury. In this review, we examine the contribution that insulin, as a potential anabolic agent in bone, may make to the pathophysiology of diabetic bone disease. Specifically, we have assimilated human and animal data examining the effects of endogenous insulin production, exogenous insulin administration, insulin sensitivity, and insulin signaling on bone. In so doing, we present evidence that insulin, acting as an anabolic agent in bone, can preserve and increase bone density and bone strength, presumably through direct and/or indirect effects on bone formation.
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PMID:Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues. 1621 65

Bone disease in patients with type 2 diabetes mellitus (DM) is characterized by low bone turnover, resulting from either impaired secretion of parathyroid hormone or osteoblasts dysfunction. We have reported that intracellular sorbitol accumulation via. sorbitol pathway might be involved in the development of osteoblast dysfunction and osteoclast formation, as evidenced by either in vitro or in vivo study. The importance of metabolic pathway is further supported by the protective effect of aldose reductase inhibitor against the development of galactose-induced bone diseases in vivo and of functional impairments of human osteoblasts-like MG-63 cells. In conclusion, sorbotol pathway might be important in the development of low bone turnover disease in DM patients, and thus aldose reductase inhibitor might be clinically useful in the protection against the development of bone diseases in DM patients.
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PMID:[Effect of aldose reductase on the abnormality of calcium metabolism in diabetic patients]. 1688 45

Vitamin D is essential for the maintenance of good health. Its sources can be skin production and diet intake. Most humans depend on sunlight exposure (UVB 290-315 nm) to satisfy their requirements for vitamin D. Solar ultraviolet B photons are absorbed by the skin, leading to transformation of 7-dehydrocholesterol into vitamin D3 (cholecalciferol). Season, latitude, time of day, skin pigmentation, aging, sunscreen use, all influence the cutaneous production of vitamin D3. Vitamin D deficiency not only causes rickets among children but also precipitates and exacerbates osteoporosis among adults and causes the painful bone disease osteomalacia. Vitamin D deficiency has been associated with increased risk for other morbidities such as cardiovascular disease, type 1 and type 2 diabetes mellitus and cancer, especially of the colon and prostate. The prevalence of hypovitaminosis D is considerable even in low latitudes and should be taken into account in the evaluation of postmenopausal and male osteoporosis. Although severe vitamin D deficiency leading to rickets or osteomalacia is rare in Brazil, there is accumulating evidence of the frequent occurrence of subclinical vitamin D deficiency, especially in elderly people.
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PMID:Vitamin D deficiency: A global perspective. 1711 89

A model of chronic kidney disease (CKD)-induced vascular calcification (VC) that complicates the metabolic syndrome was produced. In this model, the metabolic syndrome is characterized by severe atherosclerotic plaque formation, hypertension, type 2 diabetes, obesity, and hypercholesterolemia, and CKD stimulates calcification of the neointima and tunica media of the aorta. The CKD in this model is associated the adynamic bone disorder form of renal osteodystrophy. The VC of the model is associated with hyperphosphatemia, and control of the serum phosphorus both in this animal model and in humans has been preventive in the development of VC. This article reports studies that demonstrate reduction of established VC by the addition of sevelamer carbonate to the diets of this murine metabolic syndrome model with CKD. Sevelamer, besides normalizing the serum phosphorus, surprisingly, reversed the CKD-induced trabecular osteopenia. Sevelamer therapy increased osteoblast surfaces in the metaphyseal trabeculae of the tibia and femur. It also increased osteoid surfaces and, importantly, bone formation rates. In addition, sevelamer was found to be effective in decreasing serum cholesterol levels. These results suggest that sevelamer may have important actions in decreasing diabetic and uremic vasculopathy and that sevelamer carbonate may be capable of increasing bone formation rates that are suppressed by diabetic nephropathy.
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PMID:Reversal of the adynamic bone disorder and decreased vascular calcification in chronic kidney disease by sevelamer carbonate therapy. 1718 86

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

Diabetes mellitus induces alterations in bone and mineral metabolism. Diabetic bone disorder causes an increase in bone fractures, delays healing of fractures, and affects the quality of life. There are few optimal therapies for these disorders and the mechanisms responsible for their complications have not been clearly identified. Bone histology studies in humans and animals have demonstrated that decreased bone formation is a critical mechanism of bone mass reduction in diabetes. A major hypothesis about the mechanisms of diabetic complications is a diabetes-induced increase in oxidative stress, because reactive oxygen species (ROS) are increased under diabetic conditions and are known to induce cellular dysfunction in a wide variety of cell types. Oxidative stress is induced by a variety of mechanisms including formation of increased advanced glycation end-products (AGEs), increased polyol pathway flux, activation of protein kinase C isoforms, glucose autoxidation, and mitochondrial overproduction of superoxide under diabetic conditions. Other circulating factors that are elevated in diabetes, such as free fatty acids and leptin, also contribute to increased ROS generation. It is now widely accepted that ROS can cause severe damage to DNA, proteins, and lipids. Concerning bone metabolism, in vitro studies have shown that oxidative stress inhibits osteoblastic differentiation and induces osteoblast insults and apoptosis. Moreover, we have demonstrated that both streptozotocin-induced diabetic mice, an animal model of type 1 diabetes, and spontaneously diabetic Torii (SDT) rats, an animal model of type 2 diabetes, have low-turnover osteopenia associated with increased oxidative stress and that markers of oxidative stress are inversely associated with the histomorphometric parameters of bone formation. Growing evidence suggests that the increase in oxidative stress may at least partly contribute to the development of diabetic osteopenia. This review focuses on the impact of diabetes-induced oxidative stress in the development of diabetic bone disorder.
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PMID:Role of oxidative stress in diabetic bone disorder. 1923 2


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