Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duration of disease is the major susceptibility factor for microangiopathy. Microangiopathy does not occur without the metabolic abnormality of diabetes and there is much circumstantial evidence to implicate poor diabetic control in its pathogenesis. The rate of development and severity of complications, however, are variable even in patients with apparently similar control and about 25% of diabetics will never develop clinical evidence of microangiopathy. Studies of identical twins suggest a genetic component in the pathogenesis of retinopathy in NIDDM, and less so in IDDM, but increased capillary basement membrane thickness does not occur in the non-diabetic identical co-twins of insulin dependent diabetics. There may also be genetic heterogeneity not only of diabetes, but also of its complications, although for a given type of diabetes the prevalence of microangiopathy is often very similar in different racial groups. Associations between several different HLA molecules (particularly DR4) and microangiopathy in IDDM have been reported but not consistently confirmed. Recently the finding of an increased frequency of the B3 allotype of the fourth component of complement C4B3 in subjects with retinopathy has suggested that there is an HLA linked association. Both complement and the immunoglobulins are concerned with humoral immunity and the report of an association between a phenotype of the IgG heavy chain markers on chromosome 14 and retinopathy is of particular interest. These associations appear to be additive but independent. These reports need confirmation but provide the best evidence we have for an immunogenetic component (HLA and non-HLA linked) of the aetiology of microangiopathy, at least in IDDM. The studies of identical twins, HLA and Gm associations provide good evidence that genetic factors are involved in susceptibility to microangiopathy, at least in some diabetics, although the most relevant genes may not have been identified. Searches for better genetic markers must continue in order to identify those patients at increased risk of developing microangiopathy.
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PMID:The genetics of diabetic complications. 353 96

Type II, non insulin dependent diabetes mellitus is commonly diagnosed after the age of 45 years. For this reason it was previously called maturity onset diabetes. Type II diabetes occurring in young subjects has generally been described in selected pedigrees. The purpose of this work was to review data from all the unrelated type II diabetics (with fasting hyperglycemia) diagnosed before the age of 45 and observed in our department over the last four years. A total of 90 such patients including 44 men and 46 women were included in this study. Of 43 cases diagnosed before the age of 30, there were 30 women compared to only 16 women out of 47 cases diagnosed between 30 and 45 years (p less than 0.001). At the time of diagnosis 42 patients had a relative body weight lower than 120%. In 66,7% of the cases, one parent was a known diabetic. The rate of diabetes in the sibships was 50%. Differences in family history of diabetes were not observed in relation to age or weight at diagnosis. Comparison with a series of 150 conventional type II diabetics in whom diagnosis was made between 45 and 60 years of age showed a significantly greater frequency of obesity (86%) and fewer diabetic parent (36%). The mean apparent duration of diabetes was 14 years (range 5-42). Microangiopathy was not infrequent in these diabetic patients. Twenty-three patients had retinopathy, proliferative in 8 cases, and 3 were blind. Nine had renal insufficiency, severe in 3 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Type II diabetes in young subjects. A study of 90 unrelated cases. 359 70

Diabetes mellitus has recently markedly increased among elderly patient's diseases. There are no recent epidemiological reports on the relative number of male and female diabetic patients. So, an epidemiological study was performed on 746 Non-Insulin-Dependent Diabetes Mellitus patients, whose data were obtained from members of the Himeji Internal Medicine Association, divided into six groups according to sex and duration of illness. The following results were obtained. 1) The number of male patients was greater by about 20% than that of female patients, while elderly patients accounted for a larger proportion, nd age at onset of disease was about ten years higher in female than in male patients. 2) All indicators of diabetes mellitus became worse with longer duration of illness. 3) There was a correlation between the prevalence of complications and the duration of illness: The prevalence of complications increased in parallel with increasing duration of illness, and this tendency was more marked in female than in male patients. 4) Female patients had a more marked tendency to develop hypertension, hyperlipidemia and obesity than male patients. 5) Microangiopathy generally manifested itself earlier than macroangiopathy, and the increase in the prevalence of angiopathy in accordance with prolonged duration of illness was more marked for microangiopathy than for macroangiopathy. Clinical features of Japanese diabetics are found to be similar to those of Europeans, especially dominant in females. This might be due to the changing life style in japan.
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PMID:The prevalence of diabetic complication of elderly diabetics in Himeji. 886 5

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

Diabetic eye disease is the major cause of blindness and vision loss among working-age people in developed countries. Microangiopathy and capillary occlusion underlie the pathogenesis of disease. While laser treatment is regarded as the standard therapy, intensive medical management of glycaemia and hypertension is also a priority in order to reduce the risk of diabetic retinopathy. Recent data have prompted a re-evaluation of the role of lipid-modifying therapy in reducing diabetic retinopathy. The Fenofibrate Intervention for Event Lowering in Diabetes (FIELD) study demonstrated a significant 30% relative reduction in the need for first retinal laser therapy in patients with (predominantly early-stage) type 2 diabetes treated with fenofibrate 200 mg daily, from 5.2% with placebo to 3.6% with fenofibrate, p=0.0003. The benefit of fenofibrate was evident within the first year of treatment. These promising data justify further evaluation of the mechanism and role of fenofibrate, in addition to standard therapy, in the management of diabetic retinopathy.
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PMID:Diabetic retinopathy: treatment and prevention. 1793 59

Retinopathy has been increasing in prevalence as a consequence of type 2 diabetes and a cluster of coexisting risk factors characterized as the metabolic syndrome. However, the combined effects of these conditions on the retina are poorly understood. Therefore, we focused on the spontaneously hypertensive corpulent rat (SHR/N-cp), a model with type 2 diabetes, obesity and features of the metabolic syndrome to characterize retinal changes at a structural and functional level. SHR/N-cp males at 4 and 8 months of age were used in this study. Metabolic parameters and blood pressure were measured by standard methods. Morphology was investigated by histological techniques supplemented by nicotinamide adenine dinucleotide phosphate-diaphorase staining of whole mounts and fluorescein angiography to analyze the retinal vasculature. The in vivo function of the retina was examined by electroretinography (ERG). Obese SHR/N-cp rats were hypertensive and showed significant increases in body weight, serum levels of glucose, triglycerides, total cholesterol and urinary glucose excretion compared with lean controls (P < 0.01 for each). Histology indicated an overall intact integrity of the retina and aspects of microangiopathy in obese SHR/N-cp rats. ERG revealed intact processing of light signals but significantly decreased amplitudes of b-waves for all (P < 0.01) and of a-waves for some examined light intensities (P < 0.05). Oscillatory potentials were significantly protracted (P < 0.01), whereas amplitudes were not reduced. Microangiopathy and electroretinographic deficits combine to produce an early non-proliferative retinopathy phenotype in the obese SHR/N-cp rats. Thus, this model represents a valuable experimental tool to obtain further insights into the mechanisms of retinopathy in the context of obesity, type 2 diabetes and metabolic syndrome.
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PMID:Microangiopathy and visual deficits characterize the retinopathy of a spontaneously hypertensive rat model with type 2 diabetes and metabolic syndrome. 2092 14

The purpose of this study was to examine whether exercise training can prevent microangiopathy of skeletal muscles in rats with type 2 diabetes and if succinate dehydrogenase (SDH) activity, an indicator of mitochondrial oxidative enzyme activity, is involved in the prevention of microangiopathy. Six-week-old male Goto-Kakizaki (GK) rats and age-matched male Wistar rats (control group (Con)) were used. GK rats were randomly assigned to nonexercise (DB) and exercise (DBEx) groups. The DBEx group was trained on a treadmill 5 times a week for 3 weeks. No significant differences in the capillary-to-fibre ratio or the capillary density were observed between the 3 groups. The luminal capillary diameter of the DB group was significantly lower than that of the Con group, whereas the capillary diameter of the DBEx group was significantly higher than that of the DB group. In addition, SDH activity was significantly higher in the DBEx group than in the Con and DB groups. Microangiopathy of skeletal muscles in type 2 diabetes was correlated with a decrease in the luminal capillary diameter, which was prevented by exercise training. Thus, the mitochondrial oxidative capacity appears to be involved in the overall mechanism by which exercise prevents microangiopathy.
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PMID:Exercise training prevents decrease in luminal capillary diameter of skeletal muscles in rats with type 2 diabetes. 2292 84