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

Croatian Endocrine Society and Croatian Academy of Medical Sciences organized Symposium on Hyperandrogenaemia on March 22nd, 1996. Different aspects of this syndrome were discussed: epidemiology, classification and clinical features, steroid biosynthesis in the adrenal gland and ovarium, the genetics of polycystic ovarian syndrome (PCOS), clinical significance of testosterone and dihydrotestosterone metabolism, androgen excess and metabolic syndrome (syndrome X), insulin disturbances in PCOS, increased risk for development of non insulin dependent diabetes mellitus, androgen effects on serum lipoproteins, insulin like growth factors and function of ovarium, Doppler parameters in PCOS, treatment of hyperandrogenaemia, skin changes in PCOS, tests for adrenal and ovarial function, arterial hypertension and hyperinsulinism. National Board of Hyperandrogenaemia has been elected.
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PMID:[National consensus on hyperandrogenemia]. 901 36

Noninsulin-dependent diabetes mellitus is a genetically determined form of diabetes, due to impaired insulin secretion by the B-cells as well as to insulin resistance of the peripheral tissues. According to the glucose toxicity theory hyperglycemia and hyperinsulinemia exist in a vicious circle. Therefore, it is a major therapeutical aim to put the B-cell to rest and improve insulin sensitivity by a strict control of fasting blood glucose and of postprandial hyperglycemia. Furthermore, associated abnormalities within the metabolic syndrome, such as hypertension, dyslipoproteinemia and hemostatic disorders should be corrected to avoid vessel complications. Therefore, it should be started with basic measures as body weight reduction, carbohydrate-rich and fat-poor diet and exercise. If these measures fail to achieve acceptable glycemic control, antihyperglycemic drugs (acarbose, metformin) are indicated, eventually in a combination with small doses of short-acting sulfonylureas. Further impairment of insulin secretion is the indication for sulfonylurea and/or insulin application. HbA1c of 7 to 7.5% should be the goal of antidiabetic therapy, also for patients in advanced age. The main criterion for the choice of antidiabetics is the present insulin secretion capacity. Simple indicators in this respect are changes of body weight, plasma triglycerides and C-Peptide after i.v. glucagon stimulation. Application of insulin in combination with other antidiabetics or in the form of intensified insulin therapy should not be too much postponed.
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PMID:[Rational therapy of Type II diabetes]. 903 69

The high prevalence of atherosclerotic (macrovascular) complications in diabetes (1.5-6x higher than in non-diabetics) stimulated evaluation of new pathogenetic findings which could have an impact on prevention. In type 1 diabetics the development of nephropathy is a factor hastening the development of macroangiopathy. In type 2 diabetics on whom attention is concentrated at the moment interaction of various metabolic deviations is involved which include changes of lipoproteins (drop of HDL, changes in the size and composition of LDL), insulin resistance and glycosylation of proteins. There is an enhanced tendency to lipoprotein oxidation (LDL) which promote the development of cholesterol rich plaques in the arterial walls. Their rupture may cause occlusion and ensuing risks for life. Possibilities of prevention are not adequately made use of. This is due to a tendency to underrate the serious character of type 2 diabetes and also the high percentage of diabetics where the disease was diagnosed late. The metabolic syndrome which develops as a result of insulin resistance precedes for years manifestations of diabetes. Its detection makes it possible to screen subjects at risk, some of whom develop diabetes. At the same time it is also a pathogenetic factor of macrovascular complications. It leads to the cumulation of a number of risk conditions. More effective prevention can be implemented by intervention of all associated risk factors (smoking, hypertension), in the application of lifestyle provisions of energy reduction by promoting physical activity and by a rational diet (diabetes, obesity, hyperlipidaemia). The justification of pharmacotherapy for the high risk groups of diabetics with hyperlipidaemia is supported by results of recently published investigations where statins were used. For the sub-population of subjects at risk the perspective should be screening of risk factors, early diagnosis of diabetes, education, continuous primary care, comprehensive prevention using lifestyle provisions as well as advances in modern pharmacotherapy.
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PMID:[Prevention of atherosclerosis in diabetics]. 944 Oct 11

Turner syndrome afflicts approximately 50 per 100,000 females and is characterized by retarded growth, gonadal dysgenesis, and infertility. Much attention has been focused on growth and growth promoting therapies, while less is known about the natural course of the syndrome, especially in adulthood. We undertook this study to assess the incidence of diseases relevant in the study of Turner syndrome. The study period was from January 1, 1984 to December 31, 1993, and the study base was all women living in Denmark during the study period. We used data from the Danish Cytogenetic Central Register and the Danish National Registry of Patients to assess morbidity. This study supports several earlier studies reporting increased morbidity and confirms results of a recent study on cancer in Turner syndrome. Women with Turner syndrome seem to have an increased incidence of fractures, osteoporotic fractures in adulthood, and non-osteoporotic fractures in childhood. Furthermore, diabetes mellitus, both NIDDM and IDDM, was found with a markedly increased incidence in Turner syndrome, as well as ischemic heart disease, hypertension, and stroke. The risk of cancer, except cancer of the large bowel, does not seem to be elevated in Turner syndrome. Our data suggest that patients with Turner syndrome are extraordinarily prone to abnormalities constituting the metabolic syndrome (e.g., hypertension, dyslipidaemia, NIDDM, obesity, hyperinsulinemia and hyperuricemia). The present data may help to explain the decreased life span found in patients with Turner syndrome.
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PMID:Morbidity in Turner syndrome. 947 75

According to the actual knowledge obesity is a serious, nutrition-dependent pathology with a high number of consequences. Endocrine sequence of obesity such as PCO-HAIR-syndrome (polycystic ovarian syndrome, hyperandrogenemia-insulin-resistance) with its cycle disorders and sterility are beginning already in adolescent and women of young reproductive age. With ageing more serious risks such as non-insulin dependent diabetes mellitus (NIDDM), arteriosclerosis followed by coronary disease, stroke and hypertension, metabolic syndrome and a higher prevalence of malignant diseases will appear. Based on these five risks obesity should be treated early when therapeutic strategies are more successful than in older ages. The definition of a diagnosis and the beginning of a weight reduction programme combined with intense motivating treatment as well as medical and psychotherapeutic guidance is an important preventive contribution.
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PMID:[Obesity--significance in adolescence and for reproduction]. 962 28

Recent studies in Europe, North America, and the developing world have shown that low birth weight and other indices of abnormal fetal growth in babies born at term are linked with a higher prevalence of glucose intolerance and NIDDM in adult life. Reduced fetal growth is also associated with a higher prevalence of the metabolic syndrome (in particular, hypertension and vascular disease) and with insulin resistance in adult life. Because birth size is determined largely by nongenetic factors, these findings have led to the "fetal origins" hypothesis, which proposes that fetal adaptations to an adverse intrauterine environment that reduces fetal growth program lifelong physiological changes. These changes in turn predispose to diabetes and the metabolic syndrome. The mechanisms are unknown, but evidence from animal studies and preliminary human evidence suggests that adverse events in early life may influence the neuroendocrine development of the fetus. This results in long-term alterations in the setpoint of several major hormonal axes, including an increase in adrenal glucocorticoid secretion. These hormonal alterations may contribute to the predisposition to diabetes and the metabolic syndrome in people who were small at birth.
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PMID:Birth weight and the future development of diabetes. A review of the evidence. 970 43

Impaired glucose tolerance (IGT) was standardized in 1979 by the National Diabetes Data Group and the World Health Organization as a risk factor for type 2 diabetes, replacing groups such as 'borderline' and 'chemical' diabetes. IGT was defined by a blood/plasma glucose value 2 h after a 75 g glucose load that was clearly abnormal but did not convey a risk of microangiopathy in those with non-diabetic fasting blood/plasma glucose levels. IGT is not uncommon, having a prevalence of 2-25% in adults. Determinants include age, obesity (total and central), family history of type 2 diabetes, physical inactivity and triglyceride levels. The main clinical significance of IGT is: (1) as a risk factor for type 2 diabetes, with 20-50% of individuals developing type 2 diabetes over 10 years; (2) as a risk factor for cardiovascular disease (CVD); and (3) as a component of the metabolic syndrome. IGT can be treated and this may prevent or delay progression to type 2 diabetes, though the effect of treatment on the risk of CVD is unknown.
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PMID:Impaired glucose tolerance: what are the clinical implications? 974 Apr 95

Death from myocardial infarction was a rare clinical entity at the beginning of this century, but with an ageing population it is poised to become the most common cause of death worldwide. Ample epidemiological evidence confirms the clinical impression that cardiovascular risk factors--hypertension, glucose intolerance, dyslipidaemia, obesity--tend to 'cluster' in individual patients. This metabolic syndrome, or 'Syndrome X', which is thought to be underpinned by decreased insulin sensitivity, was first described in 1966 by Camus and popularized by Reaven in 1988. The enthusiasm and interest generated have led to the elucidation of some details concerning the pathogenesis of insulin resistance and coronary artery disease but have done little to change treatments or outcomes. Meanwhile, a global epidemic of Type 2 diabetes mellitus is said to be on the horizon- and it has been calculated that by the year 2230, 100% of the adult United States population will be obese.
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PMID:The metabolic syndrome: overeating, inactivity, poor compliance or 'dud' advice? 982 66

Obesity is an essential risk factor for hypertension, coronary heart disease and stroke as well as for metabolic disturbances, especially for type 2 diabetes, hyper- and dyslipidemia, and it is responsible for the metabolic syndrome with insulin resistance and hyperinsulinemia. Disturbances in the lung function are also induced by obesity, as a higher risk for arthrosis on the lower extremities. Some oncological diseases like breast-, endometrial-, and prostatic cancer are associated with obesity. It is evident, that the fat distribution plays an important role in the development of obesity associated diseases: the accumulation of visceral fat has a higher risk as the peripheral fat, probably due to the different metabolism.
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PMID:[Obesity: entrance port to multimorbidity]. 988 99

The aim of the study was 1) to establish the prevalence of GAD antibodies (GADab) in a population-based study of type 2 diabetes in western Finland, 2) to genetically and phenotypically characterize this subgroup, and 3) to provide a definition for latent autoimmune diabetes in adults (LADA). The prevalence of GADab was 9.3% among 1,122 type 2 diabetic patients, 3.6% among 558 impaired glucose tolerance (IGT) subjects, and 4.4% among 383 nondiabetic control subjects. Islet antigen 2 antibodies (IA2ab) or islet cell antibodies were detected in only 0.5% of the GADab- patients. The GADab+ patients had lower fasting C-peptide concentrations (median [interquartile range]: 0.46 [0.45] vs. 0.62 [0.44] nmol/l, P = 0.0002) and lower insulin response to oral glucose compared with GADab- patients. With respect to features of the metabolic syndrome, the GADab+ patients had lower systolic (140 [29.1] vs. 148 [26.0] mmHg, P = 0.009) and diastolic (79.2 [17.6] vs. 81.0 [13.1] mmHg, P = 0.030) blood pressure values, as well as lower triglyceride concentrations (1.40 [1.18] vs. 1.75 [1.25] mmol/l, P = 0.003). GADab+ men had a lower waist-to-hip ratio compared with GADab- patients. Compared with GADab- patients and control subjects, the GADab+ patients had an increased frequency HLA-DQB1*0201/0302 (13 vs. 4%; P = 0.002) and other genotypes containing the *0302 allele (22 vs. 12%; P = 0.010). However, the frequency of these high-risk genotypes was significantly lower in GADab+ type 2 patients than in type 1 diabetes of young or adult onset (0201/0302 or 0302/X: 36 vs. 66 vs. 64%, P < 0.001). The GADab+ type 2 group did not differ from control subjects with respect to genotypes containing the protective DQB1-alleles *0602 or *0603, nor with respect to the type 1 high-risk genotype in the IDDM1 (Hph1 +/+). We conclude that GADab+ patients differ from both GADab- type 2 diabetic patients and type 1 diabetic patients with respect to beta-cell function, features of the metabolic syndrome, and type 1 diabetes susceptibility genes. Further, we propose that LADA be defined as GADab positivity (>5 relative units) in patients older than 35 years at onset of type 2 diabetes.
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PMID:Clinical and genetic characteristics of type 2 diabetes with and without GAD antibodies. 989 37


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