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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An account is given of the present conception of asymptomatic (chemical) diabetes in the pediatric age group, which also has been named MODY (maturity-onset type of diabetes of young people). Long-term studies show that about 10% will eventually decompensate to overt diabetes. In contrast to classical juvenile-onset type of diabetes the inheritance of MODY seems to be autosomal dominant in many cases. Some authors have suggested that insulin resistance exists in non-obese patients with asymptomatic diabetes, but this view is not supported by observations of the author. Obese patients should reduce their body fat, but other therapeutic approaches are difficult to evaluate because of the normal fluctuation of the disease. There is no general agreement in the literature concerning the value of insulin treatment. The author supports the view that insulin treatment should be started in the late stages of chemical diabetes just before symptomatic disease emerges. In the long run this approach may ameliorate the condition due to the preservation of some beta-cell function for long periods. An unsettled question is whether early insulin treatment in asymptomatic diabetes will delay diabetic vascular complications.
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PMID:Asymptomatic diabetes in childhood and adolescence. A review. 35 15

Physical training is useful as a therapeutic means to obtain a decrease in body fat. The success in terms of lost fat is dependent on the ability to adhere to the programme, and probably also on regulatory factors associated with the degree of filling of adipose tissue (adipocyte volume). The rate of weight loss is usually slower than with dietary treatment but physical exercise may be more successful and less uncomfortable in the long run as a means to lose weight and prevent regaining it. Physical training is also effective against the metabolic complications associated with obesity such as decreased glucose tolerance, hyperinsulinemia and hypertriglyceridemia and should therefore be a method of choice to prevent or treat adult onset diabetes mellitus and endogenous hypertriglyceridemia in obesity. The feasibility of training in different groups of subjects seems to be dependent on, among other factors, selection of subjects and design of the training programme.
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PMID:Physical training in the treatment of obesity. 71 62

We investigated a family in which at least 4 men in 3 generations had a syndrome of obesity, mild mental retardation, delayed puberty, macroorchidism, acanthosis nigricans, hyperinsulinemia, and later overt insulin-resistant diabetes mellitus (non-insulin-dependent diabetes mellitus, NIDDM). The patients have markedly curly scalp hair, deficient face and body hair. Their teeth were healthy and normal in size and position. The clinical and biochemical findings and characteristics of the insulin receptors investigated in fibroblasts are reported. There was normal insulin binding to fibroblasts in the 2 brothers and their father. However, insulin-stimulated RNA synthesis was decreased as compared to that of normal control individuals. These findings suggest a postbinding defect of insulin action. The pedigree documents an autosomal dominant mode of inheritance. The diagnosis is of practical importance since it enables medical supervision of gene carriers in a preclinical state of atherosclerotic complications and overt diabetes. The findings in this family have relevance also to the explanation of familial mild mental retardation and to the study of different forms of insulin resistance due to a disturbance in biosignal transfer.
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PMID:Autosomal dominant insulin resistance syndrome due to postbinding defect. 128 80

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37

Insulin sensitivity of insulin dependent tissues (muscle, adipose tissue, liver) is subject to a variety of influences. Any change in insulin sensitivity is compensated in healthy subjects by a dynamic change in insulin secretion, which will decrease following a rise in insulin sensitivity and increase if insulin sensitivity is impaired (i.e. during insulin resistance induced by obesity, pregnancy, oral contraceptives, dehydration, saturated fatty acids, fever, drugs, etc.). In contrast to secondary insulin resistance idiopathic insulin resistance in type 2 diabetic individuals is associated with impaired insulin secretion, which thus is unable to overcome impaired insulin sensitivity. Idiopathic insulin resistance in type 2 diabetes is additionally characterized by reduced glucose storage, the basis of which may reside in an insulin receptor defect, in the presence of insulin receptor antibodies, in a postreceptor defect or in the synthesis of abnormal insulin molecules.
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PMID:[Insulin resistance]. 129 Mar 22

The purpose of this study was to determine the association of the prevalence of non-insulin-dependent diabetes (NIDDM) with central obesity, obesity, and family history of diabetes. This survey consisted of 1590 subjects (646 men, 944 women) aged 30 years or more from the Sun-Ming district of Kaoshiung city. Glucose tolerance status was ascertained by both medical history and a 75-g oral glucose tolerance test according to World Health Organization criteria. In men and women with central obesity (WHR > or = 0.92 in men and > or = 0.85 in women) or obesity (BMI > or = 27.6 kg/m2 in men and > or = 28.3 kg/m2 in women) (WHR: waist-hip ratio; BMI: body mass index), the prevalence of impaired glucose tolerance (IGT) and diabetes was significantly higher, except the prevalence of diabetes in both sexes with obesity and the prevalence of IGT in women with central obesity were not statistically different, as compared with nonobese subjects. The prevalence of diabetes in men significantly increased from the first quartile to the fourth quartile of BMI and the waist-hip ratio (WHR) (4.48% to 9.21% in BMI, 3.67% to 13.61% in WHR), while the prevalence in women also significantly increased from the first to fourth quartile (2.45% to 11.76% in BMI, 2.04% to 13.49% in WHR). Multiple logistic regression analyses revealed similar increase in the prevalence of diabetes among both men and women for every 1 kg/m2 increase in BMI and every 0.05 increase in WHR (1.07-fold and 1.09-fold in BMI, 1.34-fold and 1.32-fold in WHR, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of central obesity and obesity level on the prevalence of NIDDM and impaired glucose tolerance. 129 46

A primary goal of treatment in obese individuals with NIDDM is weight loss and maintenance. Obesity is a precipitating factor for the development of NIDDM in individuals who are genetically at risk. A variety of weight-loss regimens are available to match the specific needs and lifestyles of individuals. Hypocaloric high-fiber diets have been found to be effective in achieving weight loss, as well as aiding in glycemic and lipid control. Very low calorie diets, administered under medical supervision, are useful for obese NIDDM patients with 18-55 kilograms of weight to lose. Lifestyle education appears to be an important element of any successful weight loss program.
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PMID:Management of obesity in diabetes mellitus. 129 90

Socioeconomic development and changes in lifestyles have been accompanied by the emergence of diabetes as a major problem in Eastern Mediterranean countries, but reliable epidemiological data are still scarce and comparability is generally poor. For non-insulin-dependent diabetes (NIDDM) in adults, risk is higher in urban than in rural subjects, and in all populations prevalence increases with advancing age. Whereas several surveys have reported prevalence of the order of 5%, a recent national survey in Oman, which used the full WHO criteria for diagnosis, based upon the 2 hour blood glucose concentration after a 75 g oral glucose load in all subjects, reported a prevalence of diabetes of 10% in those aged 20 years and over. A further 8% of men and 13% of women had impaired glucose tolerance (IGT). Insulin-dependent diabetes (IDDM) was reported to be considerably rarer in Kuwait than in Europe and North America, but some more recent data suggest variability in frequency within the region. IDDM is frequently accompanied by ketoacidosis at diagnosis. For NIDDM, 75% of cases are associated with obesity. Long-term complications appear to occur to the same extent as in Western countries. A recent WHO Task Force meeting has set goals and targets for diabetes prevention and control within the Eastern Mediterranean Region.
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PMID:Diabetes in the eastern Mediterranean region. 129 77

In both humans and rodents the occurrence and severity of obesity-associated non-insulin dependent diabetes mellitus (NIDDM) may be influenced by both gonadal hormones and genetic background. Early gonadectomy (at 3-5 days of age) of female and male Wistar diabetic fatty (WDF) rats and of male Zucker rats allowed us to examine these effects in genetically obese rats carrying the fatty (fa) gene. Impairment of glucose tolerance and insulin sensitivity by obesity, and amelioration or exacerbation (in the case of female rats) of this impairment by gonadectomy were assessed by intragastric glucose tolerance tests when the rats reached adulthood. Both glucose tolerance and insulin sensitivity were significantly deranged in obese WDF rats of both sexes and in obese male Zucker rats compared to lean controls of the same sex and strain. Obese male WDF rats were less glucose tolerant and insulin sensitive than were obese male Zucker rats. Glucose intolerance was not ameliorated by castration in lean or obese male WDF or Zucker rats. Insulin sensitivity was significantly improved by castration in obese male rats of both strains, as fasting plasma insulin levels and total areas under the insulin curves were significantly reduced compared to obese sham-operated controls. This effect was greater in the Zucker than in the WDF male rats. Castration significantly decreased the insulin response areas in obese male Zucker rats, but did not alter those of the obese male WDF rats. Ovariectomy did not alter glucose homeostasis of obese female WDF rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of gonadectomy on glucose tolerance of genetically obese (fa/fa) rats: influence of sex and genetic background. 131 24

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6


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