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

The therapy of gout is discussed taking into consideration the concomitant diseases occurring significantly frequently in patients with gout: Hypertension, uric acid-nephrolithiasis, hyperlipoproteinaemia, obesity, premature arteriosclerosis as well as diabetes mellitus. In contrast to other opinions the authors are of the opinion that the dietetic treatment is furthermore of essential importance. It is referred to the still allowed sufficiently great number in the supply of nourishment, in which cases, however, the limitations in the supply of calories, protein or purin bodies, respectively, lipid and carbohydrate do not remain unmentioned. The propositions for the medicamentous treatment essentially correspond to the central therapeutic recommendations. For the acute attack of gout, however, following to the international experiences, the colchicine therapy is more emphasized again. The medicamentous therapy of the asymptomatic hyperuricaemia is to be included into the considerations after full exhaustion of all dietetic and other possibilities in constant increase of the serum-uric acid-level more than 8 mg/dl.
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PMID:[Therapy of gout]. 33 84

A patient with obesity and diabetes mellitus had insulin secretion studies done during a 3-year cycle of weight loss and regain in the course of which she progressed from frank diabetes to a normal state of carbohydrate tolerance and then back to her original diabetic state. The results suggest that therapeutic weight reduction not only reverses insulin resistance but also restores beta cell sensitivity and enhances beta cell capacity. The eventual re-establishment of a degree of obesity, hyperinsulinemia, and carbohydrate intolerance virtually identical to that originally seen is compatible with a primary disorder involving hypothalamic control of adipose stores and insulin secretion.
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PMID:Insulin secretion in obesity and diabetes: an illustrative case. 33 68

Mutation diabetes in the mouse occurs in the C57BL/Ks strain. All homozygous animals (db/db) develop obesity, elevated blood sugar levels and increased or normal blood insulin concentration. The defects in cellular immunity in db/db mice and their littermate controls were examined both in vivo and in vitro. Significant suppression of delayed footpad swelling and first and second set skin allograft rejection time were observed. In addition, DNA synthesis in spleen cells after nonspecific mitogen stimulation was markedly inhibited. Diabetic animals with a mean blood sugar of 512 +/- 101 mg/100 ml did not respond to exogenous insulin therapy by lowering their blood sugar levels or reversing the defect in DNA synthesis. Adding insulin to spleen cell culture in vitro had no demonstrable effect on their response to mitogens. Thus, mutation diabetic mice with their known defect in the peripheral utilization of insulin have markedly suppressed cell-mediated immune mechanisms.
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PMID:Impairment of cell-mediated immunity in mutation diabetic mice (db/db). 34 1

The incidence of cardiovascular risk factors was studied in 83 renal transplant recipients: 84.3% showed at least one cardiovascular risk factor, hyperuricaemia was found in 42.2%, hypertension in 39.7%, hypercholesterolaemia in 31.3%, hypertriglyceridaemia in 27.7%, diabetes mellitus in 19.3%, obesity in 14% and nicotine abuse in 13.2% of the patients. Patients aged from 30 to 39 and 40 to 49 showed a mean incidence of 2.7 and 2.9, respectively out of the 7 investigated cardiovascular risk factors. The results demonstrate that renal transplant patients are a high-risk group for the development of degenerative cardiovascular diseases.
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PMID:[Frequency of cardiovascular risk factors in renal transplant patients (author's transl)]. 35 73

This paper reviews and discusses the evidence supporting the involvement of defective fibrinolysis in the pathogenesis of atherosclerosis, with emphasis on diabetes mellitus. According to the literature, defective fibrinolysis has been observed in association with virtually every major "risk factor" for coronary heart disease, including diabetes mellitus, hypercholesterolemia, hypertriglyceridemia, hypertension, obesity, cigarette smoking and lack of physical exercise. The interrelationships between disturbances in carbohydrate and fat metabolism and fibrinolysis are considered. Attention is drawn to the need for increased clinical attention to the potential role of defective fibrinolysis in atherogenesis, and periodic assessments of the fibrinolytic status are suggested as a promising approach toward early recognition of atherosclerotic tendency and risk. The judicious use of physiologic, dietary and pharmacologic means to correct defective fibrinolysis prophylactically and for the treatment of some forms of atherosclerosis is advocated.
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PMID:Fibrinolysis and risk factors of atherosclerotic disease, with special emphasis on diabetes mellitus. 35 70

Plasma insulin responses to a 4-hour glucose tolerance (100 g) were studied in urbanized Black people. Persons of normal weight without diabetes (12) and obese persons without diabetes (18) were compared with obese diabetics (19). Fasting serum ketone levels were measured, and the plasma potassium, triglyceride and growth hormone responses during the glucose tolerance test were determined. Obese subjects without diabetes had a twofold greater total plasma insulin response (area under curve) than their counterparts of normal weight, but there was a progressive fall in total plasma insulin response from subjects with mild diabetes (with fasting normoglycaemia) to those with severe diabetes (with fasting hyperglycaemia). The early plasma insulin responses of the group with mild diabetes were significantly impaired, and the peak response was only reached at 120 minutes. The subjects with severe diabetes had a flat insulin response curve. Fasting serum ketone levels were highest in the group with severe diabetes. The growth hormone responses were similar in all the groups. Plasma potassium and tryglyceride levels fell less during the glucose tolerance test in the group with severe diabetes than in the other three groups. These data indicate that insulin secretion is reduced in obese Blacks with chemical evidence of diabetes and this reduction becomes severe in the symptomatic diabetic.
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PMID:Hormonal and metabolic responses to an oral glucose load in obese Black diabetics. 35 29

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

The authors examined 48 patients with different endocrine pathology (relatives of patients with diabetes mellitus with a normal glucose tolerance test, patients with diabetes mellitus, obesity, thyrotoxicosis, and hypothyroidism) and a group of healthy persons. Blood glucagon concentration was determined radioimmunologically on fasting stomach and against the background of insulin hypoglycemia. A marked reduction of glucagon on fasting stomach was noted in patients with diabetes mellitus, and a reduction of the hormone concentration 30 and 60 min after the insulin injection. In obese patients and relatives of diabetic patients the initial blood glucagon level was not different from that in healthy persons. At the same time there was a significant reduction, and in relatives of diabetes patients also a retardation of glucagon secretion against the background of insulin hypoglycemia. The pattern of glucagon secretion in thyrotoxicosis and hypothyroidism proved to be changed.
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PMID:[Glucagon secretion in several endocrine diseases]. 36 65

The kinetics of unlabeled porcine insulin were studied in 69 nondiabetic male subjects aged 18-83 yr with obesity indexes of 0.93 - 1.51 and in 12 maturity-onset diabetics age 46-78 yr with obesity indexes of 0.95-1.56 by using the euglycemic clamp technique. Analysis of the insulin kinetic data by using a mathematical model permitted the determination, for each individual, of steady state distribution masses and degradation rate constants. The individuals were grouped to allow comparison of the results on the basis of age, obesity index, or diabetes. The responses over a period of 120 min to an infusion and wash out of insulin show some transient as well as steady state differences with age, obesity, or diabetes. Analysis of these data by use of compartmental models leads to the conclusion that in the steady state the ratio of insulin in extravascular spaces to that in plasma (T/P) is decreased in the moderately obese group (26%) and in the diabetic group (17%) but increased in the older group (13%) when each is compared with the appropriate control. Since extravascular insulin includes both insulin bound to receptors and insulin in the interstitial fluid, the observed changes in the extravascular to plasma mass ratio most likely reflect changes in in vivo binding to receptors, although the magnitude of the change would be modified somewhat by changes in the size of the interstitial spaces relative to plasma. In addition, the rate of entry of new insulin into plasma (BSDR) was increased in the diabetic population (45%; P less than 0.02) as well as in the moderately obese group (27%) but was decreased somewhat in the older group (11%). The following general conclusions can be drawn from the results: The pattern of parameter changes seen with obesity is similar to that seen with maturity-onset diabetes. The decrease in T/P seen with obesity and with maturity-onset diabetes cannot be accounted for solely by changes in fasting plasma insulin levels in these populations. The pattern of changes seen in the older subjects is opposite that seen in the maturity-onset diabetics, which suggests that diabetes is a perturbation distinct from the normal aging process. Finally, the changes in the metabolism of insulin are not large, making it unlikely that they are the sole cause of the major alterations in glucose tolerance seen with aging, obesity, or diabetes.
Diabetes 1979 Feb
PMID:Kinetics of native insulin in diabetic, obese, and aged men. 36 27

Obesity in the Zucker rat is accompanied by hyperlipemia, hyperinsulinism, insulin resistance, pancreatic hyperplasia, and islet hypertrophy. This study correlates the morphologic heterogeneity of isolated pancreatic islets with secretion of insulin and glucagon in the perifusion system. Islet size was arbitrarily defined as large (greater than 0.45 mm) or small (smaller than 0.12 mm). Protein content and volume (V = 4/3pir3) were calculated for groups and individual islets, respectively. Islets from obese rats secreted more insulin in response to glucose and aminophylline than islets from lean rats (peak 7.8 +/- 2.4 vs. 1.5 +/- 0.37 microU/islet/min, P less than 0.005). Insulin release was related directly to islet size and protein content. Small islets from lean and obese animals produced less insulin per islet than large islets (P less than 0.005). In terms of islet volume, however, large islets were inefficient insulin releasers as compared to small islets (P less than 0.005). Stimulation with Br-cAMP released glucagon from islets of lean but not from large islets of obese animals (peak 11 +/- 3.3 vs. 4.1 +/- 0.3 pg/microgram protein per minute, P less than 0.05). Arginine produced the same effect on glucagon release (P less than 0.05) as stimulation with Br-cAMP. The observed increased insulin release rates and the blunted glucagon response are related to islet size in the pancreas of the Zucker rat.
Diabetes 1979 Jun
PMID:Correlation between morphology and function in isolated islets of the Zucker rat. 37 79


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