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 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The composition of the diet of the type II-diabetics should correspond to the principles of a lactovegetarian diet: relatively many carbohydrates, vegetables, fruits and little fat, in particular little animal fats. By such a pathogenetically orientated nutrition one is at the earliest able to treat successfully preventively and therapeutically the development of the arteriosclerosis which is connected with the type 2 diabetes and with metabolic syndrome. Thereby the weight reduction is of course integrated into such a dietary prescription. The number of meals a day should not routine-like be established to 5 to 6, and only in a bad metabolic condition the subdivision into many smaller meals is necessary. In the calculation of the food type 2 diabetics with overweight stabilised on diet alone should estimate the energy of food and reduce it. At this stage the calculation of carbohydrates is not necessary. Only when a blood sugar decreasing therapy is added (insulin and perhaps sulfonylureas) we have additionally to begin the calculation of carbohydrates. In order to obtain a useful compliance unnecessary reglementations must be removed so that only there where necessary a strict discipline is observed.
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PMID:[New knowledge of diet therapy of type 2 (non-insulin-dependent) diabetes]. 220 10

We have compared the capillary density and muscle fiber type of musculus vastus lateralis with in vivo insulin action determined by the euglycemic clamp (M value) in 23 Caucasians and 41 Pima Indian nondiabetic men. M value was significantly correlated with capillary density (r = 0.63; P less than or equal to 0.0001), percent type I fibers (r = 0.29; P less than 0.02), and percent type 2B fibers (r = -0.38; P less than 0.003). Fasting plasma glucose and insulin concentrations were significantly negatively correlated with capillary density (r = -0.46, P less than or equal to 0.0001; r = -0.47, P less than or equal to 0.0001, respectively). Waist circumference/thigh circumference ratio was correlated with percent type 1 fibers (r = -0.39; P less than 0.002). These results suggest that diffusion distance from capillary to muscle cells or some associated biochemical change, and fiber type, could play a role in determining in vivo insulin action. The association of muscle fiber type with body fat distribution may indicate that central obesity is only one aspect of a more generalized metabolic syndrome. The data may provide at least a partial explanation for the insulin resistance associated with obesity and for the altered kinetics of insulin action in the obese.
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PMID:Skeletal muscle capillary density and fiber type are possible determinants of in vivo insulin resistance in man. 330 99

To investigate the metabolic effects of medroxyprogesterone acetate, carbohydrate and lipid metabolism in women with polycystic ovary syndrome was evaluated before and after long-term therapy with this drug. The effects of suppression of pituitary gonadotropins and ovarian sex steroids were correlated with the response to an oral glucose load and with a serum lipid profile. Twenty of 25 women with polycystic ovary syndrome weighted more than 150% of their ideal body weight. None of the patients had fasting hyperglycemia. Fasting and peak serum insulin responses to glucose were abnormally high in most patients with polycystic ovary syndrome. Fasting serum insulin had a significant positive correlation with percent ideal body weight (r = .7, P less than .01). High density lipoprotein cholesterol was low in all patients studied, whereas total cholesterol and serum triglyceride levels were normal. Therapy with medroxyprogesterone acetate did not affect body weight, glucose tolerance, or serum lipids. The correlations between serum testosterone and high-density lipoprotein cholesterol or insulin levels were not significant (P greater than .1). The authors conclude that medroxyprogesterone acetate does not affect the metabolic syndrome of obesity, hyperinsulinemia, and decreased high-density lipoprotein cholesterol that is commonly seen in patients with polycystic ovary syndrome.
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PMID:Abnormalities of fuel metabolism in the polycystic ovary syndrome. 621 33

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

Albeit physical exercise and training have been recommended as an integral part of diabetes therapy only limited data are available to prove such beneficial effects of physical exertion in normalizing the metabolism in diabetes. It is the purpose of this review to critically summarize studies concerning the effects of physical training in maturity-onset diabetes. Based upon available evidence in animal experimentation, i.e. in normal and fat ZUCKER rats, as well as on data in non-diabetic man, physical training is expected to increase peripheral insulin sensitivity; thus a decrease of insulin requirements might be achieved in the course of a physical training program. So far, however, the preliminary evidence of only two studies on the effect of training in maturity-onset diabetes has been presented: slight improvements of glucose tolerance and a considerable, but--at least in one study--short-lived decrease of circulating insulin levels have been described. These improvements have to be weighed against the possible hazards of physical training programs in maturity-onset diabetic patients who--as a group--have to be considered at high coronary risk. More and more detailed and prolonged studies, however, are urgently needed to document and to prove beyond any doubt the benefits of physical training in the metabolic syndrome of maturity-onset diabetes mellitus.
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PMID:Physical training as a part of the therapy for adult-onset diabetes. 675 75

The effect of treadmill training on intravenous glucose tolerance and insulin sensitivity was investigated in Zucker rats (fafa). In 25-week-old fafa animals with the typical metabolic syndrome of massive obesity, glucose intolerance, hypertriglyceridaemia and insulin resistance, treadmill exercise of only very mild intensity was carried out for 6 weeks. The training programme induced a marked reduction in basal and post-glucose challenge plasma insulin levels and a slight but significant improvement of intravenous glucose tolerance. No alteration in insulin sensitivity of the isolated perfused hindquarter was demonstrable. In another study a 9-week training programme was started in 7-week-old fafa rats before the development of their metabolic syndrome. In the sedentary control animals glucose intolerance and insulin resistance developed during the study period; in the training group, both the deterioration of glucose tolerance and the decrease of insulin sensitivity were prevented. This study demonstrates in fafa rats that (a) in young animals physical training may prevent a genetically predisposed deterioration of glucose tolerance and insulin sensitivity and (b) in adult animals mild physical training may improve intravenous glucose tolerance and insulin sensitivity.
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PMID:Treadmill training improves intravenous glucose tolerance and insulin sensitivity in fatty Zucker rats. 704 3

A large segment of the population gradually develops insulin resistance, and the related metabolic syndrome is one of the most frequent causes of atherosclerosis. Searching for a practical indicator of insulin resistance, we studied the correlations between fasting serum insulin level, the general manifestations of insulin resistance syndrome, and various aspects of coronary artery disease in 797 men and 322 women. After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). We also noted a higher prevalence of hypertension, diabetes mellitus, and type IV hyperlipidemia. Significantly more women in the fourth than in the first quartile had angiographically documented significant stenosis of the coronary arteries (p = 0.0016, odds ratio 2.9, 95% confidence interval 1.5 to 5.6) and previous myocardial infarction (p = 0.0297, odds ratio 2.1, 95% confidence interval 1.1 to 4.1). Men in both the first and the fourth quartile had a more disturbed lipid profile and a higher prevalence of significant stenoses of coronary arteries and/or previous myocardial infarction than women; there was a tendency toward a lower prevalence of alcohol consumption (p = 0.0503), a higher prevalence of gout (p = 0.0634), and previous myocardial infarction (p = 0.0791) in men in the fourth than in the first quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fasting hyperinsulinism, insulin resistance syndrome, and coronary artery disease in men and women. 748 1

Epidemiological studies have revealed that elevated fibrinogen concentrations are associated with an increased risk of myocardial infarction, stroke, intermittent claudication, and cardiovascular mortality. The manner in which fibrinogen operates in atherogenesis has not yet been elucidated, but genetic control of fibrinogen levels is partially responsible. Fibrinogen frequently acts in concert with hyperlipidemia, diabetes, hypertension, physical inactivity, and age, variables that are influenced by insulin action. Because the offspring of hypertensive men tend to be hyperinsulinemic and insulin resistant from a young age, we hypothesized that their increased fibrinogen levels might reflect decreased insulin action and thus play a role in the metabolic syndrome. We chose 48 adult offspring (mean age, 38.4 years) of 30 fathers who had been treated for hypertension, and the former were matched by age, body mass index, sex, and smoking habits with 37 control subjects. Elevations in fibrinogen concentration (3.63 +/- 0.93 versus 2.87 +/- 0.54 g/L, P < .001) paralleled increases in blood glucose and insulin levels, estimates of insulin resistance, and blood pressure. In the offspring, in contrast to the control group, correlations between fibrinogen and metabolic-syndrome variables (ie, insulin, glucose, and waist and hip circumferences) were found. In stepwise multiple regression analyses, age and smoking habits were entered as variables in both study groups, but postload insulin and high-density lipoprotein cholesterol were entered as variables in the offspring group only. We propose that familial predisposition influences the relationship between insulin concentration and fibrinogen, an effect that may contribute to the clinical importance of the metabolic syndrome.
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PMID:Increased fibrinogen levels in the offspring of hypertensive men. Relation with hyperinsulinemia and the metabolic syndrome. 748 47

The relationship between insulin resistance and hyperinsulinaemia on one hand and hypertension on the other hand has become apparent during the last few years. Insulin resistance, which may be genetically determined, is, according to our present understanding, the 'key player' in the metabolic syndrome. However, the pathophysiology of the combination of factors has not yet been fully elucidated. Early therapeutic intervention for insulin resistance, hyperinsulinaemia and hypertension may prevent the clinical manifestation of non-insulin-dependent (type 2) diabetes. Preliminary results of an ongoing study investigating the effects of trandolapril or the diuretic combination of hydrochlorothiazide and triamterene on serum glucose and insulin levels are presented.
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PMID:Hypertension and insulin resistance. Glycaemia and insulinaemia in overweight hypertensive patients. 751 73

The metabolic syndrome is discussed in terms of insulin resistance linked to an increased regulation of metabolism by cortisol and fatty acids. This change in hormonal balance is associated with diabetes, android (visceral) obesity, hypertension, hypertriglyceridemia, hyperapobetalipoproteinemia and low concentrations of HDL; a cluster of risk-factors that predisposes to the development of premature atherosclerosis. It is proposed that the metabolic syndrome is accompanied by a derangement in the hypothalamic-pituitary-adrenal-axis such that the effects of cortisol are exaggerated relative to those of CRF. Excessive action of fatty acids and cortisol causes insulin resistance and increase the hepatic secretion of glucose and VLDL. Furthermore, cortisol can decrease the uptake of LDL by the liver. Cortisol in the presence of relatively high insulin concentrations can promote the deposition of energy and lead to obesity. Chronic treatment of rats with D-fenfluramine has been shown to decrease the release of cortisol and fatty acids in response to stress, and to improve insulin sensitivity. The effects of D-fenfluramine were also tested in male JCR:LA corpulent rats which are prone to develop atherosclerosis and myocardial lesions. D-fenfluramine improved insulin sensitivity, decreased the hypertriglyceridemia, and prevented the development of necrotic myocardial lesions caused by ischemia. The data presented demonstrates a link between excessive action of cortisol and fatty acids in predisposing to insulin resistance and the pathologies that are associated with the metabolic syndrome.
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PMID:Role of glucocorticoids and fatty acids in the impairment of lipid metabolism observed in the metabolic syndrome. 755 May 41


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