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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A large body of evidence has been accumulating that insulin plays a role in coronary heart disease (CHD). Hyperinsulinemia has been considered a risk factor for CHD according to prospective studies. Cross-sectional studies found an association between hyperinsulinemia and prevalence of CHD, while population studies have shown that populations at increased risk for CHD are hyperinsulinemic. Strong relations between hyperinsulinemia and atherosclerotic coronary lesions have been demonstrated by angiographic studies. It has recently been observed that also patients with microvascular angina are hyperinsulinemic. Several mechanisms have been proposed to explain the role of hyperinsulinemia in the development of atherothrombosis. Hyperinsulinemia is the consequence of insulin resistance, a defect in insulin-mediated glucose uptake. Experimental evidence suggests that insulin has actions that may promote atherosclerosis, which clinical studies suggest the existence of a metabolic syndrome characterized by the presence of major coronary risk factors in which insulin resistance is the common link.
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PMID:[Hyperinsulinemia and cardiovascular risk]. 763 61

The study was undertaken to evaluate the development and association of parameters related to the metabolic syndrome during celiprolol treatment. Hyperinsulinemic euglycemic clamp and independent oral glucose tolerance tests (OGTT) were performed on 25 nondiabetic patients with controlled hypertension and dyslipidemia. The tests were carried out during the patients' previous antihypertensive monotherapy (beta- or Ca-blocker, or an ACE inhibitor), and after 6 and 12 months of celiprolol treatment. About one third of patients were randomized to a control group in which treatment was kept unchanged. Insulin sensitivity index (ISI), measured by the euglycemic clamp test, increased 35% in the celiprolol group at 6 months and remained at that level at 12 months, independent of the previous treatment (p = 0.03, compared to the change in the control group). During a 2 hour OGTT, incremental glucose area under the curve (AUC) decreased from 4.5 to 1.9 hr x mmol/l during 6 months of celiprolol treatment, and decreased further to 1.5 hr x mmol/l at 12 months (p < 0.001). Insulin AUC decreased from 113 to 72 hr x mU/l, and decreased further to 68 hr x mU/l (p < 0.01). All insulin parameters in OGTT were highly significant (p < 0.0001) and inversely associated with ISI. Insulin AUC had the best linear correlation with ISI (r = -0.682, p < 0.0001). Glucose parameters in OGTT correlated only weakly and inversely with insulin sensitivity. From the fasting serum lipids, triglycerides showed an inverse (p < 0.001) and HDL a weak (p < 0.05) positive association with ISI. Four out of 20 metabolic, clinical, and demographic parameters proved to be independently significant predictors for ISI in multiple regression analysis. These were insulin AUC, fasting insulin levels, triglyceride values, and age. The coefficient of determination in this four-parameter linear model was 69%. In this preliminary, observer-masked trial with a limited control group, celiprolol improved the impaired insulin sensitivity and glucose tolerance of dyslipidemic hypertensive patients. A fairly predictive model can be formulated to evaluate the peripheral insulin sensitivity of hypertensive patients with suspected metabolic syndrome using OGTT with serum insulin determinations.
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PMID:Association between serum lipids, glucose tolerance, and insulin sensitivity during 12 months of celiprolol treatment. 766 96

The metabolic syndrome usually goes along with abdominal obesity: diabetes type II, hypertension, dyslipidemia, and gout are often associated. The common characteristic is the resistance to insulin action. Reasons for the metabolic syndrome are--besides a genetic determination--overnutrition, physical inactivity, and alcohol consumption. Therefore, a causal therapy aims at the elimination of these factors. Consequently, the non-pharmacological therapy of the metabolic syndrome should be emphasized. The most important treatment is the reduction of body weight in the presence of obesity which is relevant for almost 90% of the patients. Body weight can rapidly be diminished by hypocaloric diets. Both, conventional reducing diets or formula diets may be used for weight reduction. Total fasting should not be performed for several reasons. For minor weight reduction or weight maintenance following a period of rapid weight loss with a hypocaloric diet, increased physical activity also lowers weight or prevents relapsing. Aims of therapeutical procedures are the elimination or amelioration of insulin resistance and subsequently the diseases of the metabolic syndrome. Both methods, reducing diet and physical training, act on various factors related to insulin resistance. For example, hypocaloric diets activate thyroxine kinase of the insulin receptor and reduce glucose and insulin in plasma. Physical training reduces not only insulin and glucose in plasma but also free fatty acids in addition and increases capillary density in skeletal muscle. Using the glucose clamp technique, diets and training are equally effective in improving glucose metabolism. Compared to these non-pharmacological methods drugs are less convincing. Since the non-pharmacological treatment implies behavioral changes with regard to nutrition, physical activity and alcohol consumption, simple instructions are not sufficient. Usually long-lasting changes in life style are necessary in order to achieve health improvement. Therefore, health care programs on individual or social basis are required in order to improve nutrition and increase physical activity. However, long-acting effects are difficult to achieve in adults; more promising is the prevention of insulin resistance.
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PMID:[Non-pharmacological therapy of metabolic syndrome]. 771 78

The author summarizes mechanisms by which insulin resistance and compensatory hyperinsulinism are manifested in the clinical picture. He divides the mechanisms into prereceptor, receptor and postreceptor mechanisms. The latter dominate in the population quantitatively and thus also by their impact because they create the so-called 5H syndrome (association of hyperinsulinism with hyperglycaemia (NIDDM), hyperlipoproteinaemia, hypertension, hirsutism and the polycystic ovary syndrome) or the so-called hormonal metabolic syndrome X, lethal tetrad, metabolic syndrome, syndrome of insulin resistance). The term syndrome X does not appear suitable as it is frequently mistaken for coronary X syndrome which probably is also conditioned by hyperinsulinism, for the hormonal metabolic X syndrome and probably also fot the "fragile X syndrome" in genetics. The 5H syndrome is caused by a postreceptor disorder of insulin efficiency for which so far the molecular basis and dominating organ site have not yet been defined adequately. Hyperinsulinism is conceived as an insulin resistance compensating phenomenon. In its development participates, however, in addition to compensatory hypersecretion also impaired insulin utilization (liver, muscles) and an impaired primary secretory response caused probably by a disorder of blood sugar control (glucokinase, GLUT 2). This is suggested by the frequently inadequate response of the blood sugar level, IRI and C-peptide during the oral glucose tolerance test (OGGT). A hyperinsulinaemic response may be encountered when the blood sugar curve is normal, flat, in impaired glucose tolerance and in diabetes. Thus OGGT alone is not suited for the early detection of the 5H syndrome unless concurrently the IRI and C-peptide response is recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical manifestations of the insulin resistance syndrome. The hormonal-metabolic syndrome X, the 5H syndrome and their etiopathogenesis]. 772 46

Obesity is a remarkable heterogeneous condition as shown by the variety of metabolic complications encountered. Imaging techniques with computed tomography have made it possible to quantify adipose tissue deposited within the abdominal cavity (visceral fat) which has been found to be correlated with serum glucose, insulin and lipid levels. Individuals with excessive visceral fat have hypertriglyceridaemia, high apolipoprotein B levels and hypoalphalipoproteinaemia. Several genes could modulate the degree of dyslipidaemia in patients with excessive visceral fat. Consequently, these patients should be managed as a genetically identifiable subgroup at risk of developing metabolic complications of obesity. It would also be justified to focus treatment on mobilizing visceral fat and improving the metabolic syndrome rather than simply on weight loss, an often unrealistic and clinically unjustified objective.
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PMID:[Grouping of risk factors for cardiovascular diseases in visceral obesity. Therapeutic implications]. 775 34

Despite recent progress in therapy and management of diabetes mellitus, diabetes remains a serious disease with life-threatening complications. It is by far the most common metabolic disease and affects 5% of the population in industrialized countries. Noninsulin-dependent diabetes mellitus (NIDDM) is a complex disorder characterized by insulin resistance and impaired insulin secretion and is associated with an increased risk of coronary heart disease, peripheral vascular disease, arterial hypertension and dyslipidemia. Predisposing factors for NIDDM are obesity and a family history of diabetes. Greater physical activity has been associated inversely with the prevalence of NIDDM in several cross-sectional studies. Physical activity increases the sensitivity to insulin, and regular endurance exercise can induce and maintain weight loss, improve glucose tolerance and ameliorate most of the abnormalities in the metabolic syndrome. Type I diabetes mellitus arises as a consequence of immunologically mediated pancreatic islet beta-cell destruction in genetically susceptible individuals. It is an insidious process that may occur over years. During the stage of disease evolution (prediabetes), individuals may be identified by the presence of immunological markers and a decline of beta-cell function. The autoimmune nature of the disease process has led to attempts to stop this process by immune intervention strategies. A variety of immune interventions has been used, some immunosuppressive and some immunomodulatory. Several screening programs are used in order to identify high-risk subjects (i.e. first-degree relatives of individuals with type I diabetes) who may benefit from an early intervention. The ultimate goal of all these efforts is to prevent the development of overt type I diabetes mellitus in those at risk for the disease, using strategies that are both safe and specific. This review summarizes the results of the various studies conducted to date and outlines the approaches currently being tested.
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PMID:[Is prevention of diabetes mellitus possible?]. 783 27

About 3 decades ago insulin resistance has been described as the pathogenetic factor leading from abnormal fat metabolism to diabetes mellitus. Within the metabolic syndrome insulin resistance is related to the upper body (android) type of obesity, hypertriglyceridaemia, hypertension, and diabetes mellitus ("deadly quartet"). It precedes the development of arterial hypertension and the metabolic disorders. The pathomechanisms leading from obesity and hypertriglyceridaemia to insulin resistance may be described by the glucose fatty acid cycle of Randle et al. According to their metabolic scheme increased supply of fatty acids results in reduced glucose oxidation. Concomittantly hepatic glucose production is increased. On the other hand insulin resistance combined with hyperinsulinaemia may lead to an elevation of VLDL-triglycerides and to a decrease of HDL-cholesterol in blood, thus creating a vicious cycle, in which elevated VLDL-triglycerides reinforce insulin resistance via the glucose fatty acid cycle. Interventions to improve insulin sensitivity and thereby lower plasma insulin should reduce obesity and hypertriglyceridaemia by dietary treatment. They usually improve promptly diabetic metabolism. New developments in pharmacological inhibition of fatty acid oxidation are discussed.
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PMID:[Lipid metabolism and insulin resistance--clinical aspects and pathobiochemistry]. 784 95

We investigated the association between fasting insulin concentration--an indicator of insulin resistance in nondiabetic individuals--cardiovascular risk factors, and coronary heart disease in a study of 390 men in the town of Zutphen. In 1990, an extensive examination was carried out on the participating men (aged 70 to 89 years). Fasting insulin levels were determined and a number of other risk factors measured. Known and newly diagnosed diabetics were excluded from the data analyses. Fasting insulin concentration was significantly associated with levels of glucose, triglycerides, uric acid, serum albumin, creatinine, and fibrinogen as well as resting heart rate. Inverse associations with high-density lipoprotein cholesterol and factor VII activity were observed. These results were independent of confounding factors such as age, body mass index, ratio of subscapular to triceps skinfold thicknesses, cigarette smoking, physical activity, and alcohol consumption. Men with a fasting insulin level higher than 80 pmol/L (highest quartile of the distribution) had a significantly higher prevalence of coronary heart disease and especially of myocardial infarction. This result was independent of potential confounding variables as well as of possible intermediates (total and high-density lipoprotein cholesterol, hypertension, serum triglycerides, fasting glucose, and other risk factors related to fasting insulin) (odds ratio, 2.2; 95% confidence interval, 1.2-4.0). No association between fasting insulin level and hypertension or blood pressure was observed. These results show that fasting insulin is an important indicator of coronary heart disease in elderly men. Clotting factors, resting heart rate, uric acid, serum albumin, and creatinine may also play a role in this metabolic syndrome.
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PMID:Hyperinsulinemia, risk factors, and coronary heart disease. The Zutphen Elderly Study. 791 15

Microalbuminuria is defined in principle as abnormally increased albumin excretion below the level that is characteristic for proteinuria. In diabetes, microalbuminuria is defined as having an excretion rate of 20 to 200 micrograms/min. This level of albuminuria predicts overt renal disease in both non-insulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus patients, and it is also associated with increased mortality. In nondiabetic individuals, the albumin excretion rate is not normally distributed with a skewed upper distribution. Excretion rate is lower during daytime, even during rest, than overnight. The median values in several studies for daytime and overnight albumin excretion rates are approximately 4 and 3 micrograms/min, respectively, with the upper 90th percentile approximately 15 and 10 micrograms/min, respectively. Microalbuminuria in population studies is significantly, but weakly, correlated to blood pressure, triglycerides, and low high-density lipoprotein cholesterol, as well as plasma glucose and obesity. These parameters are elements of the so-called metabolic syndrome. New studies in insulin-dependent diabetes mellitus on the transition from normo- to microalbuminuria show that high normal excretion rate and poor metabolic control are associated with progression. In non-insulin-dependent diabetes mellitus, microalbuminuria is quite common (20% to 25% of patients) in both newly diagnosed patients and patients with established diabetes. In many studies, a prevalence of approximately 20% is found, and again microalbuminuria is associated with components of the metabolic syndrome, which includes poor metabolic control and blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of microalbuminuria in diabetes and in the background population. 792 49


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