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

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

Insulin resistance with consecutive hyperinsulinemia is associated with dyslipidemia in individuals with metabolic syndrome or "syndrome x". This dyslipidemia is characterized by a hypertriglyceridemia and reduced levels of HDL-(high density lipoprotein)cholesterol in plasma. Table 1 summarizes the alterations of lipoproteins in insulin resistance. In severe forms of insulin resistance LDL-(low density lipoprotein)cholesterol can be elevated as well. The hypertriglyceridemia is caused by an elevated synthesis and secretion of VLDL (very low density lipoprotein) in the liver and by reduced metabolism, mediated e.g. by lipoprotein lipase. The alterations of VLDL-metabolism are associated with a reduced concentration of HDL-cholesterol. In addition the composition of lipoprotein particles can be altered, which might interfere with their normal metabolism. Furthermore addition direct effects of insulin on cellular cholesterol metabolism have been described. These alterations in lipid metabolism which are due to an insulin resistance and hyperinsulinemia might be related to the increased coronary risk which has been observed in patients with metabolic syndrome. Therefore the diagnostic approach in patients with hypertriglyceridemia should consider the possibility of an underlying glucose intolerance or Type 2 diabetes. Therapeutic aims and strategies are discussed. In accordance to guidelines of the American Heart Association the goals of lipid-lowering therapy take into account the prevalence of various cardiovascular risk factors in an individual patient (Table 2). Principle actions of lipid-lowering drugs on plasma lipids are outlined in Table 3. Table 4 summarizes the effect of antihypertensive drugs on plasma lipids and lipoproteins, which should be considered in the treatment of patients with dyslipidemia.
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PMID:[Disorders of lipid metabolism in insulin resistance]. 771 75

The relationship between overweight and cardiovascular disease was a matter of debate for many years. Recent studies have demonstrated that obesity defined as body mass index of 30 kg/m2 or higher is associated with an exponential increase of cardiovascular complications. This effect is largely mediated by the induction of established risk factors such as dyslipidemia, hypertension and type 2 diabetes mellitus. Recently, there is growing evidence that the occurrence of most complications of obesity depends not only on the degree of overweight but also on the pattern of body fat distribution. Many data suggest that the anatomical localization of body fat is more important for the risk of developing complications than the adipose tissue mass per se. An abdominal, upper-body type of fat distribution, which can be easily determined by the measurement of waist and hip circumferences (waist/hip ratio = WHR), is also a confirmed risk factor for metabolic disturbances, hypertension and atherosclerosis, independent of body weight. However, the clinical appearance of these disturbances is frequently associated with the development of obesity. This network of metabolic disorders and their vascular complications is termed "metabolic syndrome" or "syndrome X" (Table 2). Abdominal obesity is now known to be closely associated with the metabolic syndrome and is regarded to represent its readily recognizable phenotypic feature. The components of the metabolic syndrome are characterized by varying forms and degrees of insulin resistance. It is assumed that insulin resistance, defined as diminished biological response to the action of insulin, represents the primary defect or at least the common pathogenetic link between these disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Abdominal obesity and coronary heart disease. Pathophysiology and clinical significance]. 771 76

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

In the treatment of the metabolic syndrome which comprises the most serious risk factors of atherosclerosis education is a basic prerequisite of treatment and prevention of complications. In the submitted review the authors analyze basic procedures of education from the general aspect as well as in individual disorders and diseases which characterize the metabolic syndrome (dyslipoproteinaemia, obesity, diabetes mellitus and impaired glucose tolerance, hypertension). They emphasize that a comprehensive change of the patient's life style and the life style of his whole family is necessary. This cannot be achieved within a short time and therefore motivation of the patient as well as of the health professionals engaged in the educational work is essential.
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PMID:[Patient education in the metabolic syndrome]. 772 42

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

Members of Jehovah's Witnesses refuse blood transfusions and blood products under any circumstances. Because of an improvement in blood salvage techniques in our centre, they are not excluded from open-heart surgery. In recent years recombinant human erythropoietin (rhEPO) has been applied to correct perioperative anemia in these patients. METHODS. Seventeen members of Jehovah's Witnesses who were more than 18 years of age were operated on using various blood salvage technique, e.g., haemoseparation and a high dose of Aprotinin. We present the first three patients treated with 4 x 500 U of i.v. rhEPO/kg body wt. given within 11 days preoperatively. Thirteen of the patients operated on had elevated preoperative risk factors, for instance poor left ventricle, severe aortic valve stenosis, metabolic syndrome, age older than 70 years, etc. In other centres that perform cardiac operations on members of Jehovah's Witnesses, these risk factors represent contraindications for open-heart surgery in these patients. RESULTS. Patients with rhEPO treatment showed a preoperative hematocrit increase of 7 Vol.% within 10 days and no postoperative complications. At the 6th postoperative hour the hematocrit returned to the starting values; in patients without rhEPO, however, the hematocrit generally had not increased to preoperative values even by the 8th day after operation. In 9 patients with preoperative elevated risk factors and a postoperative relative decrease in hematocrit below 33% we observed an uncomplicated postoperative period. Four patients with these risk factors, a pronounced decrease in hematocrit and blood loss postoperatively had various severe complications. CONCLUSIONS. Preoperative treatment with a high dose of rhEPO to enhance the hematocrit and maturity by precursor red blood cells in patients with a hematocrit below 45 Vol.% is a possibility to compensate for the blood loss perioperatively and to avoid complications from a decrease in oxygen transport capacity. The anaemia and high blood loss postoperatively are the main causes for a slightly elevated operation risk in members of Jehovah's Witnesses in all heart centres that perform cardiac operations on these patients. Nevertheless, Jehovah's Witnesses should be not excluded from cardiac operations, since open-heart surgery without use of homologous blood is becoming a routine procedure.
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PMID:[Operations with a heart-lung machine in adult members of Jehovah's Witnesses]. 778 54

Type IIB muscle fibres are among the most insulin-insensitive muscle fibres and are not adapted to oxidation of fat during muscle work. The first characteristic of this type of muscle fibre most probably reflects or contributes to further development of insulin resistance contribute to further perpetuation of obesity and to the channeling of excess free fatty acids to the liver followed by secondary deterioration of its function. The impaired functioning of the liver is epitomized, among other changes, by impairment of insulin extraction. The increasing hyperinsulinaemia is followed by inhibition of synthesis of specific proteins such as carrier proteins for transporting testosterone (sex hormone binding globulin, SHBG). This results in an increased free testosterone concentration which induces androgenization in women and may further increase insulin insensitivity in abdominal obesity in women. The poor capillarization and changed muscle morphology in spite of great interindividual variety is observed in several pathological conditions characterised by insulin sensitivity (stroke, PCO, hypertension, diabetes, obesity). It is suggested that, in addition to the previous concept of the main role of intraabdominal adipose tissue, even muscles and liver are also important organs contributing to the pathogenesis and development of the metabolic syndrome.
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PMID:Role of muscle morphology in the development of insulin resistance and metabolic syndrome. 783 Dec 32


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