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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of insulin to stimulate glucose disposal by muscle varies widely within the population at large. Individuals with muscle insulin resistance develop type 2 diabetes if they cannot compensate for this defect by secreting large amounts of insulin. Although this philanthropic effort on the part of the pancreatic B-cell may prevent gross decompensation of glucose homeostasis, it renders such individuals at increased risk to develop a cluster of abnormalities (syndrome X) associated with coronary heart disease. Although the kidney is not considered to be an insulin sensitive tissue, two features of syndrome X, hyperuricemia and hypertension, are likely to be dependent on the retention of normal insulin action on the kidney. More specifically, there is evidence to support the hypothesis that elevated plasma insulin concentrations may enhance renal sodium retention and decrease urinary uric acid clearance. As such, it is possible that a normal kidney response to the compensatory hyperinsulinemia associated with insulin resistance in nondiabetic subjects contributes to the development of hyperuricemia and hypertension in such individuals.
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PMID:The kidney: an unwilling accomplice in syndrome X. 939 43

We demonstrated that the fructose-induced hypertensive rat, representative of the principal metabolic abnormalities found in a majority of hypertensive patients, i.e. hypertriglyceridemia, hyperinsulinemia and insulin resistance (Syndrome X), is associated with an impaired response to endothelium-dependent vasodilators and that fructose may directly contribute to this impairment. Twelve male Wistar rats were divided into two groups, one given 10% fructose (n=6); the other no fructose (n=6) for 40 days in the drinking water. Systolic blood pressure was measured via the tail cuff method. Perfusion pressure responses to acetylcholine, were measured in the isolated perfused mesenteric vascular bed. Constrictor or dilator responses were measured as increases or decreases, respectively, of the perfusion pressure at a constant flow (4 ml/min). Fructose-fed rats had significantly higher blood pressure, insulin and triglyceride levels than control animals. In phenylephrine constricted beds, the endothelium-dependent dilatation to acetylcholine (0.001 to 1 micromol) was attenuated in the fructose-fed group compared to control animals. Whether this abnormality results from the syndromes (hyperinsulinemia, hypertension and hypertriglyceridemia) associated with the fructose-fed animal model is unknown. We therefore hypothesized that fructose can impair the endothelium-dependent vasodilator response. This was evaluated by perfusing mesenteric arteries from normal rats with control mannitol (40 mM) or fructose (40 mM). Endothelium-dependent dilation to acetylcholine was impaired in fructose-perfused mesenteric arteries. Indomethacin restored the vasodilator response to acetylcholine, suggesting that a cyclooxygenase derivative mediates the impaired response. Thus, we conclude that fructose can contribute to the impaired endothelium-dependent response in the fructose-induced hypertensive rat model.
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PMID:Fructose perfusion in rat mesenteric arteries impairs endothelium-dependent vasodilation. 945 May 8

The term syndrome X has been applied to the association of hypertension, non-insulin-dependent diabetes mellitus (NIDDM), android obesity, insulin resistance, and dyslipidemia. In this paper, based on population samples from Tecumseh, Michigan, and Hiroshima, Japan, characterized by persons > or = 40 years of age, we examine the validity of regarding this constellation of traits as a true syndrome, i.e., an array of traits with a single, unifying pathophysiology underlying its components. Data were not available on insulin resistance and dyslipidemia, and obesity was expressed as body mass index (BMI) without the division into android and non-android types. The four ethnic-gender data sets were analyzed on the basis of two age classes, age > or = 40 years and age > or = 50 years, and two obesity classes, BMI > or = 27 and > or = 30. A simple chi 2 test of goodness-of-fit under a model of independence revealed non-random associations between hypertension, NIDDM, and BMI which were in part attributable to an excess of persons with all three traits. However, when the four data sets were subjected to separate log-linear analyses of the three-way association tables, none of the three-factor interaction terms (i.e., syndrome X) was significant. High significance was, however, observed in the two-factor interaction term for BMI*hypertension. It is concluded that the significant association between these three traits is driven by the BMI*hypertension interaction, and there is no evidence in these data sets of a significant role for a syndrome X. Genet.
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PMID:Syndrome X: is it for real? 952 8

Cardiovascular risk factors were compared between 126 people with non-insulin-dependent diabetes mellitus (NIDDM) and 530 non-diabetics (controls), in a random sample of people (Chinese, Malays, and Asian Indians) aged 40-69 years from the general population of Singapore. Data were adjusted for age and ethnicity. For both genders, people with NIDDM had higher mean body mass indices, waist-hip ratios and abdominal diameters. They also had a higher prevalence of hypertension, higher mean levels of fasting serum triglyceride, slightly lower mean levels of serum high-density-lipoprotein cholesterol, and higher mean levels of plasma plasminogen activator inhibitor-1 and tissue plasminogen activator (antigen). These factors are components of syndrome X (metabolic syndrome) and increase the risk of atherosclerosis and thrombosis. In contrast, there were no important differences for cigarette smoking, serum total and low-density-lipoprotein cholesterol, serum apolipoproteins A1 and B, plasma factor VIIc and plasma prothrombin fragment 1 + 2. Females with NIDDM, but not males, had a higher mean serum fibrinogen level than non-diabetics, which could explain why NIDDM has a greater cardiovascular effect in females than males. Serum lipoprotein(a) concentrations were lower in people with NIDDM. Mean levels of serum ferritin, a pro-oxidant, were higher in people with NIDDM than controls, but there were no important differences for plasma vitamins A, C and E, and serum selenium, which are anti-oxidants.
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PMID:Cardiovascular risk factors in non-insulin-dependent diabetics compared to non-diabetic controls: a population-based survey among Asians in Singapore. 954 28

Measurements of coronary flow reserve, once used only for research, have gained wide acceptance as an additional diagnostic approach in the decision-making process of diagnostic cardiac catheterization and coronary interventions. Apart from the noninvasive determination of coronary flow reserve, intracoronary Doppler flow wires have facilitated decision making in the catheterization laboratory. Different techniques, unstandardized procedures, and data from uncomparable patient populations have remained a confounding factor. This review examines current concepts of coronary flow reserve as well as methodologic considerations and pitfalls. Applications of coronary flow reserve for periinterventional assessment are evaluated on the background of practical guidance. According to a detailed examination of arterial structure and function, a normal coronary flow reserve exceeds a value of 3.0. Values below 3.0 suggest involvement of microvascular disease caused by functional or structural alterations. The influences of various factors such as age, hemodynamics, hypercholesterolemia, hypertrophy, hypertension, syndrome X, and coronary artery disease are discussed in relation to the effect on coronary flow reserve. From available information, measurements of coronary flow reserve are an adjunct to current interventional technology to optimize individual patient care. Further efforts should be undertaken to incorporate these new methods into our routine clinical decision making.
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PMID:Current concepts of coronary flow reserve for clinical decision making during cardiac catheterization. 966 31

The sympathoadrenal system plays an important role in the regulation of metabolic and cardiovascular activity. With respect to carbohydrate metabolism, specifically, catecholamines affect both insulin secretion and insulin action. Alterations in sympathoadrenal system function have been suggested to contribute to the constellation of disorders referred to as syndrome X (obesity, hypertension, NIDDM, and dyslipoproteinemia). The origin of any such abnormalities in sympathoadrenal function is unknown. The sympathoadrenal system, like other parts of the mammalian nervous system, is susceptible to environmental influences during development. Although these neurological alterations in rats are particularly prominent during the postpartum period, they are also apparent during intrauterine life. Moreover, the effects of these early environmental factors last well into adulthood and may represent permanent alterations in sympathetic nervous system behavior. Although the impact of maternal diabetes on sympathetic neural development has not been examined extensively, limited data available indicate that maternal diabetes may affect sympathetic nervous system development in the offspring. Although the full impact of maternal diabetes on neurological development in the offspring is unknown, given the myriad effects of the sympathoadrenal system on mammalian physiology, lasting changes in autonomic nervous system function may have potentially profound consequences for metabolic and cardiovascular regulation in adulthood.
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PMID:Effects of fetal and neonatal environment on sympathetic nervous system development. 970 44

Resistance to insulin-mediated glucose disposal has been postulated to predispose individuals to a cluster of associated abnormalities (Syndrome X) known to increase risk of cardiovascular disease (CVD). Although several abnormalities subsumed under the rubric of Syndrome X have been shown to predict CVD, there has been no prospective study evaluating the power of insulin resistance, the putative fundamental defect in the syndrome, in this context. Therefore, this study was initiated to evaluate the hypothesis that resistance to insulin-mediated glucose disposal would predict the development of CVD in healthy volunteers. To accomplish this goal, 147 normal, healthy, nonobese, volunteers were evaluated [4.7 +/- 0.1 yr (mean +/- SEM)] after baseline measurements of steady state plasma glucose concentration (an estimate of insulin-mediated glucose disposal), as well as other CVD risk factors. Clinical end points developed in 13 subjects during the follow-up period; hypertension in 5, coronary artery disease in 4, cerebrovascular accident in 3, and peripheral vascular disease in 1. There was a significant univariate relationship between SSPG and CVD (P < 0.002), with the majority of the events taking place in the tertile of subjects with the highest SSPG concentration, i.e. the greatest degree of insulin resistance. In contrast, no CVD events were observed in the tertile with the lowest SSPG concentrations; the most insulin sensitive. SSPG was also related significantly to diastolic blood pressure, triglyceride, and low-density lipoprotein and high-density lipoprotein cholesterol concentrations, and the glucose and insulin responses to oral glucose. All of these relationships were independent of age, gender, body mass index, estimates of physical activity, and smoking history. When SSPG was paired with each of the other variables in a series of multiple regression models, only SSPG, or insulin response, were independent predictors of CVD events. In conclusion, approximately one of every five healthy, nonobese subjects in the most insulin-resistant tertile, followed for approximately 5 yr, had a serious clinical event. These data highlight the importance of insulin resistance as a predictor of CVD.
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PMID:Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease. 970 45

During the past decade, the potential implications of insulin resistance were recognised by clinicians ranging from endocrinologists to cardiologists. Central to this expanding interest is Reaven's hypothesis that tissue resistance to the effects of insulin is a factor linking various metabolic disorders and coronary heart disease. This review critically describes the different approaches for the evaluation of insulin sensitivity in vivo. Qualities and limitations of several investigative techniques are discussed, such as anthropometric indexes, basal biological indexes, insulin suppression tests and insulin tolerance tests. The two most widely used methods for quantifying insulin sensitivity are the euglycaemic hyperinsulinaemic clamp and the intravenous glucose tolerance test with minimal model analysis. Insulin resistance occurs in many aetiologically diverse human disorders. Genetic syndromes with extreme insulin resistance are very uncommon. Insulin resistance is frequently associated with obesity, type 2 diabetes and essential hypertension. The insulin resistance syndrome called syndrome X includes impaired insulin-mediated glucose uptake, impaired glucose tolerance, hyperinsulinaemia, hypertension, dyslipidaemia and haemostatic disorders. Finally, the clinical significance of high values of insulin sensitivity is discussed.
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PMID:[In vivo evaluation of insulin sensitivity and clinical applications]. 975 76

Leptin levels in subjects with android obesity with the insulin resistance syndrome (syndrome X, 5H) are in general elevated, as compared with non-obese subjects and correlate with the BMI, with the percentage of body fat, WHR, IRI levels and sex (they are higher in women), as it is the case in the general population. In the elevated leptin level in syndrome 5H (association of hyperinsulinism, hyperglycaemia-NIDDM, hyperlipoproteinaemia with android obesity, arterial hypertension and hirsutism in females with the polycystic ovaries syndrome) participate in a significant way also elevated basal IRI and cortisol levels as well as an elevated postprandial IRI response during oGTT despite the fact that leptin and endothelin-1 levels do not rise significantly during oGTT despite hyperinsulinaemia. Leptin levels were however higher in men (liminally significant in women) with an hyperinsulinaemic response during oGTT, as compared with probands with a normal insulin response. Optimal insulin and glucocorticoid levels are the prerequisite for a rise of leptin because proadipocytes in vitro begin to produce leptin as soon as insulin is added to the medium and this effect is trebled, if cortisol is added. It appears that the insulin and leptin resistance in syndrome 5H are parallel phenomena which potentiate each other. Elevated insulin and cortisol levels maintain elevated leptin levels which in turn enhances the insulin resistance in muscles and at the same time has an impact on the IRI response to postprandial hyperglycaemia. In the background of this insulin and leptin resistance in the majority of subjects with the 5H syndrome there is apparently no actual molecular defect of the hormone and its receptors in target tissues but a possible defect in mechanisms of postreceptor transduction of the hormonal signal. In the hormonal resistance participate moreover also two general and non-specific mechanisms such as: 1. increased consumption or uptake of hormonal receptors by elevated levels of the appropriate hormone ("down regulation" phenomenon), 2. disorders of paracrine endothelial mechanisms of the vascular wall which determine via the control of the inflow in the regional microcirculation the availability of insulin, leptin and metabolic substrates to target tissues. Impaired vasodilatation reserves and the development of paradoxical vascular spasms in response to stimuli which normally cause vasodilatation (strain, administration of acetylcholine, histamine, ATP etc.) are constant, associated phenomena in hyperlipoproteinaemias, arterial hypertension and in type 2 diabetics. These phenomena are the syndrome of insulin resistance and syndrome 5H-X resp. Endothelin-1 levels assessed in the systemic circulation are however due to their short biological half-life and the paracrine action of endothelin-1 not sensitive markers of endothelial dysfunction in syndrome X.
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PMID:[Relation between levels of leptin, insulin and cortisol in persons with the 5H (X) syndrome]. 982 79

Death from myocardial infarction was a rare clinical entity at the beginning of this century, but with an ageing population it is poised to become the most common cause of death worldwide. Ample epidemiological evidence confirms the clinical impression that cardiovascular risk factors--hypertension, glucose intolerance, dyslipidaemia, obesity--tend to 'cluster' in individual patients. This metabolic syndrome, or 'Syndrome X', which is thought to be underpinned by decreased insulin sensitivity, was first described in 1966 by Camus and popularized by Reaven in 1988. The enthusiasm and interest generated have led to the elucidation of some details concerning the pathogenesis of insulin resistance and coronary artery disease but have done little to change treatments or outcomes. Meanwhile, a global epidemic of Type 2 diabetes mellitus is said to be on the horizon- and it has been calculated that by the year 2230, 100% of the adult United States population will be obese.
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PMID:The metabolic syndrome: overeating, inactivity, poor compliance or 'dud' advice? 982 66


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