Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological data reveal that hyperuricemia is a risk factor of atherosclerosis. The risk is possibly caused by a link between hyperuricemia and insulin resistance-related metabolic syndrome. Recently it has been proposed that a missense mutation (Trp64Arg) in the beta3-adrenergic receptor (beta3-AR) gene may contribute to the accumulation of multiple risk factors related to insulin resistance. The present study was undertaken to further clarify an association between the Trp64Arg mutation and the metabolic syndrome in 47 Japanese men with hyperuricemia, who are substantially at high risk of atherosclerosis. One patient (2%) had the homozygous mutation, 12 (26%) were heterozygous for the mutation, and 31 (72%) had no mutation found by the PCR-RFLP analysis. The Trp64Arg mutation was not related to past maximal body mass index (BMI), BMI and waist/hip ratio. The subjects with the heterozygous mutation showed a slightly higher incidence of impaired glucose tolerance and diabetes mellitus in the 75 g oral glucose challenge (67%), as compared with those without the mutation (39%). Serum insulin response at 60 min and the sum of serum insulin in the glucose challenge were greater in the former subjects than those in the latter subjects (P=0.041 and 0.076, respectively). An increase in serum lipoprotein(a) was also observed in the subjects with the heterozygous mutation, but the Trp64Arg mutation was not associated with other dyslipidemia, blood pressure or ischemic changes on the electrocardiogram. These results indicate that the heterozygous mutation of Trp64Arg in the beta3-AR gene partly contributes to the accumulation of multiple risk factors in male subjects with hyperuricemia. A larger prospective study is necessary to elucidate a possible role of the Trp64Arg mutation in atherosclerotic diseases in future.
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PMID:Contribution of a missense mutation (Trp64Arg) in beta3-adrenergic receptor gene to multiple risk factors in Japanese men with hyperuricemia. 1039 34

The purpose of this study was to test the hypothesis of a causal relationship between high insulin levels and the development of benign prostatic hyperplasia (BPH) and to determine the clinical, anthropometric, metabolic and insulin profile in men with fast-growing BPH compared with men with slow-growing BPH. The present study was designed as a risk factor analysis of BPH in which the estimated annual BPH growth rate was related to components of the metabolic syndrome. Two hundred and fifty patients referred to the Urological Section, Department of Surgery, Central Hospital, Varberg, Sweden, with lower urinary tract symptoms with or without manifestations of the metabolic syndrome were consecutively included. The prevalences of atherosclerotic disease manifestations, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained. Data on blood pressure, waist and hip measurement, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, total cholesterol, triglycerides, HDL and LDL cholesterol, uric acid, alanine aminotransferase (ALAT) and prostate-specific antigen (PSA). The prostate gland volume was determined using ultrasound. The median annual BPH growth rate was 1.04 ml/year. Men with fast-growing BPH had a higher prevalence of NIDDM (p = 0.023) and treated hypertension (p = 0.049). These patients were also taller (p=0.004) and more obese as measured by body weight (p<0.001), BMI (p=0.026), waist measurement (p <0.001), hip measurement (p = 0.006) and WHR (p=0.029). Moreover, they had elevated fasting plasma insulin levels (p = 0.018) and lower HDL cholesterol levels (p = 0.021) than men with slow-growing BPH. The annual BPH growth rate correlated positively with diastolic blood pressure (rs = 0.14; p = 0.009), BMI (rs = 0.24; p < 0.001) and four other expressions of obesity and fasting plasma insulin level (rs = 0.18; p = 0.008), and negatively with the HDL cholesterol level (rs = -0.22; p = 0.001). In conclusion, the data suggest that NIDDM, hypertension, tallness, obesity, high insulin and low HDL cholesterol levels constitute risk factors for the development of BPH. The results also suggest that BPH is a component of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinaemia, as patients with the metabolic syndrome. The findings support the hypothesis of a causal relationship between high insulin levels and the development of BPH, and give rise to a hypothesis of increased sympathetic nerve activity in men with BPH.
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PMID:Clinical, anthropometric, metabolic and insulin profile of men with fast annual growth rates of benign prostatic hyperplasia. 1041 80

There is increasing recognition that hypertension is only one facet of a metabolic syndrome that represents a cluster of risk factors including insulin resistance evident during long-term development of cardiovascular disease. The objectives of the present study were to evaluate glucose metabolism and insulin sensitivity in the Dahl genetic salt-sensitive rat model of hypertension and to find out whether there is a correlation between high blood pressure, salt sensitivity and insulin sensitivity. The experiments were performed in Wistar and Dahl salt-resistant (DSR) and salt-sensitive (DSS) rats given a normal or salt-loaded (2% NaCl in the drinking water) diet for 2 months. Glucose turnover, metabolic clearance of glucose and insulin sensitivity were determined using the euglycemic clamp technique in anesthetized animals. Four different concentrations of insulin were used (2.1, 4.2, 8.4 and 16.8 mg/kg/min) with results showing that there were no significant differences in serum glucose and insulin levels, glucose utilization and clearance and insulin sensitivity between Wistar and DSR; these groups remained normotensive throughout the 2-month experiment. However, DSS rats, even on a normal diet, developed hypertension by the end of the experiment and consistent with their hypertensive condition, significantly decreased glucose utilization and clearance and decreased insulin sensitivity were observed. The changes were more marked at higher insulin infusion rates (8.4 and 16.8 mg/kg/min). These results demonstrate that DSS rats with fully developed hypertension were insulin resistant. In contrast, DSR rats remained normotensive despite sodium loading. Sodium loading significantly exaggerated the hypertensive state of DSS rats but did not further increase insulin resistance. The results from respective weanling rats showed that even at this early stage before development of hypertension, DSS rats already had significantly increased serum insulin suggesting insulin resistance. In conclusion, the present results suggest that DSR genetically hypertensive rats were insulin resistant although insulin resistance was unrelated to high blood pressure or NaCl intake.
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PMID:Glucose metabolism and insulin sensitivity in Dahl hypertensive rats. 1044 35

Metabolic syndrome is a clustering of many insulin resistance-associated cardiovascular risk factors such as hypertension, hypertriglyceridaemia, low high-density lipoprotein (HDL) cholesterol, abnormal glucose metabolism and hyperinsulinaemia. Furthermore, it is known that obesity is the most common clinical state characterized by insulin resistance. Central adiposity, in particular, has been shown to be the most distinctive feature of this syndrome. Some studies have also suggested that obesity per se would be necessary for the expression of metabolic defects associated with centrally distributed fat. It has been presented that undernutrition in utero might 'programme' blood pressure, insulin resistance, blood coagulation and cholesterol metabolism and would thus have a role in the aetiology of cardiovascular disease and type 2 diabetes in adult life. Some studies have also found associations between low birthweight and metabolic syndrome in adulthood. However, criticism on this hypothesis of fetal programming has recently been presented. It has been suggested that the origins of adulthood risk of cardiovascular disease and type 2 diabetes can be related to somatic growth as a child, not necessarily to intrauterine growth. In westernized countries, the relative proportion of underweight newborn children is decreasing, and thus considering entire populations low birthweight has lost its theoretical role in the aetiology of type 2 diabetes and cardiovascular disease. On the other hand, as obesity is known to be increasing in the industrialized countries among all age groups, the association between weight gain in childhood and metabolic syndrome in adulthood is more than noteworthy. Instead of undernutrition during pregnancy, sedentary lifestyle and lack of physical exercise pose a new threat. This results in an increased occurrence of overweight in childhood, which may be the first sign of insulin resistance and future metabolic syndrome.
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PMID:Childhood weight and metabolic syndrome in adults. 1048 Jul 53

It has been increasingly recognised in recent years that type 2 (non-insulin-dependent) diabetes is part of a cluster of cardiovascular risk factors known as the metabolic syndrome, but also endorsed with such names as the deadly quartet, syndrome X and the insulin resistance syndrome. Atherosclerosis is the most common complication of type 2 diabetes among Europeans, and coronary artery, cerebrovascular and peripheral vascular disease are 2 to 5 times more common in people with this condition than in those without diabetes. These observations indicate that the treatment of type 2 diabetes requires agents that do more than simply lower blood glucose levels, and a therapy with both antihyperglycaemic effects and beneficial effects on dyslipidaemia, hypertension, obesity, hyperinsulinaemia and insulin resistance is likely to be most useful. In this respect, metformin has an important and established role: this drug has been shown to lower blood glucose and triglyceride levels, and to assist with weight reduction and to reduce hyperinsulinaemia and insulin resistance. Studies in the Israeli sand rat, Psammomys obesus, have indicated hyperinsulinaemia/insulin resistance to be the initial and underlying metabolic disorder in obesity and type 2 diabetes. Thus, the well established effect of metformin in reducing insulin resistance makes this drug an excellent candidate for the prevention of progression of impaired glucose tolerance to type 2 diabetes, and for the reduction of mortality associated with cardiovascular disease.
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PMID:Clinical efficacy of metformin against insulin resistance parameters: sinking the iceberg. 1057 21

The purpose of this study was to examine characteristics associated with the insulin metabolic syndrome, including insulin resistance, abnormal glucose tolerance, dyslipidemia, obesity, and elevated blood pressure, among women who have experienced gestational diabetes. 39 nondiabetic, young (20-42 years), postpartum (3-18 months) white women were recruited from obstetrical clinics. Twenty-one women had a history of gestational diabetes; 18 had uncomplicated pregnancies. Multivariate analyses revealed a significant difference between groups in insulin resistance (M, measured by euglycemic clamp) and insulin levels (from an oral glucose tolerance test), with insulin resistance showing a statistically stronger difference than insulin levels. Groups also differed significantly when compared on a set of variables associated with insulin metabolic syndrome: glucose tolerance, triglycerides, blood pressure, and body-mass index. Using insulin resistance as a covariate eliminated these group differences, suggesting that insulin resistance is the key factor underlying insulin metabolic syndrome. The higher risk of later developing type 2 diabetes and hypertension in women who have a history of gestational diabetes is explicable by their poorer profile on variables associated with insulin metabolic syndrome, and appears to be attributable to insulin resistance. Thus, insulin resistance appears to distinguish young women at risk for cardiovascular disease.
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PMID:History of gestational diabetes, insulin resistance and coronary risk. 1061 62

We examined the effects of the potassium channel opener KRN4884 (5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine ) on cardiovascular metabolic syndrome (i.e., syndrome X), in rats. High-fructose diet rats developed hypertension, hypertriglyceridemia, increased total cholesterol/HDL (high-density lipoprotein)-cholesterol ratio, and hyperinsulinemia, KRN4884 (0.3-3.0 mg/kg, twice a day for 14 days, p.o.) alleviated the risk factors in fructose-fed rats. Furthermore, fructose-fed rats exhibited impairment of glucose tolerance and excess insulin secretion when loaded with glucose orally. Treatment with KRN4884 (1.0 mg/kg, twice a day for 14 days, p.o.) improved the glucose intolerance and inhibited hypersecretion of insulin in the glucose-loaded, fructose-fed rats. In contrast, KRN4884 (0.3-1.0 mg/kg, twice a day for 10 days, p.o.) did not affect serum triglyceride, cholesterol, glucose, or insulin concentrations in normal rats. LPL (lipoprotein lipase) activities in skeletal muscle and adipose tissue, and HTGL (hepatic triglyceride lipase) activity in liver were measured after administration of KRN4884 or vehicle twice a day for 14 days in fructose-fed rats. KRN4884 caused a significant increase in LPL activity in muscle and tended to increase LPL activity in adipose tissue in fructose-fed rats. HTGL was decreased in fructose-fed rats as compared with normal controls and was unaffected by KRN4884. These findings suggested that KRN4884 enhances insulin sensitivity and LPL activity, which are related to glucose and lipid metabolism and may be useful for the treatment of syndrome X.
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PMID:Effects of the K+ channel opener KRN4884 on the cardiovascular metabolic syndrome model in rats. 1067 63

Serum mannose concentration increases in diabetic patients and correlates closely with blood glucose. In patients with glomerulonephritis, serum mannose and mannose/glucose ratio positively correlate with dyslipidemia and the extent of urinary protein excretion. We investigated whether changes in serum mannose mark subjects with features of metabolic syndrome, including obesity, hypertension, glucose intolerance, and dyslipidemia. The study comprised 20 patients with mean age of 68 (SD 11) years, body mass index 27.2 (SD 5.1) kg/m2, blood glucose 6.2 (SD 1.6) mmol/L, serum total cholesterol 6.3 (SD 1.2) mmol/L, triglyceride 2.0 (SD 0.08) mmol/L, uric acid 320 (SD 109) micromol/L, mannose 60.0 (SD 17) micromol/L, and mannose/glucose ratio 9.7 (SD 1.8) micromol/mmol. Serum mannose correlated with blood glucose (r=0.758, p=0.012), triglyceride (r=0.478, p=0.023), and HDL-cholesterol (r = approximately 0.427, p=0.022). Mannose/glucose ratio correlated with BMI (r=0.581, p=0.033), mannose (r=0.491, p=0.035), and uric acid (r=0.608, p=0.027). The rate of VLDL lipoprotein turnover may be instrumental in the regulation of serum mannose concentration. We conclude that an altered mannose metabolism is a novel consideration among the metabolic abnormalities in the metabolic syndrome.
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PMID:Metabolic syndrome is associated with changes in D-mannose metabolism. 1069 Oct 51

The association between both plasma viscosity and fibrinogen concentration with clustering of metabolic risk markers was examined within a cross-sectional study of employed middle-aged men. Analyses were performed on a subsample of 629 non-smokers (46.7+/-7.8 years) without diabetes. The effect of obesity and cardiorespiratory fitness on these haemorheological parameters and their association with the metabolic syndrome was also investigated. The cohort was grouped by the number of metabolic markers present. Metabolic markers included high-density lipoprotein-cholesterol (<1.13 mmol/l), triglycerides (> or =1.805 mmol/l), glucose (> or =5.5 mmol/l) and diastolic blood pressure (> or =90 mm Hg). The age-adjusted odds ratio for hyperviscosity (> or =1.67 mPa/s) was 2.08 [95% confidence interval (CI), 1.06-4.05; P = 0.031] for the subjects with the metabolic syndrome (three or more metabolic markers) when compared with those with no metabolic abnormalities. The comparable age-adjusted odds ratio for hyperfibrinogenaemia (> or = 3.47 g/l) was non-significantly higher at 1.69 (95% CI, 0.87-3.27; P = 0.119). The mean age-adjusted plasma viscosity level and the prevalence of hyperviscosity increased significantly from 1.629 to 1.692 mPa/s (P = 0.0005) and from 21.0 to 36.0% with accumulating metabolic markers (P = 0.006). Plasma viscosity and fibrinogen concentration both increased with higher quartiles of skinfolds (P = 0.003 and P = 0.01, respectively) following adjustment for age, lipids and leucocyte count. Plasma viscosity was also significantly lower with higher levels of predicted maximum oxygen consumption (VO2max) (P = 0.0005). The odds ratio for hyperviscosity in subjects with the metabolic syndrome as compared with those with no metabolic markers was attenuated following adjustment for age, sum of skinfolds and predicted maximum oxygen consumption (VO2max) (1.44; 95% CI, 0.72-2.90; P = 0.307). These cross-sectional results suggest that plasma viscosity is associated with increased clustering of metabolic markers in middle-aged men of high socio-economic status. Obesity and poor cardiorespiratory fitness may be important in the development of haemorheological abnormalities associated with the metabolic syndrome.
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PMID:Plasma viscosity, fibrinogen and the metabolic syndrome: effect of obesity and cardiorespiratory fitness. 1069 Nov 1

The severity of metabolic syndrome is usually determined according to static variables (blood glucose, insulin level, body mass index etc.) The most important classification is dynamic and prognostic classification which can be used to determine the ability to decrease elevated metabolite and hormone levels or to lose weight. Different mathematical approaches were used to determine these phenomena: 1. Mathematical modelling e.g. (Bergman minimal model or glycation model). 2. Predictive calculations using multiple regression (using static and dynamic parameters to determine weight loss in obesity treatment). 3. One day starvation test (finding very variable hormone and metabolic changes in obese patients). We can conclude There are 3 types of metabolic parameters: A. Static (basic) description, B. Functional (actual) description, C. Dynamic-stability describing variables. Mathematical modelling is a complicated method needing many blood samples. It is very invasive for patients and it is difficult to be repeated. Predictive importance can have also repeated measured metabolic data which are able to classify the stability (fixation) of metabolic state. Some basic parameters and simple dynamic tests like one day starvation test can be used in prognostic classification of patients who are able to change their fixed metabolic state.
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PMID:Classification of metabolic patients using dynamic variables. 1072 67


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