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

The aim of this study was to determine noninvasive predictive factors of significant liver fibrosis in patients with increased serum aminotransferases associated with features of metabolic syndrome (abdominal obesity, systemic hypertension, fasting hyperglycemia, and dyslipidemia). One hundred seventy-three patients were prospectively examined, regardless of alcohol consumption. Biometric, metabolic, and hepatic biochemical variables were tested for association with fibrosis assessed on liver biopsy according to the Metavir score system. Significant fibrosis, defined as Metavir scores F2, F3, or F4, was observed in 42 of 173 patients (24%). A logistic regression model and receiver operating characteristic curve were used to construct a simple index predictive of significant fibrosis. None of the patients with serum hyaluronate levels of 35 microg/L or less had significant fibrosis. In patients with serum hyaluronate levels >35 microg/L, no case of fibrosis stage F3 or F4 was found when serum carbohydrate-deficient transferrin/transferrin ratio was less than 0.9. In conclusion, in patients with increased serum aminotransferases associated with features of metabolic syndrome, a simple algorithm, including serum hyaluronate and serum carbohydrate-deficient transferrin/transferrin ratio, allows the exclusion of clinically relevant hepatic fibrosis, regardless of current or past alcohol consumption.
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PMID:Prediction of liver fibrosis in patients with features of the metabolic syndrome regardless of alcohol consumption. 1644 Mar 40

We evaluated various anthropometric indices(BMI, waist circumference, and waist-to-height ratio[W/Ht]) to find a simple method for assessing the risk of metabolic syndrome during routine health checkups. W/Ht correlated more closely than any other index to the sum of 4 or 5 coronary risk factors(hypertension, hyperglycemia, hypertriglyceridemia, and low HDL cholesterol; or these four combined with hypercholesterolemia). W/Ht index(> or = 0.5) was capable of identifying approximately all overweight individuals, and also identified more individuals of normal weight as at risk than any other measure of central fat distribution. Even normal-weight subjects with W/Ht > or = 0.5 demonstrated significantly higher risk for clustering of > or = 2 coronary risk factors, other metabolic risks, and a sedentary history than those with W/Ht < 0.5.
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PMID:[A simple and practical index for assessing the risk of metabolic syndrome during routine health checkups]. 1520 55

The common clustering of glucose intolerance, insulin resistance, abdominal adiposity, elevated blood pressure, and low HDL cholesterol is referred to as metabolic syndrome. Individuals with this syndrome have an increased risk of developing cardiovascular disease (CVD). The World Health Organisation and the National Cholesterol Education Programme's Adult Treatment Panel III (NCEP-ATP III) have outlined specific diagnostic criteria for the diagnosis of the metabolic syndrome to help in the identification of this syndrome in clinical practice. While the WHO criteria were specifically developed for use in research, the NCEP criteria are useful in clinical diagnosis of the metabolic syndrome. The metabolic syndrome is amenable to lifestyle modifications such as increased physical activity, weight loss, and possibly intake of low-glycemic foods. Drug therapy may be used to treat individual components of the syndrome such as elevated blood pressure and dyslipidemia. To control elevated glucose levels (when there is failure of lifestyle modification), medications such as metformin, thiazolidinedione derivatives and alpha glucosidase inhibitors may be used.
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PMID:The metabolic syndrome: an emerging risk state for cardiovascular disease. 1523 Apr 89

The metabolic syndrome is a cluster of risk factors for coronary heart disease that seemingly have an underlying metabolic causation. Central obesity is the centerpiece of the metabolic alterations. Accordingly, increased abdominal adiposity contributes to dyslipidemia, hyperglycemia, and hypertension. In about 20% of the cases with metabolic syndrome, there is also beta-cell dysfunction that leads to the clinical manifestation of diabetes mellitus. Recent evidence suggests that increased obesity is also associated with inflammation. The role of adipose tissue in the causation of metabolic alterations that lead to the clinical manifestation of the metabolic syndrome has become a focus of active research. Adipose tissue not only secretes non-esterified fatty acids that contribute to atherogenic dyslipidemia, steatosis and lipotoxicity. This organ is also an active endocrine and paracrine system. It can secrete pro-inflammatory factors, pro-insulin resistance factors, and other cytokines and hormones that can contribute to hypertension and impaired fibrinolysis. Therefore, the metabolic alterations commonly associated with increased central obesity of the metabolic syndrome are pro-atherogenic partly because the metabolites are proinflammatory.
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PMID:Obesity and the metabolic syndrome. 1525 55

Epidemiological associations are now well-established between insulin resistance, the metabolic syndrome and worsened cardiovascular outcomes. A direct role of insulin in vascular biology is also now broadly recognized. Specifically, insulin can directly stimulate the action of nitric oxide synthase, an effect that can be demonstrated both in vitro and in vivo. Insulin resistance, whether present endogenously or produced experimentally through exposure to fatty acids, glucosamine or tumour necrosis factor alpha, is associated with impaired endothelium-dependent vasodilation and, specifically, with impaired insulin-stimulated vasodilation. A number of potential molecular explanations for these observations are being pursued, with evidence to support a number of concurrent pathogenic mechanisms. These include insulin resistance-associated reductions in nitric oxide availability due to increases in oxidative stress (not requiring the presence of hyperglycemia), reduced availability of tetrahydrobiopterin and excess levels of asymmetrical dimethylarginine. A strong body of evidence also supports an excess of the vasoconstrictor endothelin, which may result directly from hyperinsulinemia and/or indirectly due to a loss of the suppressive effects of nitric oxide on endothelin production and action. The current leading edge of investigations into the association between insulin-resistant states and vascular dysfunction involves the expanding repertoire of adipocyte-derived hormones. Of these, particular interest has been focused on adiponectin, which has both vascular and metabolic actions, and may contribute importantly to the connection between metabolism and vascular function. Progress along these novel lines of investigation will continue to expand the understanding of the mechanisms linking insulin resistance, the metabolic syndrome and vascular disease.
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PMID:Insulin resistance, metabolic syndrome and vascular diseases: update on mechanistic linkages. 1530 8

Zucker diabetic fat (ZDF) rats with the metabolic syndrome and hyperlipidemia develop focal and segmental sclerosis. The role of oxidative and nitrosative stress in the nephropathy in ZDF was studied. Renal histology, function, and immunohistologic and biochemical parameters of oxidative and nitrosative stress were evaluated at 8 and 22 wk of age in ZDF and Zucker lean (ZL) rats and after chronic treatment with ebselen, an antioxidant and peroxinitrite scavenger. At 8 wk, ZDF rats showed hyperglycemia, no proteinuria or nephropathy, but higher levels of dihydrobiopterin and 3-nitrotyrosine (3-NT)-modified proteins compared with age-matched ZL rats. At 22 wk, ZDF rats developed focal and segmental sclerosis, proteinuria, decreased creatinine clearance, and renal tissue levels of glutathione and tetrahydrobiopterin with further elevation in dihydrobiopterin and 3-NT-modified proteins, in contrast to age-matched ZL rats. Renal immunohistologic expression of lipid peroxidation products and 3-NT-modified proteins also increased in 22-wk-old ZDF but not in ZL rats. Chronic ebselen treatment of ZDF rats restored renal tissue levels of glutathione and tetrahydrobiopterin; prevented significant accumulation of dihydrobiopterin, lipid peroxidation products, and 3-NT-modified proteins; and ameliorated focal and segmental sclerosis, proteinuria, and fall in creatinine clearance without affecting mean BP, body weight, and blood glucose, compared with the untreated ZDF rats. Chronic ebselen therapy also ameliorated vasculopathy with lipid deposits and tubulointerstitial scarring, inflammation, and upregulated alpha-smooth muscle actin expression. These findings suggest that ZDF rats develop a progressive nephropathy with glomerular, vascular, and tubulointerstitial pathology. Oxidative and nitrosative stress predates the nephropathy, which is improved by peroxinitrite scavenger ebselen, and thus considered its cause and not consequence.
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PMID:Nephropathy in Zucker diabetic fat rat is associated with oxidative and nitrosative stress: prevention by chronic therapy with a peroxynitrite scavenger ebselen. 1533 88

In 1990-1992, the authors investigated the association of total and free testosterone with the metabolic syndrome in postmenopausal US women not taking hormone replacement therapy (n=362) in a prevalent case-control study of carotid atherosclerosis. Free testosterone was estimated by using the free androgen index (FAI) (total testosterone/sex hormone-binding globulin ratio). The metabolic syndrome was defined as the presence of three or more of the following criteria: waist circumference > or =35 inches (88.9 cm), triglycerides > or =150 mg/dl, high density lipoprotein cholesterol <40 mg/dl, blood pressure >130/80 mmHg, fasting insulin > or =100 pmol/liter, or impaired glucose homeostasis (fasting glucose > or =110 mg/dl or diagnosed diabetes mellitus). FAI, but not total testosterone, was strongly associated with the metabolic syndrome. Compared with women in the lowest FAI quartile, those in the highest quartile had a fivefold greater odds of having the metabolic syndrome (odds ratio=5.38, 95% confidence interval: 2.70, 10.7) after adjustment for age, race, and carotid atherosclerosis status. In multivariate analyses, the three-component metabolic syndrome combinations that contained both hyperinsulinemia and hyperglycemia were most strongly associated with increased FAI (absolute increase=0.41-0.54 compared with that for women who did not have these combinations; all p's < 0.001). Higher FAI was associated with the hyperinsulinemia and hyperglycemia components of the metabolic syndrome. The role of androgens in glucose homeostasis in postmenopausal women requires further study.
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PMID:Glucose and insulin components of the metabolic syndrome are associated with hyperandrogenism in postmenopausal women: the atherosclerosis risk in communities study. 1535 14

Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that can lead to hepatic fibrosis and cirrhosis. Portal fibrosis in the absence of NASH, called isolated portal fibrosis (IPF), has received less attention and has not been classified as a spectrum of NAFLD. The aims of this study were to determine the prevalence of IPF in subjects undergoing gastric bypass surgery, to identify biochemical variables associated with IPF, and to assess the metabolic syndrome as defined by the AdultTreatment Panel III criteria. We analyzed liver biopsies from 195 morbidly obese subjects after excluding all other causes of liver disease. The prevalence of fatty liver (FL) only, IPF, and NASH was 30.3%, 33.3%, and 36.4%, respectively. Several biochemical parameters significantly trended across the 3 groups, with IPF falling between FL and NASH. Hyperglycemia was the only metabolic parameter associated with NASH (OR, 5.4; 95% CI, 2.4-12; P < .0001) and IPF (OR, 2.8; 95% CI, 1.2-6.5; P = .01). Subjects with diabetes had the greatest risk for NASH (OR, 8; 95% CI, 3.3-19.7; P < .0001) and IPF (OR, 4.3; 95% CI, 1.6-11.6; P = .003). The metabolic syndrome was identified in 78.5% of subjects, and a significant trend for the number of metabolic criteria was observed across the spectrum of FL, IPF, and NASH. In conclusion, a significant subset of morbidly obese individuals has portal fibrosis in the absence of NASH that is associated with glycemic dysregulation. Therefore, IPF should be considered a spectrum of NAFLD that may prelude NASH in morbid obesity.
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PMID:Portal fibrosis and hepatic steatosis in morbidly obese subjects: A spectrum of nonalcoholic fatty liver disease. 1536 53

Factors related to metabolic syndrome were investigated in a sample of 249 Moroccan Sahraoui women, ages 15 years and older. Body weight, height, waist and hip circumference, total cholesterol, triglycerides, fasting blood glucose, and blood pressure were measured. The results indicate that central obesity was the most common comorbid factor (75%) followed by hypertension (28.6%), hypertriglyceridemia (22.4%), hyperglycemia (11.9%), and hypercholesterolemia (11.6%). The overall prevalence of metabolic syndrome was 16.3%, and it was more prevalent in obese, older, married, and women without education than nonobese, younger, single, and educated women. Also, the prevalence of all metabolic syndrome components decreased with physical activity. The results suggest that prevention of obesity, particularly central obesity, could be the most direct route to prevention of this syndrome and its complications.
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PMID:Metabolic syndrome among Moroccan Sahraoui adult Women. 1536 8

To delineate the roles of the lactogens and GH in the control of perinatal and postnatal growth, fat deposition, insulin production, and insulin action, we generated a novel mouse model that combines resistance to all lactogenic hormones with a severe deficiency of pituitary GH. The model was created by breeding PRL receptor (PRLR)-deficient (knockout) males with GH-deficient (little) females. In contrast to mice with isolated GH or PRLR deficiencies, double-mutant (lactogen-resistant and GH-deficient) mice on d 7 of life had growth failure and hypoglycemia. These findings suggest that lactogens and GH act in concert to facilitate weight gain and glucose homeostasis during the perinatal period. Plasma insulin and IGF-I and IGF-II concentrations were decreased in both GH-deficient and double-mutant neonates but were normal in PRLR-deficient mice. Body weights of the double mutants were reduced markedly during the first 3-4 months of age, and adults had striking reductions in femur length, plasma IGF-I and IGF binding protein-3 concentrations, and femoral bone mineral density. By age 6-12 months, however, the double-mutant mice developed obesity, hyperleptinemia, fasting hyperglycemia, relative hypoinsulinemia, insulin resistance, and glucose intolerance; males were affected to a greater degree than females. The combination of perinatal growth failure and late-onset obesity and insulin resistance suggests that the lactogen-resistant/GH-deficient mouse may serve as a model for the development of the metabolic syndrome.
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PMID:Roles of the lactogens and somatogens in perinatal and postnatal metabolism and growth: studies of a novel mouse model combining lactogen resistance and growth hormone deficiency. 1538 48


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