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

Gender-specific differences in the incidence of cardiovascular disease have long been known, and estrogens have been considered to be responsible for this dissimilarity. Recently, the steep increase in cardiovascular risk in the no longer fertile woman has become evident. The postmenopausal metabolic syndrome is very frequent, with obesity, insulin resistance, and hyperinsulinemia, which convey increased sodium reabsorption, stimulation of the sympathetic nervous system, and smooth muscle growth. The clinical corollary of these overall changes is hypertension. Gender differences in components of the renin-angiotensin system have been shown to exist, and may play a central role in blood pressure control. In normotensive populations, plasma renin activity is significantly higher in men than in women, and is higher in postmenopausal versus premenopausal women. Two angiotensin-converting enzyme inhibitors, ramipril and moexipril, have undergone trials aimed specifically at older people with cardiovascular risk and with postmenopausal hypertension, and could be the first therapeutic choice. However, a comprehensive treatment should include nonpharmacologic measures with strong emphasis on weight normalization and regular physical activity, prevention of osteoporosis, as well as decisions on the use of estrogen replacement therapy and treatment of the menopausal metabolic syndrome. Finally, education of both patients and physicians on the nature and prognosis of untreated hypertension is crucial.
Curr Hypertens Rep 2002 Dec
PMID:Systemic hypertension in postmenopausal women: a clinical approach. 1241 76

The World Health Organization (WHO) and the National Cholesterol Education Program (NCEP) recently proposed definitions for the metabolic syndrome. Little is known of their validity, however. The authors assessed the sensitivity and specificity of the definitions of the metabolic syndrome for prevalent and incident diabetes mellitus in a Finnish population-based cohort of middle-aged men (n = 1,005) followed for 4 years since the late 1980s. Four definitions based on the WHO and NCEP recommendations were compared. All definitions identified persons at high risk for developing diabetes during the 4-year follow-up (odds ratios = 5.0-8.8). The WHO definition including waist-hip ratio > 0.90 or body mass index >or= 30 kg/m(2) was the most sensitive (0.83 and 0.67) and least specific (0.78 and 0.80) in detecting the 47 prevalent and 51 incident cases of diabetes. The NCEP definition in which adiposity was defined as waist girth > 102 cm detected only 61% of prevalent and 41% of incident diabetes, although it was the most specific (0.89 and 0.90). The WHO definition seems valid as judged by its relatively high sensitivity and specificity in predicting diabetes. The NCEP definition including waist > 102 cm also identifies persons at high risk for diabetes, but it is relatively insensitive in predicting diabetes.
Am J Epidemiol 2002 Dec 01
PMID:Metabolic syndrome and development of diabetes mellitus: application and validation of recently suggested definitions of the metabolic syndrome in a prospective cohort study. 1244 65

The human transcription factor FOXC2 has recently been shown to protect against diet-induced insulin resistance in transgenic mice. We investigated the expression of FOXC2 in fat and muscle and performed a genetic analysis in human subjects. FOXC2 mRNA levels were increased in visceral compared with subcutaneous fat from obese subjects (12 +/- 4-fold; P = 0.0001), and there was a correlation between whole-body insulin sensitivity and FOXC2 mRNA levels in visceral fat (fS-insulin R = -0.64, P = 0.01, and homeostasis model assessment of insulin resistance [HOMA-IR] R = -0.68, P = 0.007) and skeletal muscle (fS-insulin R = -0.57, P = 0.03, and HOMA-IR R = -0.55, P = 0.04). Mutation screening of the FOXC2 gene identified a common polymorphism in the 5' untranslated region (C-512T). The T allele was associated with enhanced insulin sensitivity (HOMA-IR P = 0.007) and lower plasma triglyceride levels in females (P = 0.007). Also, the higher expression of FOXC2 in visceral than in subcutaneous fat was restricted to subjects homozygous for the T allele (P = 0.03 vs. P = 0.7). Our data suggest that increased FOXC2 expression may protect against insulin resistance in human subjects and that genetic variability in the gene may influence features associated with the metabolic syndrome.
Diabetes 2002 Dec
PMID:FOXC2 mRNA Expression and a 5' untranslated region polymorphism of the gene are associated with insulin resistance. 1245 13

Sibutramine-induced weight loss and weight maintenance lead to clinically relevant reductions in risk factors associated with the metabolic syndrome. Treatment with the drug decreases visceral fat, improves lipid levels, decreases glycosylated haemoglobin and decreases uric acid concentrations. Sibutramine is effective in achieving weight loss in patients with type 2 diabetes but weight loss occurs more slowly than in non-diabetic patients. The criteria for predicting response to treatment in uncomplicated patients may not be appropriate to those with type 2 diabetes. Furthermore, it is important to set realistic goals for weight loss in type 2 diabetes to avoid the risk of denying effective treatment to patients.
Int J Obes Relat Metab Disord 2002 Dec
PMID:Metabolic benefits associated with sibutramine therapy. 1245 98

This review presents recent concepts of how beta-agonists affect glucose homeostasis by modulating insulin secretion, liver metabolism, and uptake of glucose into muscle, with attention to the influence of hypoglycemia on beta-agonist sensitivity and the effects of beta(3)-adrenergic receptor (beta(3)AR) polymorphisms on adipocyte metabolism. Specific beta(2)-agonist effects on the pancreatic beta cell result in increased insulin secretion, yet other mechanisms, such as increased glucagon secretion and hepatic effects, cause an overall increase in serum glucose and an apparent decrease in insulin sensitivity. Human studies confirm the presence of beta(2)ARs on pancreatic beta cells. Intensive treatment of diabetes mellitus with insulin, especially in type 1 diabetes, has led to increased incidence of hypoglycemia. Repeated episodes of hypoglycemia lead to unawareness of neuroglycopenia, a major limitation to intensive treatment. Hypoglycemic unawareness is associated with reduced beta-agonist sensitivity. Scrupulous avoidance of hypoglycemia over many weeks to months can restore beta-agonist sensitivity and improve detection of hypoglycemia. beta-agonists have also been employed to prevent hypoglycemia. beta-agonists can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. While beta(1)ARs and beta(2)ARs mediate many of these actions, it is likely that beta(3)ARs in the adipocyte membrane also play an important role. Specific beta(3)AR subtypes have been associated with obesity and the metabolic syndrome.
J Allergy Clin Immunol 2002 Dec
PMID:beta-Agonists and metabolism. 1246 41

Non-alcoholic steatohepatitis (NASH) is a disease of emerging identity and importance. It is frequently associated with obesity, especially visceral fat, and is intimately related to fatty liver and markers of the insulin resistance syndrome. Both the prevalence and the severity of liver steatosis are related to body mass index, waist circumference, hyperinsulinaemia, hypertriglyceridaemia and impaired glucose tolerance or type 2 diabetes. The identification of obese patients who may progress from steatosis to NASH and from NASH to fibrosis/cirrhosis is an important clinical challenge. Substantial weight loss is accompanied by a marked attenuation of insulin resistance and related metabolic syndrome and, concomitantly, by a remarkable regression of liver steatosis in most patients, although increased inflammation may be detected in some subjects. Thus, NASH may be considered as another disease of affluence, as is the insulin resistance syndrome, and perhaps being part of it, especially in obese patients.
Best Pract Res Clin Endocrinol Metab 2002 Dec
PMID:Obesity and liver disease. 1246 16

Beta-cells possess inherent mechanisms to adapt to overnutrition and the prevailing concentrations of glucose, fatty acids, and other fuels to maintain glucose homeostasis. However, this is balanced by potentially harmful actions of the same nutrients. Both glucose and fatty acids may cause good/adaptive or evil/toxic actions on the beta-cell, depending on their concentrations and the time during which they are elevated. Chronic high glucose dramatically influences beta-cell lipid metabolism via substrate availability, changes in the activity and expression of enzymes of glucose and lipid metabolism, and modifications in the expression level of key transcription factors. We discuss here the emerging view that beta-cell "glucotoxicity" is in part indirectly caused by "lipotoxicity," and that beta-cell abnormalities will become particularly apparent when both glucose and circulating fatty acids are high. We support the concept that elevated glucose and fatty acids synergize in causing toxicity in islets and other organs, a process that may be instrumental in the pleiotropic defects associated with the metabolic syndrome and type 1 and type 2 diabetes. The mechanisms by which hyperglycemia and hyperlipidemia alter insulin secretion are discussed and a model of beta-cell "glucolipotoxicity" that implicates alterations in beta-cell malonyl-CoA concentrations; peroxisome proliferator-activated receptor-alpha and -gamma and sterol regulatory element binding protein-1c expression; and lipid partitioning is proposed.
Diabetes 2002 Dec
PMID:Malonyl-CoA signaling, lipid partitioning, and glucolipotoxicity: role in beta-cell adaptation and failure in the etiology of diabetes. 1247 83

Low serum magnesium levels are related to diabetes mellitus (DM) and high blood pressure (HBP), but as far as we know, there are no previous reports that analyzed the serum magnesium concentration in individuals with metabolic syndrome (MS). We performed a cross-sectional population-based study to compare 192 individuals with MS and 384 disorder-free control subjects, matched by age and gender. Magnesium supplementation treatment and conditions likely to provoke hypomagnesemia, including previous diagnosis of diabetes mellitus (DM) and/or high blood pressure (HBP), were exclusion criteria. In this regard, only incident cases of DM and HBP were included. MS was defined by the presence at least of two of the following features: hyperglycemia (> or =7.0 mmol/l); HBP (> or =160/90 mmHg); dyslipidemia (fasting triglycerides > or =1.7 mmol/l and/or HDL-cholesterol <1.0 mmol/l); and obesity (body mass index > or =30 kg/m(2) and/or waist-to-hip ratio > or =0.85 in women or > or =0.9 in men). Low serum magnesium levels were identified in 126 (65.6%) and 19 (4.9%) individuals with and without MS, p<0.00001. The mean serum magnesium level among subjects with MS was 1.8+/-0.3 mg/dl, and among control subjects 2.2+/-0.2 mg/dl, p<0.00001. There was a strong independent relationship between low serum magnesium levels and MS (odds ratio (OR)=6.8, CI(95%) 4.2-10.9). Among the components of MS, dyslipidemia (OR 2.8, CI(95%) 1.3-2.9) and HBP (OR 1.9, CI(95%) 1.4-2.8) were strongly related to low serum magnesium levels. This study reveals a strong relationship between decreased serum magnesium and MS.
Acta Diabetol 2002 Dec
PMID:Low serum magnesium levels and metabolic syndrome. 1248 95

The metabolic syndrome is an important risk factor for major chronic diseases in women. A key component of the syndrome, central adiposity, is correlated with psychological risk factors associated with coronary artery disease in prior epidemiological studies. We evaluated if psychological risk factors predicted the metabolic syndrome and if the metabolic syndrome predicted psychological distress. A population-based cohort of 425 women who were middle-aged, and pre-, peri-, and postmenopausal was followed for an average 7.4 years. Psychological risk factors, including depression, anxiety, tension, current perceived stress, and anger, and biological components of the metabolic syndrome, including glucose, triglycerides, high-density lipoprotein (HDL)-cholesterol, waist circumference, and blood pressure (BP) were measured at baseline and at examinations 1 to 8 years postmenopause. Women were classified according to the National Heart, Lung, and Blood Institute (NHLBI) criteria for metabolic syndrome. Women who exhibited high levels of depression, tension, and anger at baseline, and increased in anger during the follow-up had elevated risk for developing the metabolic syndrome during follow-up, P <.04. The metabolic syndrome at baseline, in turn, predicted increasing anger and anxiety 7.4 years later, P <.001. Psychological risk factors affect the development of the metabolic syndrome. The association between anger and the metabolic syndrome is reciprocal. Reduction in the level of psychological distress may prevent the development of the metabolic syndrome in women.
Metabolism 2002 Dec
PMID:The relationship between psychological risk attributes and the metabolic syndrome in healthy women: antecedent or consequence? 1248 70

The most common and clinically important complication in adults with diabetes is cardiovascular disease (CVD), which includes coronary heart disease, peripheral vascular disease, and stroke. Both type 2 diabetes and the insulin resistance syndrome are associated with a marked increase in the risk for CVD. The metabolic syndrome and the closely related insulin resistance syndrome have recently been recognized as important disorders, each being associated with an increase in CVD risk even in the absence of glucose intolerance. Given the significant public health burden of CVD, risk reduction has emerged as a significant clinical challenge for most practitioners. Diabetes and the insulin resistance syndrome are closely related disorders, with insulin resistance being more than a key pathogenic defect in type 2 diabetes. Even in the absence of glucose intolerance, these 2 disorders are both associated with a number of distinct pathologic findings, including hypertension, atherogenic dyslipidemia, a prothrombotic environment, and significant vascular and hemodynamic abnormalities that result from endothelial cell dysfunction. Insulin resistance is now recognized to be closely associated with the development of each of these risk factors. This article uses a case-based approach to discuss the unique features of insulin resistance and type 2 diabetes considered to be key contributors to CVD risk. A systematic approach to both evaluation and management is proposed, with priority given to therapies of demonstrated clinical benefit. Because of its critical and central role in the development of many CVD risk factors, targeted treatment of insulin resistance will also be discussed as such therapy may prove to be a critical component of care in years to come.
Am J Manag Care 2002 Dec
PMID:The metabolic syndrome, type 2 diabetes, and cardiovascular disease: understanding the role of insulin resistance. 1251 Jul 88


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