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

Levels of basal insulinemia, malondialdehyde (an index of oxidative stress) and some metabolic parameters were studied in 143 men and 83 women aged 48.3+/-0.7 years with incomplete metabolic syndrome: hypertension, abdominal obesity, dyslipoproteinemia with normoglycemia. Basal insulinemia correlated significantly with malondialdehyde levels both in men and women. Slose relationship was also found between basal insulinemia and waist circumference.
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PMID:[On the possible prooxidant role of insulinemia in formation of metabolic syndrome in men and women.]. 1547 68

Recent definitions of the metabolic syndrome from the World Health Organization (WHO) and National Cholesterol Education Program (NCEP) have given us a clearer picture of the prevalence of the metabolic syndrome and the risks it poses for cardiovascular disease and type 2 diabetes. Solid epidemiological and trial evidence support lifestyle changes as the main modifiable risk factors, including abdominal obesity, sedentary lifestyle and a diet rich in saturated fat and low in fiber content, in the treatment of individual components of the metabolic syndrome. Physical activity may prevent the metabolic syndrome as defined by the WHO and NCEP, but the evidence for lifestyle changes using these definitions is still sparse. No trials on the treatment of the metabolic syndrome to prevent diabetes have been published. However, both the Finnish Diabetes Prevention Study and the Diabetes Prevention Program found that moderate lifestyle interventions in persons with impaired glucose tolerance, a condition related to the metabolic syndrome. decreased the incidence of type 2 diabetes by 58%. Some drugs may also prevent diabetes. Further research on lifestyle modifications in the prevention and treatment of the metabolic syndrome, and on how best to promote lifestyle changes, is needed. In the meantime, efforts to curb obesity and overweight, increase physical activity and improve compliance with current dietary recommendations should continue.
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PMID:Epidemiology and treatment of the metabolic syndrome. 1547 8

Development of hypertension has been linked to chronic low-grade inflammation. However, it is not known whether this connection is mediated by features of the metabolic syndrome or smoking, or their changes, which themselves have been linked to inflammation. We studied the predictive value of highly sensitive C-reactive protein (hs-CRP), smoking, and abdominal obesity to the development of hypertension in an 11-year follow-up of a population-based study cohort comprising 379 middle-aged normotensive men. During the follow-up, 124 men (33%) developed hypertension. Men with hs-CRP > or =3.0 mg/L were 2.8x (95% confidence interval, 1.2 to 6.6) more likely to develop hypertension than with hs-CRP <1.0 mg/L even after adjustment for features of the metabolic syndrome, lifestyle factors, and their changes. Cigarette smoking was also associated with development of hypertension independently of inflammation and other confounders. Waist girth increased more in men who quit smoking than in other men. An increase in waist girth during follow-up strongly predicted incident hypertension. The decrease in smoking was not associated with a lower risk of hypertension in age-adjusted analyses. Hypertension is preceded by low-grade chronic inflammation in middle-aged white men independently of smoking or features of the metabolic syndrome. Furthermore, smoking may be a risk factor for hypertension. Although stopping smoking is beneficial with respect to health outcomes, the subsequent increase in weight and waist girth associated with smoking cessation may offset the decrease in the risk of hypertension that one may otherwise expect.
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PMID:Inflammation, abdominal obesity, and smoking as predictors of hypertension. 1549 31

Nutrition is a key environmental factor that is particularly involved in the pathogenesis and progression of several polygenic, diet-related diseases. Nutrigenomics refers to the interaction between nutrition and the human genome. Dietary fatty acids interact with multiple nutrient-sensitive transcription factors. This explains the molecular basis of some of the health effects associated with altered dietary fatty acid composition. The metabolic syndrome is a very common condition, characterized by insulin resistance, abdominal obesity, dyslipidaemia and hypertension. It often precedes Type 2 diabetes mellitus, and is associated with a greater risk of cardiovascular disease. Several lines of evidence suggest that the interaction between nutrient-derived metabolic stressors and pro-inflammatory signals play an important role in the aetiology of insulin resistance and the development of the metabolic syndrome. This paper will address the interaction between several nutrient-sensitive transcription factors, including SREBP (sterol-regulatory-element-binding protein) and NFkappaB (nuclear factor kappaB), demonstrating how this interaction may be altered with dietary fatty acid interventions.
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PMID:Dietary lipids and gene expression. 1550 46

The diagnosis of metabolic syndrome is based on identification of the following parameters: abdominal obesity, triglycerides, HDL-cholesterol, blood pressure, fasting glycemia, as recommended by ATP III. In order to simplify the clinical practice, at least two parameters should be screened for. The most frequent couple, easy to be determined in practice, is hypertensive waist, followed by hypertriglyceridemic waist, hypertensive dyslipidemia, dysglycemic dyslipidemia and hypertensive dysglycemia. Based on these couples the next step would be to identify the triads that diagnose the metabolic syndrome. A global assessment of cardiovascular risk should be made. Suggested method is to apply the Framingham Score. Therapeutic intervention is structured according to levels of cardiovascular risk. Clinical management is structured on THEME Programs (therapy, education, monitoring, evaluation), applied to all risk factors.
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PMID:Metabolic syndrome--practical approach. 1552 14

The metabolic syndrome (MetS) is a huge public health problem worldwide, being one of the major causes of cardiovascular disease, responsible for a growing number of premature deaths throughout the world. MetS includes a cluster of anomalies, such as: abdominal obesity, insulin resistance, hyperinsulinemia, hypertension, type 2 diabetes mellitus or glucose intolerance, hypertriglyceridemia etc. The number of people with MetS increases with age, affecting more than 40% of people in their 60s and 70s. About 30% of European people over 50 have MetS. Some experts estimate that as many as two thirds of Americans may be suffering from MetS. The exact cause of MetS is not known: genetics play a minor role, acquired in-utero factors also play a role (prenatal malnutrition, toxin exposure, exposure to high levels of maternal cortisol). For most people, the MetS results primarily from lifestyle factors, such as: chronic stress, inadequate exercise. The MetS can be avoided and reversed in most cases. Weight loss is both a treatment and goal for MetS patients. Moderate weight loss, in the range of 5-10% of body weight, can help restore body's ability to recognize insulin and greatly reduce the chance that the syndrome will evolve into a more serious illness. In most people weight loss will lower blood pressure and improve triglyceride levels. Increased activity alone can improve insulin levels. Physical activity result in a weight loss, improved blood pressure, improved cholesterol and triglyceride level and reduced risk of developing diabetes. It is also important to treat: hyperlipidemia, hypertension, prothrombotic state.
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PMID:The metabolic syndrome--a multifaced disease. 1552 15

Metabolic syndrome is a cluster of cardiovascular risk factors. Pathogenesis of metabolic syndrome implies 3 potential etiological mechanisms: obesity and adipose tissue disorders, insulin resistance, and a constellation of independent factors. Clinical recognition of the metabolic syndrome is based on finding several well-recognized signs in clinical practice: abdominal obesity, elevated triglycerides, reduced HDL cholesterol, raised blood pressure, and elevated plasma glucose. In addition, other components commonly aggregate with the major components: elevated apolipoprotein B, small LDL particles, insulin resistance and hyperinsulinemia, impaired glucose tolerance (IGT), elevated C-reactive protein (CRP), and variation in coagulation factors (plasminogen activator inhibitor [PAI]-I and fibrinogen). Cardiovascular disease (CVD) is the primary clinical outcome of metabolic syndrome. Additionally, risk for type 2 diabetes is higher. Diabetes is itself a major risk factor for CVD. ATP III criteria for diagnosis of metabolic syndrome provide a practical tool to identify patients at increased risk for CVD. World Health Organization (WHO) and American Association of Clinical Endocrinologists (AACE) criteria require further oral glucose testing if IFG and diabetes are absent. IGT on OGTT denotes greater risk for diabetes than does metabolic syndrome without elevated fasting glucose.
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PMID:Metabolic syndrome--new insights into a growing entity. 1552 16

In men, hypoandrogenism is associated with features of the metabolic syndrome. It is not known whether men with the metabolic syndrome are at a higher risk of developing hypogonadism. We therefore assessed whether the metabolic syndrome predicts development of hypogonadism 11 yr later in 651 middle-aged Finnish men participating in a population-based cohort study. Men with the metabolic syndrome at baseline as defined by the World Health Organization (n = 114, 20%) had a 2.6-fold increased risk of developing hypogonadism as defined by total testosterone levels less than 11 nmol/liter at the 11-yr follow-up independent of age, smoking, and other potential confounders. Further adjustment for body mass index (OR, 2.0; 95% CI, 1.1-3.8) or baseline total testosterone levels (OR, 1.9; 95% CI, 1.0-3.4) attenuated the association. The association of the metabolic syndrome with hypogonadism as defined by calculated free testosterone levels less than 225 pmol/liter was similar, but weaker. The adjusted decrease in testosterone concentrations during the 11-yr follow-up was also greater in men with than without the metabolic syndrome. Smokers had a nonsignificantly lower risk of developing hypogonadism during follow-up, whereas a decrease in smoking increased the risk of hypogonadism. The metabolic syndrome predisposes to development of hypogonadism in middle-aged men. Prevention of abdominal obesity and the accompanying metabolic syndrome in middle age may decrease the risk of hypogonadism in men, especially in those who quit smoking.
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PMID:The metabolic syndrome and smoking in relation to hypogonadism in middle-aged men: a prospective cohort study. 1553 58

Adipose tissue type 1 11beta-hydroxysteroid dehydrogenase (11beta-HSD1), which generates hormonally active cortisol from inactive cortisone, has been shown to play a central role in adipocyte differentiation and abdominal obesity-related metabolic complications. The objective was to investigate whether genetic variations in the human 11beta-HSD1 gene are associated with the metabolic syndrome among French-Canadian men. We sequenced all exons, the exon-intron splicing boundaries, and 5' and 3' regions of the human 11beta-HSD1 gene in 36 men with the metabolic syndrome, as defined by the National Cholesterol Education Program-Adult Treatment Panel III, and two controls. Three intronic sequence variants were identified: two single-nucleotide polymorphisms in intron 3 (g.4478T>G) and intron 4 (g.10733G>C) and one insertion in intron 3 (g.4437-4438insA). The relative allele frequency was 19.6%, 22.1%, and 19.6% for the g.4478G, g.10733C, and g.4438insA alleles, respectively. One single-nucleotide polymorphism was identified in exon 6 (c.744G>C or G248G). The frequency of the c.744C allele was only 0.46% in a sample of 217 men. Variants were not associated with components of the metabolic syndrome except for plasma apolipoprotein B levels. In conclusion, molecular screening of the 11beta-HSD1 gene did not reveal any sequence variations that can significantly contribute to the etiology of the metabolic syndrome among French-Canadians.
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PMID:Molecular screening of the 11beta-HSD1 gene in men characterized by the metabolic syndrome. 1553 20

The metabolic syndrome is diagnosed according to criteria set by either WHO (obesity, high blood pressure, dyslipidemia, insulin resistance) or more recently by ATP III (National Cholesterol Education Program's Adult Treatment Panel III report). The latter emphasizes abdominal obesity, atherogenic dyslipidemia, high blood pressure and increased fasting glucose. Without presuming a nosologic entity, the metabolic syndrome is emerging as by far the most important precursor of an epidemic of cardiovascular disease, not only in Western countries. This epidemic calls for action at a time when our understanding of dietary intervention for maintaining weight loss remains primitive and cannot withstand critical scrutiny (because of a lack of long term randomised, prospective studies). Dietary therapy in metabolic syndrome therefore has to be aimed where success is most likely, i.e. at a reduction in energy intake and increase in output by physical activity, a prudent balance of carbohydrates, proteins and fats, taking into account secondary changes in lipid profiles and the glycemic load of nutrients. All nutritional advice must be incorporated in long term programs with continuous guidance, preferably in group therapy targeting all individual risk factors.
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PMID:[Metabolic syndrome: diagnosis and dietary intervention]. 1733 58


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