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The metabolic syndrome is a widespread clinical condition and an important cluster of atherothrombotic disease risk factors. The inclusion of this syndrome in the recently published Adult Treatment Panel III (ATP III) guidelines focused the attention of the physicians on this entity. Abdominal obesity, PPAR modulation, insulin resistance (with or without glucose intolerance), atherogenic dyslipidemia, elevated blood pressure, prothrombotic and proinflammatory states are the principal factors of this multifaceted syndrome. There are two major pathways of metabolic syndrome progress: (1) With preserved pancreatic beta cells function and insulin hypersecretion, which can recompense for insulin resistance. This pathway leads mostly to the macrovascular complications of metabolic syndrome. (2) With substantial injure of pancreatic beta cells leading to gradually reduced insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. Because macrovascular complications of insulin resistance state precede the onset of hyperglycemia, early intervention in patients with metabolic syndrome is particularly important. Since central obesity (accompanied by insulin resistance even in the absence of hyperglycemia) is the key factor leading to development of metabolic syndrome and its future macrovascular complications, we assume that next logical step is the recognition of central obesity itself as a major risk factor for cardiovascular diseases.
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PMID:Macrovascular complications of metabolic syndrome: an early intervention is imperative. 1545 79

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

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 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

Central obesity, insulin resistance, inflammation, as well as vascular changes are common in patients with type 2 diabetes. In this study we assessed the relationship among stiffness of the carotid artery, visceral fat, and circulating inflammatory markers in type 2 diabetic subjects. Carotid stiffness, quantified as the distensibility coefficient (DC), was measured by ultrasound in asymptomatic, normotensive patients with uncomplicated, well-controlled type 2 diabetes and in controls. Body fat distribution was quantified by magnetic resonance imaging. In patients, the carotid DC was inversely associated with visceral fat area (r = -0.660; P = 0.005) and plasma levels of C-reactive protein (CRP; r = -0.687; P = 0.002), but most strongly with plasma IL-6 (r = -0.766; P < 0.001). In multivariate analysis, the association between DC and visceral fat disappeared after adjustment for CRP and IL-6. Correction for age, body mass index, blood pressure, glycosylated hemoglobin, or fasting plasma glucose did not affect the association between carotid DC and inflammatory markers. Thus, carotid stiffness is associated with visceral obesity in patients with uncomplicated type 2 diabetes, but this association seems to be mediated by circulating IL-6 and CRP, of which IL-6, at least in part, originates from adipose tissue and stimulates hepatic CRP production.
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PMID:The association between abdominal visceral fat and carotid stiffness is mediated by circulating inflammatory markers in uncomplicated type 2 diabetes. 1561 16

The increased prevalence of type 2 diabetes parallels the increased prevalence of obesity. Abdominal obesity contributes to insulin resistance. To overcome the insulin resistance, the pancreas makes more insulin, keeping the glucose in the normal range. Eventually, the pancreas will fail, resulting in elevated levels of blood glucose. Thus, to develop type 2 diabetes, an individual must have a defect in insulin sensitivity with an accompanying defect in insulin secretion. In the early stages of the disease, glucose can be controlled with appropriate therapeutic lifestyle changes aimed at lowering insulin resistance. As the disease progresses, one has to use medications. Insulin secretagogues increase insulin levels, whereas insulin sensitizers, such as metformin and thiazolidinediones, decrease insulin resistance. The defect in insulin secretion is progressive, and eventually, almost every patient needs exogenous insulin, which may be delayed with appropriate lifestyle changes. Insulin resistance is associated with a clustering of metabolic abnormalities called the insulin-resistance syndrome, which is a component of the metabolic syndrome. Insulin-resistance syndrome includes obesity, hypertension, dyslipidemia, and elevated levels of plasminogen activator inhibitor type 1. These abnormalities increase the risk of cardiovascular disease. Of people with type 2 diabetes, 70% die from premature cardiovascular disease. Prevention of the complications of diabetes requires good control of not only blood glucose but also other manifestations of the insulin-resistance syndrome, including hypertension and lipid abnormalities.
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PMID:Epidemiology of diabetes and obesity in the United States. 1564 25

In excess of 50% of adult population and nearly one third of children in Mexico have overweight and obesity. This accounts for slightly >32,671,000 million persons, excluding children; thus, total numbers are even more significant. These figures are alarming for those responsible for the economic future and well-being of Mexico. Overweight and obesity lead to higher risk of mortality as well as development of multiple diseases, mainly coronary heart disease, diabetes type 2, cancer, and stroke, which are at present the principal causes of mortality in Mexico. The World Health Organization (WHO) announced that there are throughout the world more than one billion adults with overweight, of whom 300 million have obesity. In addition to the obesity epidemic in Mexico, there is high prevalence of diabetes type 2. Coexistence of both epidemics has been denominated the twin epidemic. As many as 80% of cases of type 2 diabetes are linked with overweight or obesity, particularly abdominal obesity. The disease was once thought to be limited to adults, but obese children are now developing the illness. In Mexico, we are able to refer to at least three epidemics, because not only are obesity and type 2 diabetes advancing rapidly in the country, but also cardiovascular disease, linked with high prevalence of both hypertension and metabolic syndrome as reported by scientists based on Mexican National Health Survey 2000 data.
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PMID:[The epidemiology of obesity]. 1564 67

Type 2 diabetes mellitus was modeled in newborn albino rat pups. Metabolism and contractile activity of isolated heart under conditions of hypoxia were studied on adult rats. Contractile activity of the myocardium in animals with type 2 diabetes mellitus and abdominal obesity decreased during hypoxia. It was manifested in a decrease in systolic and developed pressure and disturbances in diastolic relaxation of the myocardium. Damage to cell membranes and increased secretion of aspartate transaminase into the coronary circulation were observed under conditions of energy deficit and activation of the anaerobic pathway of energy production. These changes became more pronounced with increasing the period of hypoxic exposure.
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PMID:Effect of hypoxia on metabolism and contractile function of the heart in rats with type 2 diabetes mellitus and abdominal obesity. 1566 7

Abdominal obesity is a known risk factor for diabetes-related diseases. This study aimed to establish a formula to predict visceral abdominal fat area on the basis of simple clinical and anthropomorphic parameters easily measured in the clinic. We determined visceral fat (V) and subcutaneous fat (S) areas in 115 Japanese women using the standard procedure based on computed tomography (CT) at umbilical level. Furthermore, we measured clinical and anthropometric parameters including height, weight, waist circumference, hip circumference, skin fold thickness and body fat percentage. In 115 subjects, V area was 87.8+/-52.5 cm2 and S area was 221.1+/-99.7cm2. Abdominal obesity is diagnosed in Japan as a V area > or =100 cm2; on this basis 42 women (37%) had abdominal obesity. The prevalences of diabetes and related diseases were significantly higher among women with abdominal obesity. By simple regression analysis, V and S areas significantly correlated with anthropometric parameters: in particular, V area correlated with waist circumference (r=0.745, p<0.01) and S area with body mass index (r=0.793, p<0.01). However, these parameters were not sufficient to predict V area. By multiple regression analysis using simple parameters, we established the following formula to predict visceal fat: V area = 159.475 + 1.023(age) - 2.119(height) + 1.454(body weight) + 2.841(waist circumference) - 1.208(hip circumference) (r=0.812, p<0.01). The V area calculated by formula correlated (r=0.761) with that determined by CT in a second age-matched group of 31 Japanese women. The present study confirms that visceral adipose tissue is closely associated with type 2 diabetes mellitus, dyslipidemia and hypertension, and generated a formula to predict visceral adipose tissue accumulation.
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PMID:Evaluation of visceral adipose accumulation in Japanese women and establishment of a predictive formula. 1566 78


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