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)

Type 2 diabetes is a heterogeneous disease resulting from a dynamic interaction between defects in insulin secretion and insulin action. As most subjects are overweighted or obese, the initial treatment is optimization of the meal plan and enhancement of physical activity in order to obtain sustained weight reduction. In case of failure of life-style changes, various oral antihyperglycaemic agents may be used. Some are targeting defective insulin secretion (sulphonylureas, glinides) while others are targeting insulin resistance (metformin, thiazolidinediones). Criteria of drug selection should include both patient's characteristics (body weight, age, degree of hyperglycaemia, comorbidities) and pharmacological properties of the compound (mode of action, safety profile, cost). Monotherapy is usually recommended first, but combined therapy using drugs with additive or synergistic effects may be required to obtain appropriate blood glucose control. As the natural history of the disease is characterized by a progressive exhaustion of beta cells, exogenous insulin may be required in the long term, usually in combination with oral agents. Finally, as patients with type 2 diabetes are insulin-resistant and often have a metabolic syndrome, a multifactorial intervention including aggressive treatment of arterial hypertension and dyslipidaemia is recommended in order to reduce the incidence of cardiovascular complications.
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PMID:Treatment of type 2 diabetes. 1474 1

The purpose of the study was to examine the stability of variables associated with the metabolic syndrome from adolescence to adulthood. The sample included 48 subjects from the Aerobics Center Longitudinal Study who had one clinical visit during adolescence (mean age = 15.8 years) and a follow-up visit during adulthood (mean age = 26.6 years). The following variables were considered: treadmill time to exhaustion (TM), body mass index (BMI), waist circumference (WC), percent body fat (%BF), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), TC:HDL-C, triglycerides (TG), glucose (GLU), and systolic (SBP), diastolic (DBP), and mean (MAP) blood pressure. A composite risk factor score using variables consistent with the WHO and ATP III definition of the metabolic syndrome (WC, HDL-C, TG, MAP, and GLU) was calculated. Tracking coefficients were computed as partial correlations, controlling for length of follow-up (mean = 11 years). Tracking coefficients (r values) were moderate for all variables (TM, 0.53; BMI, 0.64; WC; 0.79;%BF, 0.44; TC, 0.62; HDL-C, 0.60; TG, 0.54; TC:HDL-C, 0.78; SBP, 0.45; and MAP, 0.41), except GLU (0.26) and DBP (0.21). The composite risk factor score also tracked moderately well (0.56) from adolescence into adulthood. The results support previous findings that variables associated with the metabolic syndrome track moderately well from adolescence to adulthood. The findings support the prevention and treatment of obesity, atherosclerosis, type 2 diabetes, and the metabolic syndrome during childhood and adolescence.
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PMID:Stability of variables associated with the metabolic syndrome from adolescence to adulthood: the Aerobics Center Longitudinal Study. 1549 27

Burnout is characterized by emotional exhaustion, physical fatigue, and cognitive weariness, resulting from prolonged exposure to work-related stress. The authors review the accumulated evidence suggesting that burnout and the related concept of vital exhaustion are associated with increased risk of cardiovascular disease and cardiovascular-related events. The authors present evidence supporting several potential mechanisms linking burnout with ill health, including the metabolic syndrome, dysregulation of the hypothalamic-pituitary-adrenal axis along with sympathetic nervous system activation, sleep disturbances, systemic inflammation, impaired immunity functions, blood coagulation and fibrinolysis, and poor health behaviors. The association of burnout and vital exhaustion with these disease mediators suggests that their impact on health may be more extensive than currently indicated.
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PMID:Burnout and risk of cardiovascular disease: evidence, possible causal paths, and promising research directions. 1671 65

Young adult women have had the greatest increase in prevalence of metabolic syndrome (MetS) over time, and prevalence is highest in Hispanic women, compared with women of other ethnicities. Factors contributing to the high prevalence of MetS in Hispanic women are unknown. This study was conducted to determine if physical activity or fitness were associated with individual features of MetS in young Mexican and Mexican-American women, and if the associations were independent of fat mass. Sixty young Mexican and Mexican-American women participated in the study. MetS was defined according to the Adult Treatment Panel III. A fasting blood sample was drawn for the measurement of glucose, insulin, high-density lipoprotein cholesterol (HDL-c), and triglycerides. Physical activity was assessed by questionnaire and accelerometer. Fitness was assessed by progressive treadmill test to exhaustion and ventilatory threshold. Body composition was assessed with Bod Pod. Multivariate regression was used to establish the independent contributions of physical activity and fitness to the individual features of MetS. After controlling for fat mass and fat-free mass, physical activity was found to be independently related to HDL-c and fitness was found to be independently related to triglycerides (p < 0.05). The independent associations between physical activity, fitness, and features of MetS were mediated by, rather than independent of, fat mass. Fat mass was independently related to triglycerides, systolic blood pressure, and diastolic blood pressure. Although physical activity and fitness were related to features of MetS, these associations were not independent of fat mass.
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PMID:Physical activity, cardiorespiratory fitness, and metabolic syndrome in young Mexican and Mexican-American women. 1923 80

AMP-activated protein kinase (AMPK) is a serine/threonine kinase that is implicated in the control of energy metabolism and is considered to be a molecular target for the suppression of obesity and the treatment of metabolic syndrome. Here, we identified and characterized nootkatone, a constituent of grapefruit, as a naturally occurring AMPK activator. Nootkatone induced an increase in AMPKalpha1 and -alpha2 activity along with an increase in the AMP/ATP ratio and an increase the phosphorylation of AMPKalpha and the downstream target acetyl-CoA carboxylase (ACC), in C(2)C(12) cells. Nootkatone-induced activation of AMPK was possibly mediated both by LKB1 and Ca(2+)/calmodulin-dependent protein kinase kinase. Nootkatone also upregulated PPARgamma coactivator-1alpha in C(2)C(12) cells and C57BL/6J mouse muscle. In addition, administration of nootkatone (200 mg/kg body wt) significantly enhanced AMPK activity, accompanied by LKB1, AMPK, and ACC phosphorylation in the liver and muscle of mice. Whole body energy expenditure evaluated by indirect calorimetry was also increased by nootkatone administration. Long-term intake of diets containing 0.1% to 0.3% (wt/wt) nootkatone significantly reduced high-fat and high-sucrose diet-induced body weight gain, abdominal fat accumulation, and the development of hyperglycemia, hyperinsulinemia, and hyperleptinemia in C57BL/6J mice. Furthermore, endurance capacity, evaluated as swimming time to exhaustion in BALB/c mice, was 21% longer in mice fed 0.2% nootkatone than in control mice. These findings indicate that long-term intake of nootkatone is beneficial toward preventing obesity and improving physical performance and that these effects are due, at least in part, to enhanced energy metabolism through AMPK activation in skeletal muscle and liver.
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PMID:Nootkatone, a characteristic constituent of grapefruit, stimulates energy metabolism and prevents diet-induced obesity by activating AMPK. 2050 76

Endothelial progenitor cells (EPCs) are an emerging biomarker of vascular health. However, there are few data on the biology and mobilizing factors of EPCs in metabolic syndrome (MS). The aim of this study was to assay EPC mobilizing factors, including granulocyte colony-stimulating factor, stem cell factor/c-kit ligand (SCF), vascular endothelial growth factor, and stromal cell-derived factor-1 levels, in patients with MS (n = 36) and age- and gender-matched controls (n = 38). There was a significant reduction of 83% in granulocyte colony-stimulating factor levels in patients with MS. Also, there were decreases in SCF and SCF soluble receptor levels. However, there was no significant difference in stromal cell-derived factor-1 levels, and paradoxically, vascular endothelial growth factor levels were increased, consistent with resistance. In conclusion, in addition to progenitor cell exhaustion as a mechanism for the decrease in EPCs in patients with MS, they also have a mobilization defect, as manifested by decreased levels of granulocyte colony-stimulating factor and SCF, resulting in a decrease in EPCs.
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PMID:Circulating levels of endothelial progenitor cell mobilizing factors in the metabolic syndrome. 2104 Jun 91

Non-alcoholic fatty liver disease (NAFLD) can be found in approximately 30% of adults in industrialized societies. Non-alcoholic steatohepatitis (NASH) is its most severe histological form and progresses to cirrhosis in 20% of these patients. Once developed, 30% to 40% of patients with cirrhosis will suffer liver-related death. NAFLD is considered the hepatic manifestation of the metabolic syndrome. Recent findings linking the components of metabolic syndrome with NAFLD and the progression to nonalcoholic steatohepatitis will be reviewed; in particular, the role of visceral adipose tissue, insulin resistance, adipocytokines, oxidative stress and diminished antioxidants within the liver in the exacerbation of these conditions. It is now widely accepted that non-hepatic mechanisms are largely responsible for the development of insulin resistance, which causes hepatic steatosis. Insulin resistance, a key feature of metabolic syndrome, is crucial for NASH development. We have a classical chicken-egg problem: insulin resistance causes hepatic steatosis or vice-versa? A possible sequence of the pathogenetic events is the following: increased free fatty acid supply - increased de novo lipogenesis - triglyceride and VLDL overproduction - atherogenic dyslipidemia- oxidative stress (lipid oxidation and peroxidation) - exhaustion of antioxidant defense system- "Tsunami" of inflammatory cytokines- fibrosis- carcinogenesis. Given the strong association of NAFLD with metabolic syndrome, early recognition, assessment and management are essential. The management emphasizes weight reduction and attention to global cardiometabolic risk factors, similar to recommendations for management of the elements of metabolic syndrome.
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PMID:[Fatty liver and global cardiometabolic risk]. 2107 6

We claim that a new level of studies is needed to answer a series of important questions about the expanding global chronic disease burden for cardiovascular disease (CVD) and for related conditions such as diabetes, metabolic syndrome, and obesity. These require a new study design structure, related to a new level of theory that goes beyond the current single-factor, a-theoretic epidemiological studies. This new platform for the design of large-scale Work/Stress/Disease studies would assess CVD-related disease mechanisms in a more general and dynamic form, based on the use of new tools for measuring autonomic functions in an occupational stress context and a new theory of disease causation. A sample outline is presented for such a study, based on Stress-Disequilibrium Theory (SDT) hypotheses, building on analytic tools developed for the assessment of stress-related exhaustion effects and chronic disease risks from Heart Rate Variability (HRV) research studies. The goal is to assess the associations between social organizational risks, particularly at work, and hypertension, metabolic syndrome, and diabetes II. The study design is multi-stage, spanning across several levels of disease-related de-regulation, and addressing co-morbidity of the conditions themselves. The study design is meant to span across a broad social population at all levels and would probably be multi-site, involving several countries, to yield the larger sample increased power for finding associations for work - physiological effects.
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PMID:Description of a large-scale study design to assess work-stress-disease associations for cardiovascular disease. 2130 75

One of the most important and complex diseases of modern society is metabolic syndrome. This syndrome has not been completely understood, and therefore an effective treatment is not available yet. We propose a possible stem cell mechanism involved in the development of metabolic syndrome. This way of thinking lets us consider also other significant pathologies that could have similar etiopathogenic pathways, like lipodystrophic syndromes, progeria, and aging. All these clinical situations could be the consequence of a progressive and persistent stem cell exhaustion syndrome (SCES). The main outcome of this SCES would be an irreversible loss of the effective regenerative mesenchymal stem cells (MSCs) pools. In this way, the normal repairing capacities of the organism could become inefficient. Our point of view could open the possibility for a new strategy of treatment in metabolic syndrome, lipodystrophic syndromes, progeria, and even aging: stem cell therapies.
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PMID:Could metabolic syndrome, lipodystrophy, and aging be mesenchymal stem cell exhaustion syndromes? 2171 67

The twenty-first century arrived in the middle of a global epidemic of metabolic syndrome (MS) and type 2 diabetes mellitus (DM2). It is generally accepted that an excess of nutrients linked to a low physical activity triggers the problem. However, the molecular features that interact to develop the MS are not clear. In an effort to understand and control them, they have been extensively studied, but this goal has not been achieved yet. Nonhuman animal models have been used to explore diet and genetic factors in which experimental conditions are controlled. For example, only one factor in the diet, such as fats or carbohydrates can be modified to better understand a single change that would be impossible in humans. Most of the studies have been done in rodents. However, it is difficult to directly compare them, because experiments are different in more than one variable; genetic strains, amount, and the type of fat used in the diet and sex. Thus, the only possible criteria of comparison are the relevance of the observed changes. We review different animal models and add some original observations on short-term changes in metabolism and beta cells in our own model of adult Wistar rats that are not especially prone to get fat or develop DM2, treated with 20% sucrose in drinking water. One early change observed in pancreatic beta cells is the increase in GLUT2 expression that is located to the membrane of the cells. This change could partially explain the presence of insulin hypersecretion and hyperinsulinemia in these rats. Understanding early changes that lead to MS and in time to pancreatic islet exhaustion is an important biomedical problem that may contribute to learn how to prevent or even reverse MS, before developing DM2.
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PMID:Early endocrine and molecular changes in metabolic syndrome models. 2190 98


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