Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome comprises a set of metabolic and physiologic risk factors associated with elevated cardiovascular disease risk. The expression of each one of its major factors (hypertriglyceridemia, low high-density lipoprotein cholesterol levels, hypertension, abdominal obesity, and insulin resistance) has been found to be the result of complex interactions between genetic and environmental factors. Moreover, obesity may play a major role in triggering the metabolic syndrome by interacting with genetic variants at candidate genes for dyslipidemia, hypertension, and insulin resistance. In support of this hypothesis, several studies at multiple candidate genes have already demonstrated the significance of these interactions; however, the data and their reliability are still very limited, and in many cases replication studies are still lacking in the literature. Therefore, more studies with better epidemiologic design and standardized adiposity measures are needed to estimate the contribution of body weight and fat distribution to the genetic predisposition to the metabolic syndrome, which is the most common cardiovascular disease risk factor in industrialized societies.
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PMID:The metabolic syndrome: a crossroad for genotype-phenotype associations in atherosclerosis. 1506 43

Metabolic syndrome is defined as a clustering of cardiovascular risk factors (abdominal obesity, hyperinsulinemia, atherogenic dyslipidemia, hypertension and hypercoagulability) that together increase the risk of developing coronary heart disease and type 2 diabetes. Inhibition of acetyl-CoA carboxylase (ACC), which results in inhibition of fatty acid synthesis and stimulation of fatty acid oxidation, has the potential to favorably affect a multitude of cardiovascular risk factors associated with metabolic syndrome. ACC exists as two tissue-specific isozymes, ACC1 present in lipogenic tissues (liver and adipose) and ACC2 present in oxidative tissues (liver, heart and skeletal muscle). Studies in both ACC2 knockout mice and animals administered isozyme-nonselective ACC inhibitors have demonstrated the utility of treating metabolic syndrome through this modality. An isozyme-non-selective ACC inhibitor may potentially provide the optimal therapeutic for beneficially affecting metabolic syndrome. However, demonstration of the full potential of isozyme-selective inhibitors, once identified, should reveal advantages and liabilities associated with single isozyme inhibition. While demonstrating clinical efficacy of an ACC inhibitor should be relatively straightforward, the heterogeneity of the patient population and the absence of established guidelines regarding approval endpoints for agents simultaneously affecting multiple aspects of metabolic syndrome will pose developmental challenges for initial market entries.
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PMID:Acetyl-CoA carboxylase inhibition for the treatment of metabolic syndrome. 1508 94

The prevalence of the polycystic ovaries syndrome (PCOS) is high but it is a heterogeneous disorder with implications in numerous medical domains. Abdominal obesity and insulin resistance, which are the main metabolic disorders, are strong links between hormonal abnormalities and long-term medical consequences. The latter begin to be better understood. Some studies suggest that PCOS may increase the risk for several conditions, including type 2 diabetes, dyslipidemia, hypertension, cardiovascular disease and some cancers.
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PMID:[Long-term risks of polycystic ovaries syndrome]. 1512 16

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

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

The National Cholesterol Education Program's Adult Treatment Panel III identifies persons with multiple metabolic risk factors or "metabolic syndrome" as candidates for intensified therapeutic lifestyle changes. This article reviews the important role of weight reduction,diet, and exercise in improving the metabolic syndrome and its risk factors of abdominal obesity, impaired fasting glucose,dyslipidemia, and coagulation/inflammatory factors. The article also provides practical strategies.
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PMID:Focus on lifestyle change and the metabolic syndrome. 1526 93

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

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 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

The metabolic syndrome comprises an array of cardiovascular disease (CVD) risk factors such as abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Insulin resistance and/or increased abdominal (visceral) obesity have been suggested as potential etiological factors. More recently, increasing evidence has associated insulin resistance and subclinical inflammation involving cytokines derived from adipose tissue, or adipocytokines. Despite the fact that precise mechanisms have yet to be established, there is a significant role for both diet and physical activity to improve the many factors associated with the metabolic syndrome, including modulation of various adipocytokines. Although both diet and physical activity have been studied for their ability to modify cytokines in more traditional inflammatory conditions, such as rheumatoid arthritis, they have been less studied in relation to inflammation as an underlying cause of the metabolic syndrome and/or CVD. A more thorough understanding of the clustering of metabolic abnormalities and their underlying etiology will help to define diet and physical activity guidelines for preventing and treating the metabolic syndrome, an important aspect of CVD prevention. This paper will address potential underlying causes of the metabolic syndrome, with a focus on the putative mechanistic role of adipocytokines, and will discuss the impact of diet and physical activity on the metabolic syndrome.
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PMID:Metabolic syndrome, a cardiovascular disease risk factor: role of adipocytokines and impact of diet and physical activity. 1563 Jan 52


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