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)

The objective of the study was to evaluate the efficiency of lovastatin correction of dyslipidemia and impaired intravascular platelet activity (IPA) in patients with arterial hypertension (AH) concurrent with metabolic syndrome (MS). Eighteen patients were given lovastatin for a month. The time course of changes in anthropometric parameters, blood lipid spectrum, plasma and lipid peroxidation, antioxidative protectiveness of the liquid blood part and platelets, and IPA were assessed. The results were processed by Student's test and correlation analysis. Lovastin was ascertained to correct dyslipoproteinemia and peroxidation syndrome and to optimize the intrathrombocytic mechanisms responsible for their function regulation in patients with AH + MS. Lovastatin inhibits in vivo increased platelet activity. These effects may be stabilized during its use. Body weight loss and diminished insulin resistance in patients with AH concurrent MS require long use of lovastatin along with low-calorie diet and exercises.
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PMID:[Thrombocytic hemostasis in hypertensive patients with metabolic syndrome and its correction with lovastatin]. 1558 98

Despite meaningful progress in the identification of risk factors and the development of highly effective clinical tools, deaths from cardiovascular disease continue to increase worldwide. Sparked by an obesity epidemic, the metabolic syndrome and the rising incidence of type 2 diabetes have led to an upsurge of cardiovascular risk. Although pharmacologic treatments with the statin class of drugs have reduced cholesterol levels and lowered mortality rates, several large controlled clinical trials, including the Scandinavian Simvastatin Survival Study, the Cholesterol and Recurrent Events trial, the Air Force/Texas Coronary Atherosclerosis Prevention studies, and Long-term Intervention with Pravastatin in Ischemic Disease study, have indicated that cardiovascular events continue to occur in two thirds of all patients. Follow-up studies, such as the Heart Protection Study and the Pravastatin or Atorvastatin Evaluation and Infection Therapy/Thrombolysis In Myocardial Infarction-22 trials, reinforced these earlier results. Although therapy with gemfibrozil, a fibric acid derivative, showed reduced occurrence of cardiovascular events in the Helsinki Heart Study and the Veterans Affairs HDL Intervention Trial, results of other studies, e.g., the Bezafibrate Intervention Program and the Diabetes Atherosclerosis Intervention study, showed less encouraging results. Although lifestyle modifications, such as improved diet and increased exercise levels, benefit general health and the metabolic syndrome and insulin resistance in particular, most people continue to resist changes in their daily routines. Thus, physicians must continue to educate their patients regarding an optimal balance of drug therapy and personal behavior.
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PMID:The forgotten majority: unfinished business in cardiovascular risk reduction. 1619 35

Guidelines from the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) focus the need for the most intensive efforts to lower low-density lipoprotein cholesterol (LDL-C) in the patients at greatest risk of a major future clinical coronary heart disease event. Major clinical trials, such as Pravastatin or Atorvastatin Evaluation and Infection Therapy and the Heart Protection Study, demonstrated the value of lowering LDL-C levels in high-risk patients to well below the ATP III target of <100 mg/dL. In 2004, the NCEP writing group suggested that a more aggressive LDL-C goal of <70 mg/dL is an option when treating high-risk patients, particularly those with the presence of established cardiovascular disease plus major multiple risk factors (especially diabetes), severe and poorly controlled risk factors (ie, cigarette smoking), multiple criteria of the metabolic syndrome, or an acute coronary syndrome. With stricter targets, high-risk patients are less likely to achieve their cholesterol goals than lower risk patients. Recent large trials comparing rosuvastatin with other statin monotherapies have shown a greater LDL-C reduction and better attainment of goals with rosuvastatin. In addition, the MERCURY [Measuring Effective Reductions in Cholesterol Using Rosuvastatin Therapy] trials demonstrate that switching to rosuvastatin significantly increased the percentage of patients who achieved their ATP III LDL-C targets.
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PMID:Rising to the challenge of treating high-risk patients. 1704 74

The fermentation products of Monascus, especially those produced by solid-state fermentation of rice, have been used as food and health remedies for over 1000 years in China. Monascus rice products (MRPs) are currently being used as health foods in the United States and many Asian countries such as Japan, Taiwan, China, Korea, Thailand, the Philippines, and Indonesia. Many studies have shown that Monascus spp. produce commercially viable metabolites, including food colorants, cholesterol-lowering agents, and antibiotics. The most important bioactive compound isolated from Monascus is monacolin K, which is identical to the potent cholesterol-lowering, antiatherosclerotic drug lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. Several species of the genus Monascus also produce citrinin, a mycotoxin harmful to the hepatic and renal systems. Monacolin K and citrinin are polyketide fungal metabolites. The biosynthetic pathways leading to the formation of polyketides, including monacolin K and citrinin, have been elucidated in Aspergillus and Monascus. The concern for safety is, therefore, high for the development of MRPs as health foods. Other attractive applications for MRPs are likely, as supported by recent studies that indicate that MRPs contain other substances (flavonoids, polyunsaturated fats, phytosterols, pyrrolinic compounds, and others) with a wide variety of biological activities and pharmacological potentials. Their effects in lowering blood sugar and triacylglycerol while raising HDL-C are more pronounced than those of monacolin K alone. Beyond cholesterol lowering, MRP may also be an ideal candidate for the treatment of metabolic syndrome.
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PMID:Monascus rice products. 1790 Apr 98

Reciprocal relationships between endothelial dysfunction and insulin resistance suggest that therapies improving endothelial dysfunction will simultaneously improve insulin sensitivity and other metabolic parameters. However, previous studies with some statins either did not alter insulin sensitivity or promoted insulin resistance despite significant improvements in endothelial dysfunction and decreases in circulating pro-inflammatory markers. This may be due to pleiotropic or off-target effects of some statins to cause insulin resistance by diverse mechanisms unrelated to endothelial dysfunction. Indeed, there is evidence of other differential metabolic actions of distinct statins including effects on hydroxymethylglutaryl-CoA reductase inhibition, isoprotenoid synthesis, calcium release, glucose transport, insulin secretion, and/or insulin resistance. Pravastatin increases expression of adiponectin mRNA, enhances adiponectin secretion, increases plasma levels of adiponectin, and enhances insulin sensitivity in mice and humans. Clinical studies including large scale randomized controlled trials demonstrate potential differences between individual statins, with pravastatin promoting risk reduction for new onset of diabetes. Conversely, other statins including atorvastatin, rosuvastatin, and simvastatin all promote significant increase in this risk. Given the frequent concordance of metabolic diseases including diabetes, obesity, and metabolic syndrome with cardiovascular diseases associated with hyperlipidemia, it is important to understand the potential metabolic risks and benefits of therapies with distinct statins. In this review, we discuss these differential effects of statins on metabolic homeostasis and insulin sensitivity.
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PMID:Differential metabolic effects of distinct statins. 2113 Apr 54

Hypercholesterolemia and hypertension are among the most important risk factors for cardiovascular (CV) disease. They are also important contributors to metabolic diseases including diabetes that further increase CV risk. Updated guidelines emphasize targeted reduction of overall CV risks but do not explicitly incorporate potential adverse metabolic outcomes that also influence CV health. Hypercholesterolemia and hypertension have synergistic deleterious effects on interrelated insulin resistance and endothelial dysfunction. Dysregulation of the renin-angiotensin system is an important pathophysiological mechanism linking insulin resistance and endothelial dysfunction to atherogenesis. Statins are the reference standard treatment to prevent CV disease in patients with hypercholesterolemia. Statins work best for secondary CV prevention. Unfortunately, most statin therapies dose-dependently cause insulin resistance, increase new onset diabetes risk and exacerbate existing type 2 diabetes mellitus. Pravastatin is often too weak to achieve target low-density lipoprotein cholesterol levels despite having beneficial metabolic actions. Renin-angiotensin system inhibitors improve both endothelial dysfunction and insulin resistance in addition to controlling blood pressure. In this regard, combined statin-based and renin-angiotensin system (RAS) inhibitor therapies demonstrate additive/synergistic beneficial effects on endothelial dysfunction, insulin resistance, and other metabolic parameters in addition to lowering both cholesterol levels and blood pressure. This combined therapy simultaneously reduces CV events when compared to either drug type used as monotherapy. This is mediated by both separate and interrelated mechanisms. Therefore, statin-based therapy combined with RAS inhibitors is important for developing optimal management strategies in patients with hypertension, hypercholesterolemia, diabetes, metabolic syndrome, or obesity. This combined therapy can help prevent or treat CV disease while minimizing adverse metabolic consequences.
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PMID:Combining Potent Statin Therapy with Other Drugs to Optimize Simultaneous Cardiovascular and Metabolic Benefits while Minimizing Adverse Events. 2876 31