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

Arterial hypertension is a global public health problem owing to its high prevalence and association with increased risk for cerebral, cardiac and renal events. Hypertension frequently clusters with other cardiometabolic risk factors, such as dysglycemia, low levels of high-density lipoprotein cholesterol and high triglyceride levels. These, along with other factors such as central obesity, increased inflammation, endothelial dysfunction and thrombosis, are components of the metabolic syndrome. All guidelines recommend that the first-line therapy in metabolic syndrome should be based on lifestyle modification, consisting of diet and moderate exercise for at least 30 min/day. Concerning drug treatment of hypertension associated with other cardiometabolic risk factors, many results of head-to-head studies have demonstrated a reduction in new-onset Type 2 diabetes in hypertensive patients treated with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, when compared with conventional antihypertensive therapy. The explanations of the different actions of both these drugs include several mechanisms related to pancreatic insulin release and insulin sensitivity improvement. Another mechanism by which the inhibition of the renin-angiotensin system may improve insulin sensitivity is through the partial peroxisome proliferator-activated receptor-gamma agonism of telmisartan. For that reason, telmisartan has been considered by some experts to be an antihypertensive agent that is particularly useful in the treatment of hypertension associated with cardiometabolic risk factors. The impact of the promising metabolic action exhibited by telmisartan on the outcome of hypertensive patients aggregating other cardiometabolic risk factors waits for adequately randomized and powered clinical trials.
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PMID:Treatment of hypertension in individuals with the cardiometabolic syndrome: role of an angiotensin II receptor blocker, telmisartan. 1832 91

Adiponectin is an adipocyte hormone that links visceral adiposity with insulin resistance and atherosclerosis. It is unique among adipocyte-derived hormones in that its circulating concentrations are inversely proportional to adiposity, and low adiponectin concentrations predict the development of type 2 diabetes and cardiovascular disease. Consequently, in the decade since its discovery, adiponectin has generated immense interest as a potential therapeutic target for the metabolic syndrome and diabetes. This review summarizes current research regarding the regulation of circulating adiponectin concentrations by physiological, pharmacological, and nutritional factors, with an emphasis on human studies. In humans, plasma adiponectin concentrations are influenced by age and gender, and are inversely proportional to visceral adiposity. In vitro studies suggest that adiponectin production may be determined primarily by adipocyte size and insulin sensitivity, with larger, insulin-resistant adipocytes producing less adiponectin. While adiponectin concentrations are unchanged after meal ingestion, they are increased by significant weight loss, such as after bariatric surgery. In addition, adiponectin production is inhibited by a number of hormones, including testosterone, prolactin, glucocorticoids and growth hormone, and by inflammation and oxidative stress in adipose tissue. Smoking decreases, while moderate alcohol consumption increases, circulating adiponectin concentrations. Dietary fatty acid composition in rodents influences adiponectin production via ligand-activated nuclear receptors (PPARs); however, current evidence in humans is equivocal. In addition to PPAR agonists (such as thiazolidinediones and fibrates), a number of pharmacological agents (angiotensin receptor type 1 blockers, ACE inhibitors, and cannabinoid receptor antagonists) used in treatment of the metabolic syndrome also increase adiponectin concentrations in humans.
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PMID:Physiological, pharmacological, and nutritional regulation of circulating adiponectin concentrations in humans. 1851 Apr 34

Metabolic syndrome (MS), typified by hypertension, abdominal obesity, dyslipidaemia and impaired glucose metabolism, is a precursor of type 2 diabetes. Thiazide diuretics (TD) and beta-blockers are associated with increased risk of diabetes in patients with hypertension; however, the role of these agents in development of diabetes in MS patients is unknown. We reviewed the literature regarding risk factors for diabetes development and compared this with data from the Study of Trandolapril/Verapamil SR And Insulin Resistance (STAR), which investigated the effects of two fixed-dose combinations (FDCs) [trandolapril/verapamil SR and losartan/hydrochlorothiazide (L/H)] on glucose control and new diabetes in MS patients. In STAR, logistic regression modelling identified haemoglobin A1c [odds ratio (OR) 4.21 per 1% increment; p = 0.003), L/H treatment (OR 4.04; p = 0.002) and 2-h oral glucose tolerance test glucose levels (OR 1.39 per 10 mg/dl increments; p < 0.001) as baseline predictors of diabetes. These data support prior analyses and suggest that choice of antihypertensive agent is important. Patients with MS may be at lower risk of diabetes when using a FDC calcium channel blocker + angiotensin-converting enzyme inhibitor compared with an angiotensin receptor blocker + TD.
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PMID:Risk factor assessment for new onset diabetes: literature review. 1856 74

Pathogenesis of erectile dysfunction (ED) is related to endothelial dysfunction and therefore associated with cardiovascular risk factors. Patients with a combination of risk factors, as in metabolic syndrome, are thus likely to have an increased risk of developing endothelial and ED. The angiotensin receptor antagonist irbesartan has been shown to improve endothelial function in cardiovascular high-risk patients, which suggests a beneficial effect of treatment with irbesartan on ED. The aim of the present study was to determine the influence of irbesartan on ED in patients with a metabolic syndrome. A total of 1069 consecutive hypertensive patients with a metabolic syndrome from the Documentation of hypertension and metabolic syndrome in patients with Irbesartan Treatment survey were included. Patients were treated with irbesartan or the combination of irbesartan/hydrochlorothiazide for 6 months. ED was assessed using the international index of erectile function. The Cologne Evaluation Questionnaire of Erectile Dysfunction served as a control. Erectile function increased significantly (P<0.0001) after 6 months of treatment with irbesartan, irrespective of dosage and independent of additional treatment with hydrochlorothiazide. Prevalence of ED declined to 63.7% from 78.5% at baseline, along with a significant increase in orgasmic function (P<0.001) and intercourse satisfaction (P<0.001). Treatment with irbesartan alone, as well as in combination with hydrochlorothiazide is associated with an improvement of sexual desire, frequency of sexual contacts and erectile function in hypertensive patients with the metabolic syndrome. These results suggest a beneficial role of angiotensin receptor antagonists in the treatment of metabolic syndrome, and ED.
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PMID:Effect of irbesartan on erectile function in patients with hypertension and metabolic syndrome. 1859 5

The identification of patients at high risk for cardiovascular events is imperative in the reduction of cardiovascular mortality and morbidity. Although coronary artery disease, peripheral arterial disease, cerebrovascular disease, hypertension, and diabetes mellitus contribute to the risk of developing cardiovascular events, we are now faced with emerging fronts because of an increase in life expectancy and the epidemic of hypertension, obesity, metabolic syndrome, and diabetes. Recent data emphasize the beneficial role of renin-angiotensin-aldosterone system (RAAS) blockers. This article addresses the role of RAAS activation in the high-risk metabolic milieu and the role of angiotensin receptor blockers in targeting and inhibiting the RAAS for cardiovascular protection.
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PMID:Angiotensin receptor blockers: novel role in high-risk patients. 1892 28

Metabolic syndrome (MS), which is composed of such factors as hyperinsulinemia, insulin resistance, glucose intolerance, abdominal obesity, arterial hypertension, and dyslipidemia, contributes to accelerated development of atherosclerosis, coronary artery disease, and type 2 diabetes. It has thus become one of the major public-health challenges worldwide. The primary goal of its clinical management is to reduce the risk for cardiovascular diseases related to atherosclerosis, especially myocardial infarction, stroke, and peripheral vascular disease, and to lower the risk for type 2 diabetes. The fi rst stage in its successful preventive management is identification of the population at high risk of developing metabolic syndrome. The therapeutic approach to metabolic syndrome consists fi rst of all of lifestyle modification, i.e. the introduction of a low calorie diet, weight reduction, and regular physical activity. For people at high risk for cardiovascular diseases and type 2 diabetes as well as those with coronary artery disease and/or type 2 diabetes, pharmacological therapy should be considered. Pharmacological management must address the multipathological process of metabolic syndrome, with each component identified and properly treated. Current therapies for metabolic syndrome treat fi rst of all obesity, insulin resistance, dyslipidemia, and hypertension. The pharmacological agents most often suggested are those which increase insulin resistance (metformin and thiazolidinediones). Among the medications used in metabolic syndrome therapy are also fibrates and statins for atherogenic dyslipidemia and those lowering blood pressure, such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. This review presents the most important aspects of the prevention and treatment of patients with metabolic syndrome, including new therapeutic strategies.
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PMID:[Metabolic syndrome. Part III: its prevention and therapeutic management]. 1893 31

Nonalcoholic fatty liver disease (NAFLD) is a condition pathogenically linked to metabolic syndrome (MS) by insulin resistance (IR), and characterized by hepatic steatosis in the absence of significant alcohol use, hepatotoxicity, and/or other known liver diseases.The principles of NAFLD therapy target IR: the key point of MS. As the renin-angiotensin system (RAS) plays a central role in IR, and subsequently in NAFLD and nonalcoholic steatohepatitis (NASH), an attempt to block the deleterious effects of RAS overexpression seems a logical target. While many potential therapies tested in NASH target only the consequences of this condition, or try to "get rid" of excessive fat, angiotensin receptor blockers (ARBs) could act as an elegant tool for adequate correction of the various imbalances that act in harmony in NASH/NAFLD. Indeed, by inhibiting RAS we can improve the intracellular insulin signaling pathway, better control adipose tissue proliferation and adipokine production, and produce more balanced local and systemic levels of various cytokines. At the same time, by controlling the local RAS in the liver we might be able to prevent at least fibrosis and also slow down the vicious cycle that links steatosis to necroinflammation. By targeting the pancreatic effects of angiotensin we should be able to preserve an adequate insulin secretion and acquire a better metabolic balance.In our opinion there are two major advantages of ARBs that make them a possible therapeutic option for treating NASH and MS: their specific antihypertensive effect, and their impact on liver fibrosis. In light of this, and based on the current evidence (including existent human studies), we can speculate that some ARBs like telmisartan, candesartan, and losartan can be beneficial in treating NASH/NAFLD and its consequences, and further larger controlled clinical trials will bring consistent data into this field.
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PMID:Angiotensin receptor blockers in the treatment of NASH/NAFLD: could they be a first-class option? 1897 77

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are thought to possess cardioprotective, cerebroprotective, and nephroprotective properties. Both classes of agents can prevent or reverse endothelial dysfunction and atherosclerosis, thereby potentially reducing the risk of cardiovascular events. Such a reduction has been shown with angiotensin-converting enzyme inhibitors in patients with coronary artery disease, but no such data are scarce with angiotensin receptor blockers (Valsartan in Acute Myocardial Infarction study). Both angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been shown to reduce damage in target organs, such as the heart and kidney, and to decrease cardiovascular mortality and morbidity in patients with congestive heart failure. These drugs (especially angiotensin receptor blockers) may successfully prevent atrial fibrillation and play a protective role in metabolic syndrome. In some clinical settings, combined therapy angiotensin-converting enzyme inhibitors with angiotensin receptor blocker (double blockade of the renin-angiotensin- aldosterone system) may appear the most effective.
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PMID:On target to dual block RAS? 1914 53

Certain cardiovascular drugs have adverse effects on glucose homeostasis, which may lead to important long-term implications for increased risks of adverse outcomes. Thiazide diuretics, niacin, and beta-adrenergic blockers impair glucose homeostasis. However, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have demonstrated beneficial metabolic effects. The newer vasodilating beta-blocking agents and calcium antagonists appear to be metabolically neutral. These considerations, in addition to meticulous attention to blood pressure control and lifestyle changes, have the potential to beneficially modify glycemia and long-term risks. These considerations have particular importance in younger patients who may also have pre-diabetes or the metabolic syndrome and who are likely to require therapy over the course of decades.
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PMID:Cardiovascular therapies and associated glucose homeostasis: implications across the dysglycemia continuum. 1917 14

The pathological mechanisms of out-of-office hypertension (e.g., masked hypertension and workplace hypertension) have been remained unclear, but several mechanisms for this unique phenomenon have been proposed. Altered neurohumoral regulations, increased activity of sympathetic nerve and renin-angiotensin-system (RAS), and reduced baroreflex gain, coupled to a prolonged endothelial dysfunction, play an important role in out-of-office hypertension. Previous studies showed that angiotensin receptor blocker (ARB) reduced not only RAS but also sympathetic activity, and improved baroreflex as well asendothelial function, which suggested that ARB may be suitable for treating subjects with out-of-office hypertension. In the TROPHY (TRial Of Preventing HYpertension) study, it has been demonstrated that treatment with ARB reduced the risk of development of true hypertension from a pre-hypertensive state. Because there were close associations between pre-hypertension and out-of-office hypertension, especially in those with obesity and metabolic syndrome, this study may also provide an important information about the treatment strategy of out-of-office hypertension.
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PMID:[The clinical utility of angiotensin receptor blockers in out-of-office hypertension (masked hypertension, workplace hypertension, and home hypertension)]. 1934 44


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