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)

Obesity and hypertension are increasing medical problems in adolescents. We evaluated the association between being overweight-particularly abdominal fat-and having hypertension and assessed the contribution of the Trp64Arg beta3-adrenergic receptor gene variant. In a population-based study, we determined family history, anthropometric variables, and arterial blood pressure of 934 high school students, out of whom we selected 121 normotensive and 54 hypertensive students. Biochemical measurements included circulating renin and angiotensin-converting enzyme activities, leptin, glucose, insulin and lipid levels, and beta3-adrenergic receptor genotypes. We used Mann-Whitney U test, chi2-test, and Spearman rank-order correlation. In the total population, hypertension prevalence increased across the entire range of body mass index (BMI) percentiles. In the sample, hypertensive students showed higher BMI, waist-to-hip ratio, triglycerides, and insulin resistance and lower HDL-cholesterol than normotensive students did. Age- and sex-adjusted systolic arterial blood pressure was correlated with BMI, waist-to-hip ratio, insulin resistance, and leptin. Leptin was correlated with BMI and homeostasis model assessment method. We found no association among hypertension, BMI, and leptin levels with beta3-adrenergic receptor genotypes. Especially in girls, the waist-to-hip ratio was, however, suggestively higher in Arg64 variant carriers than in noncarriers, independent of hypertension. In fact, there was a significantly (p < 0.01) higher frequency of carriers of the Arg64 variant across the waist-to-hip ratio quartiles. In adolescents of European origin, hypertension is associated with an increased degree of obesity among other characteristics of the metabolic syndrome; the Trp64Arg variant of the beta3-adrenergic receptor gene may favor the central adiposity gain.
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PMID:Clinical features of the metabolic syndrome in adolescents: minor role of the Trp64Arg beta3-adrenergic receptor gene variant. 1473 55

Cardiovascular disease is a major cause of mortality in individuals with diabetes. Many factors, including hypertension, contribute to the high prevalence of CVD in this population. Hypertension occurs approximately twice as frequently in patients with diabetes compared with patients without diabetes. Conversely, recent data suggest that hypertensive persons are more likely to develop diabetes than normotensive persons. In addition, up to 75% of CVD in patients with diabetes may be attributed to hypertension, leading to recommendations for more aggressive blood pressure control (ie, < 130/85 mm Hg) in persons with coexistent diabetes and hypertension. Increasing obesity further contributes to both diabetes and hypertension and significantly increases CVD morbidity and mortality. Other important risk factors for CVD in these patients include atherosclerosis, dyslipidemia, microalbuminuria, endothelial dysfunction, platelet hyperaggregability, coagulation abnormalities, and diabetic cardiomyopathy. The current knowledge regarding these risk factors has been reviewed, placing special emphasis on the metabolic syndrome, hypertension, microalbuminuria, and the role of obesity in these disorders. Although not discussed in detail, it is acknowledged that both hygienic measures (weight loss and aerobic exercise) and treatment strategies that include aspirin, statins, INS sensitizers, and antihypertensive agents that reduce renin-angiotensin-aldosterone system activity have been shown to reduce inflammation, coagulation abnormalities, endothelial function, proteinuria, and in some cases reduce CVD and renal disease progression. Additional therapeutic agents are currently being developed specifically to improve INS sensitivity and other CVD risk factors that are components of the cardiometabolic syndrome.
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PMID:Insulin and insulin resistance: impact on blood pressure and cardiovascular disease. 1487 Oct 51

Obesity, currently affecting >20% of the adult population in most Western countries, is a major risk factor for the development of hypertension. Hypertension in obese patients is, in the majority of instances, further complicated by the concomitant presence of dyslipidemia and insulin resistance. The latter is reflected by derangement of glucose homeostasis, ranging from hyperinsulinemia to frank type 2 diabetes. Hypertension in obese patients is also associated with an increased risk for left ventricular hypertrophy, endothelial dysfunction, renal hyperfiltration, microalbuminuria, and elevated markers of inflammation. Sodium retention, volume expansion, and increased cardiac output are common findings in obese individuals. These changes are largely attributable to increased activity of the sympathetic nervous system and insufficient suppression of the renin-angiotensin system. Recent data show increased expression of angiotensin II-forming enzymes in adipose tissue, and increased activity of the renin-angiotensin system has recently been implicated in the development of insulin resistance and type 2 diabetes. Accordingly, antihypertensive agents that block the renin-angiotensin system might be a beneficial strategy for treatment of obesity-related hypertension. Both angiotensin-converting enzyme inhibitors and angiotensin type-1 receptor blockers have been associated with favorable metabolic properties and end-organ protection in addition to their antihypertensive effects. Data from ongoing large trials will provide an indication of the protective and preventive effects of these treatment strategies while offering insights into the mechanisms linking obesity, hypertension, and other facets of the metabolic syndrome.
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PMID:Is there a rationale for angiotensin blockade in the management of obesity hypertension? 1517 27

Hypertension is one of most important components of metabolic syndrome. Main etiology of metabolic syndrome is supposed to be due to insulin resistance. Insulin resistance/hyperinsulinemia induces blood pressure elevation by sodium retention, activation of sympathetic nervous system and renin-angiotensin system(RAS) and promotion of vascular cell growth. Moreover, activated RAS, actually angiotensin II, and salt intake lead insulin resistance by inhibiting insulin signaling. Our laboratory revealed the close relationship between the vascular RAS and the action of insulin on the vasculature. This section reviewed recent understandings about hypertension in metabolic syndrome focusing on its pathophysiologic mechanisms and antihypertensive therapy.
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PMID:[Hypertension]. 1520 48

Potentially important new findings have recently been reported concerning the so-called metabolic syndrome in relation to the renin-angiotensin system, ie, that treatment with inhibitors of the angiotensin-converting enzyme (ACE) not only decreases blood pressure levels but prevents the development of diabetes mellitus. The new findings described in this article highlight the potential role of the ACE system in the regulation of insulin sensitivity, thus contributing to the development of type 2 diabetes and metabolic syndrome. In addition to the well known selective effects of ACE inhibitors and angiotensin II receptor blockers in reducing microalbuminuria in diabetic patients, the potential ability of these drugs to reduce the risk of diabetes and the metabolic syndrome would support their use as first line agents not only in diabetic patients but also in selected groups of hypertensive patients, who are particularly at risk of developing metabolic complications. This information supports the Joint Guidelines for the Management of Arterial Hypertension by the European Society of Hypertension and the European Society of Cardiology, which highlight the crucial role of ACE inhibitors and the angiotensin II receptor blockers in preventing the development of diabetes in hypertensive patients.
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PMID:The role of the renin angiotensin hormonal system in the metabolic syndrome and type 2 diabetes. 1524 41

The metabolic syndrome (MetS) is strongly associated with insulin resistance and consists of a constellation of factors that raise the risk for cardiovascular diseases and diabetes mellitus. Therefore, the primary goals of treating MetS are prevention of type 2 diabetes and cardiovascular events. Three levels of intervention may be considered for individuals with MetS : 1) management of underlying risk conditions by controlling weight excess, enhancing regular physical exercise and promoting healthy diet; 2) management of individual risk factors such as dyslipidaemia, hypertension, hyperglycaemia and prothrombotic state; and 3) targeting insulin resistance by using specific insulin sensitizers such as thiazolidinediones. The most important therapeutic intervention effective in subjects with MetS should focus on modest weight reduction and regular leisure-time physical activities. Although lifestyle modification is the first-line therapy, drug therapy may be necessary in many patients to achieve recommended goals regarding lipid profile, blood pressure and blood glucose control. Rather than to use a magic bullet that might fully reverse the underlying cause of the syndrome, one appealing alternative would be to use a so-called "polypill" targeting each of the components of MetS. However, such a polypill should ideally contain numerous molecules that all have shown a potential interest for the management of MetS such as metformin, acarbose, a thiazolidinedione, a statin, a fibrate, an inhibitor of the renin-angiotensin system, aspirin. The growing prevalence and high-risk nature of MetS highlights the need to identify individuals with this condition and to treat them with an aggressive multitargeted approach.
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PMID:Management of the metabolic syndrome. 1525 54

Non-insulin-dependent diabetes mellitus (NIDDM) and the metabolic syndrome separately and additively increase the risk for atherosclerotic cardiovascular disease. Considering the high cardiovascular risk associated with NIDDM and the metabolic syndrome, aggressive therapy of dyslipidemia with tailored combination therapy should be considered given informed consent and discussion of risks. In addition to statins, niacin, and fibrates, therapies shown to decrease the risk for atherosclerotic cardiovascular disease include omega-3 fatty acids, diet, exercise, and optimal blood pressure control with thiazides and blockers of the renin-angiotensin system. These therapies should also be considered to reduce the high cardiovascular risk associated with NIDDM and the metabolic syndrome.
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PMID:Combination therapy of dyslipidemia in non-insulin-dependent diabetes mellitus and the metabolic syndrome. 1546 96

The hypothalamic-pituitary-adrenal (HPA) axis, like the sympathetic nervous system and the renin-angiotensin-aldosterone (RAA) system, sustains life in stressful situations by increasing vascular tone and ensuring fuel availability. It also modulates inflammation and tissue repair processes. Untoward cardiovascular effects of chronic sympathetic and RAA activation are well recognized, illustrating that the short-term benefit of the physiologic stress response can be detrimental in the long term. Similarly, chronic tissue exposure to glucocorticoids may lead to metabolic and vascular changes that accelerate vascular senescence. Specific situations associated with chronic activation of the HPA axis-such as major depression, inflammatory disease and perhaps the metabolic syndrome-may derive some of their associated cardiovascular risk from untoward glucocorticoid effects. Since there are no definitive clinical studies directly addressing the relationship between the HPA axis and cardiovascular disease, we present indirect evidence from two types of studies: (1) studies that examine the cardiovascular effects of exogenous glucocorticoids, and (2) studies demonstrating that endogenous glucocorticoid activity varies between individuals. The effects of physiologic increases in endogenous glucocorticoid activity may not always mirror the effects of supraphysiologic glucocorticoids. Nevertheless, the known effects of exogenous glucocorticoids provide important insights into the putative effects of endogenous glucocorticoids.
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PMID:Does altered glucocorticoid homeostasis increase cardiovascular risk? 1548 80

Large longitudinal studies showed the epidemiological link between obesity and hypertension. During last years, multiple possible mechanisms involved in this association were identified. Adipose tissue has an important role in the genesis of hypertension in obese patients through several pathways: insulin resistance, leptin, renin-angiotensin-aldosteron system and mediators of inflammation (TNF-alpha, IL-6). Adipocyte may be the major player in the development of insulin resistance and hypertension, elements of the metabolic syndrome, responsible for the cardiovascular complications.
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PMID:Hypertension in obese patients: a dysmetabolic hypertension with a possible adipocyte dysfunction mechanism. 1552 95

The relationship between dietary salt, blood pressure, and risk for cardiovascular disease has been debated for decades. Microalbuminuria is a biomarker for both cardiovascular and kidney disease. The presence of microalbuminuria correlates directly with the risk for myocardial infarction and stroke and indicates individuals at risk for the development of progressive kidney disease. Since patients with the metabolic syndrome, diabetes, or chronic kidney disease often are blood pressure salt sensitive, and it is well known that increasing dietary salt may offset both the antihypertensive and antiproteinuric effects of renin-angiotensin system blocking drugs, physicians must consider increased salt intake as a potential modifiable risk factor for progression of chronic kidney disease and possibly even cardiovascular disease.
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PMID:Dietary salt, blood pressure, and microalbuminuria. 1553 8


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