Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension in metabolic syndrome is common. Basic principles of therapeutic approach like decrease of body weight are discussed. Goal blood pressure levels are < or = 130/80mm Hg. ACE-inhibitors/AT1-blockers are considered drugs of choice. In most cases it is necessary to combine at least two drugs. Preferred combination is ACE-inhibitor/AT1-blocker + calcium channel blocker.
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PMID:[Treatment of hypertension in metabolic syndrome]. 1973 67

A total of 350 (184 males and 166 females) adults participated in the study. A sample of 138 individuals was selected randomly for genotyping. The synergistic effect of ACE (I/D) and ApoE (HhaI) on metabolic syndrome (MS) showed that individuals with e4/4+D/D combination had the highest occurrence of metabolic abnormalities.
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PMID:Synergistic effects of ACE (I/D) and ApoE (HhaI) gene polymorphisms among the adult Asian Indians with and without metabolic syndrome. 2041 72

Zofenopril, is a highly lipophilic ACE inhibitor, characterized by long-lasting tissue penetration and sustained cardiac ACE inhibition, indicated for the treatment of hypertension and myocardial infarction. Comparative studies with different antihypertensive drug classes have demonstrated the good efficacy and tolerability of this compound in the management of the patient with mild-moderate hypertension. Zofenopril may also be combined with hydrochlorothiazide, a combination which has proved to be effective and safe as compared with monotherapy with either agent in three studies, including more than 600 patients. In addition, recent post hoc analyses in high-risk patients, such as those with the metabolic syndrome, impaired fasting glucose or diabetes, atherogenic dyslipidemia, and impaired renal function, have confirmed the superiority of zofenopril 30 mg plus hydrochlorothiazide 12.5 mg once-daily combination as compared with zofenopril monotherapy also in these high-risk populations of patients with hypertension. These data suggest the usefulness of this fixed combination in the treatment of patients with hypertension requiring more prompt, intensive, and sustained blood pressure reduction, according to guidelines recommendation.
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PMID:Zofenopril plus hydrochlorothiazide fixed combination in the treatment of hypertension and associated clinical conditions. 1983 45

Metabolic syndrome (MetS) are consist of central obesity, diabetes, dyslipidemia and hypertension. Previous studies have reported possible association of migraine and MetS were reviewed. Migraine is a prevalent disabling disorder and have been regarded as an episodic and functional disorder. However, recent evidence suggests that in some cases, the disease may follow a chronic and progressive course. On the basis of available evidence, obesity is considered to be associated with migraine frequency and progression. The association between diabetes and migraine is unclear. Similarly, association of migraine with hypertension is also unclear. Female migraineurs commonly have an unfavorable cholesterol profile, i.e. one with high total cholesterol and low HDL levels. Obesity can be considered as a proinflammatory state in which increased inflammatory mediators, vascular hyperreactivity, plasma calcitonin gene-related peptide (CGRP) concentrations and decreased adiponectin concentrations are observed. These alterations can cause an increase in the frequency of migraine attacks developed of central sensitization, and thereafter, chronic migraine. Migraine and obesity may share some neurobiological abnormalities. Orexins modulate both pain and metabolism. Dysfunction in the orexin pathways seems to be a risk factor for both conditions. The methylene-tetrahydrofolate reductase (MTHFR) gene and the angiotensin converting enzyme (ACE) gene exhibit polymorphism. C677Tmutation in the MTHFR gene and the D-allele of the ACE gene are the shared risk factors for the development of migraine and cardiovascular disease. Certain beta-blockers, Ca blockers, ACE inhibitors, and angionten II receptor blocker (ARB) have excellent efficacy in migraine prophylaxis. The pharmacological mechanism of these agents do not seem to stand on their antihypertensive effect, but the other mechanism of action. Appropriate meal, sleep, and exercise are important for the management of MetS and migraine headaches.
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PMID:[Metabolic syndrome and prevention of migraine headache]. 1988 41

The metabolic syndrome was initially described as an insulin-resistance syndrome characterized by the clustering of metabolic traits such as high triglycerides, low high-density lipoprotein cholesterol, high blood pressure, abdominal obesity and different degrees of impaired glucose regulation. Although different definitions have been developed by various consensus groups, epidemiological studies demonstrate that they all associate the metabolic syndrome with a similar cardiometabolic risk, which is high for diabetes (ranging between three- and 20-fold), depending on the number of components and the inclusion of impaired fasting glucose, impaired glucose tolerance or both. The latter appear to indicate the failure of the beta cell to produce enough insulin to compensate for the increased demand due to insulin resistance. There is a hyperbolic relationship between insulin production and insulin sensitivity, which can be calculated by the disposition index. When this is altered there is a higher risk of developing Type 2 diabetes. There have been no clinical trials in subjects selected by the diagnosis of metabolic syndrome, but structured lifestyle changes have been tested in people with impaired fasting glucose/impaired glucose tolerance and have been able to reduce incident Type 2 diabetes by almost 50%, as long as a weight loss of at least 5% is achieved. Oral antidiabetic and anti-obesity drugs have also been successful to a lesser degree. Some fibrates have reduced or delayed incident diabetes. Extended-release niacin has a neutral effect and statins are controversial. ACE inhibitors and ARBs are the antihypertensive agents least associated with incident diabetes.
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PMID:Metabolic syndrome as a risk factor for diabetes. 2022 18

Obesity is fast becoming a bane for the present civilization, as a result of sedentary lifestyle, atherogenic diet, and a susceptible thrifty genotype. The concept of metabolic syndrome, which is a constellation of metabolic disturbances, has crystallized over the last 80 years with the aim of identifying those at greater risk of developing type 2 diabetes and cardiovascular disease. These patients have visceral obesity and insulin resistance characterized by hypertyriglyceridemia. Recently, it has been realized that they are also at an increased risk of chronic renal disease. Release of adipocytokines leads to endothelial dysfunction. There is also activation of systemic and local renin-angiotensin-aldosterone system, oxidative stress, and impaired fibrinolysis. This leads to glomerular hyperfiltration, proteinuria, focal segmental glomerulosclerosis (FSGS), and ultimately end-stage renal disease (ESRD). Treatment consists of lifestyle modifications along with optimal control of blood pressure, blood sugar and lipids. Metformin and thiazolidenidiones reduce insulin resistance; while angiotensin converting enzyme inhibitors and angiotensin receptor blockers reduce proteinuria and have a renoprotective effect. Exciting new medical therapies on the horizon include rimonabant a cannabinoid receptor type 1 antagonist, soy proteins, and peroxisome proliferator-activated receptor (PPAR) agonist. Bariatric surgery for morbid obesity has also been shown to be effective in treating metabolic syndrome.
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PMID:Metabolic syndrome and chronic kidney disease. 2036 11

The role of aldosterone has expanded from the hormone's genomic effects that involve renal sodium transport to nongenomic effects that are independent of the effect of aldosterone on sodium transport. The nongenomic effects of aldosterone to increase fibrosis, collagen deposition, inflammation, and remodeling of the heart and blood vessels, however, are markedly increased in the presence of high sodium intake. The genomic effect of aldosterone increases renal sodium transport, but the administration of large doses of aldosterone to normal individuals does not cause edema, relating to the phenomenon of "aldosterone escape"; however, in edematous disorders including cardiac failure, cirrhosis, and nephrotic syndrome, impaired aldosterone escape leads to renal sodium retention and edema formation. There is now considerable evidence for the nongenomic effects of aldosterone in several important diseases. Thus, low dosages of mineralocorticoid antagonists, with little or no effect on urinary sodium excretion, have been shown to afford a beneficial effect on morbidity and mortality in patients with advanced cardiac failure and after acute myocardial infarction. Three-drug-resistant hypertension has also been found to respond to spironolactone in modest dosages. The combination of an angiotensin converting enzyme inhibitor (ACEI) with spironolactone to treat such resistant hypertension may be more effective than adding an angiotensin receptor blocker to an ACEI. The role of spironolactone has also been shown to decrease albuminuria in chronic kidney disease including diabetic nephropathy in the presence of maximal dosages of ACEI. The effect of aldosterone in metabolic syndrome is also discussed in this review.
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PMID:Aldosterone: role in edematous disorders, hypertension, chronic renal failure, and metabolic syndrome. 2044 74

We assessed 850 patients with a history of myocardial infarction >1 month ago who attended outpatient clinics of the Clinic of Internal Medicine and Cardiology at the Faculty Hospital Brno between 1st September 2009 and 31st December 2009. There were more men (650 vs. 200) and patients under 70 years of age (576 vs. 264) in the cohort. 87.8% of patients experienced one myocardial infarction only and the mean age at the first infarction was 59.0 years in men and 65.5 in women (p < 0.001). 75.8% of patients had been prescribed all recommended pharmacotherapeutic groups according to guidelines (RAAS blockers, beta-blockers, statins, antiagregation agents) and each group individually was used in > 90% of patients. There were no differences between men and women and older and younger patients. ACE inhibitors and statins were not always prescribed in recommended (high) doses. Perindopril was the most frequently prescribed ACE inhibitor and atorvastatin the most frequently prescribed statin. Blood pressure of< 140/90 mm Hg was identified in 60.1% of patients, 75% of men and 65% of women had cholesterol level of <5 mmol/l and > 50% of patients had cholesterol < or = 4.5 mmol/l, metabolic syndrome was found in about 1/2 of patients and smoking was admitted by 12.5% of patients.
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PMID:[BRNO Register 2: post-myocardial infarction pharmacotherapy]. 2068 66

Adiponectin is an insulin-sensitizing and anti-inflammatory fat cell hormone that has immense potential as a therapeutic target for a multitude of obesity-associated diseases, including type 2 diabetes, NASH and atherosclerosis (Chandran M, Phillips SA, Ciaraldi T, Henry RR: Adiponectin: more than just another fat cell hormone?Diabetes Care 2003, 26:2442-2450). The adiponectin gene is located in chromosome 3q27, a susceptibility locus for T2DM and metabolic disorders (Saito K, Tobe T, Minoshima S, Asakawa S, Sumiya J, Yoda M, Nakano Y, Shimizu N, Tomita M: Organization of the gene for gelatin-binding protein (GBP28). Gene 1999, 229:67-73). Increased circulating levels of adiponectin are associated with improvement in the metabolic syndrome and reductions are strongly predictive of diabetes risk (Li S, Shin HJ, Ding EL, van Dam RM: Adiponectin levels and risk of type 2 diabetes: a systematic review and meta-analysis. JAMA 2009, 302:179-188. Extensive efforts have been made to understand how adiponectin levels can be elevated. The complex post-translational processing and secretion of adiponectin provides a rich area where pharmacologic manipulation may be developed to increase adiponectin levels in humans. Circulating adiponectin levels are increased by many commonly used drugs, such as statins, angiotensin converting enzyme (ACE) inhibitors, and thiazolidinediones (TZDs) providing an important opportunity to gain insight into the mechanisms underlying their effects. This review describes the cellular processes by which adiponectin is synthesized and secreted, current therapeutics known to affect this pathway and the potential for therapeutic manipulation in human subjects.
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PMID:Mechanisms of adiponectin regulation and use as a pharmacological target. 2081 Mar 17

In this study, we investigated the effect of a high n-3 fatty acid diet (eicosapentaenoic and docosahexaenoic acids) in Zucker obese and lean rats on blood pressure in association with physiological parameters, serum biochemistry and oxidative stress analysis. After 150 days of treatment, dietary fish oil supplementation in Zucker obese rats (9 months of age) reduces bodyweight gain and serum triglyceridemia and nitrite levels, increases serum glucose and angiotensin converting enzyme activity, but does not alter blood pressure, cholesterol levels and serum markers of oxidative stress (malondialdehyde, glutathione), compared to the Zucker rats fed control diet. According to these results, we can consider that after 150 days of treatment, fish oil is not enough to regulate parameters involved in the metabolic syndrome, such as cholesterolemia and blood pressure, in a 9 month-old genetically type-2 diabetes rat.
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PMID:No altered blood pressure and serum markers of oxidative stress after a long time dietary fish oil in the genetically 9 month-old type-2 diabetes Zucker rat. 2083 9


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