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

---

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

The effect of the angiotensin converting enzyme inhibitor enalapril on serum lipids, apolipoproteins, and lipoproteins was studied in 21 patients with mild essential hypertension. The drug was administered at a dosage of 2.5 to 10 mg daily for 12 weeks. Enalapril significantly decreased the very low-density lipoprotein (VLDL) fraction at eight and 12 weeks. The apolipoprotein (apo) A-I and A-II fractions were significantly increased by 10% and 7.8%, respectively, at 12 weeks. The apo B fraction and the apo B/apo A-I ratio were significantly decreased at eight weeks (8% and 17%, respectively) and at 12 weeks (11% and 19%, respectively). Unchanged were the total cholesterol level, the lipoprotein cholesterol level, the triglyceride level, apo C-II, apo C-III, apo E, and the apo A-I/apo A-II ratio. This study confirmed that enalapril is an effective antihypertensive drug with a favorable effect on the lipid profile.
...
PMID:Effects of enalapril on serum lipoproteins in mild essential hypertension. 254 8

Correspondence of fat intake with civilisatory diseases (coronary disease and cancer) is usually attributed to adverse effects of animal fat and cholesterol. The 'field studies' themselves, undertaken to support this theory, failed. As the last environmental changes in human history are agriculture and rise of carbohydrate intake (and concomitant reduction of fat and protein consumption), the author thinks that the carbohydrates rather than the animal fats cause our civilisatory diseases. It can be shown that the spread of agriculture from the Near East to the West and North of Europe with the accompanying differences in time for the adaptation to the new food (the carbohydrates) easily explains the geographic differences in the frequency of civilisatory diseases which is highest where (in Northern Ireland, Scotland and Finland) carbohydrates came last. Highest, too, in those areas is the 'polymorphism' of genes which are related to cardiovascular diseases (ACE, apolipoprotein-B etc.) This 'adaptation theory' explains also the hitherto unexplained up and down of cardiovascular disease in the USA by immigration from regions with higher adaptation to carbohydrates.
...
PMID:The colonisation of Europe and our Western diseases. 853 31

A single base deletion (211delG) in the low density lipoprotein receptor (LDLR) gene was shown to cause familial hypercholesterolaemia (FH) in a large family from Northern Ireland. Twenty-four of 52 family members tested had this mutation, 13 of which were newly diagnosed. Mutation-positive individuals had significantly higher mean total-cholesterol (TC) and LDL-cholesterol (LDL-C) than those without 211delG. LDL-C was a more accurate indicator of disease status than TC. When TC levels alone were considered, in individuals over 16 years, a false negative rate (TC < 7.5 mmol/l) of 40% was found; however this fell to 13% based on inclusion of LDL-C levels. Individuals with coronary artery disease (CAD) had significantly higher TC levels than those without CAD and tended to have tendinous xanthomas (TX) and corneal arcus (CA). Generic polymorphisms in the angiotensin converting enzyme (ACE) and apolipoprotein (apo) B genes did not appear to be associated with lipid levels or with the clinical severity of the disease; however, the apo E epsilon4 allele did show a lipid-raising effect in individuals with the mutation.
...
PMID:A novel single base deletion in the LDLR gene (211delG): Effect on serum lipid profiles and the influence of other genetic polymorphisms in the ACE, APOE and APOB genes. 864 75

Polymorphisms of 3 apolipoprotein genes Xba I apoB, Sstl apoCIII, and apoE and the insertion-deletion polymorphism of the angiotensin-converting enzyme gene (I/D ACE) and lipid levels were studied in a random sample of 403 children and adolescents aged 6 to 18 years living in St. Petersburg. The children were divided in 4 age groups with consideration for the relative body weight index: group 1.6 to 9 years; II, 10-12; III, 13-15; and IV, 16-18 years. The first three groups were divided by sex, the fourth was not because it was the smallest. Relationships between lipid levels and DNA polymorphisms of the above genes were analyzed in all groups. Effects of apoB Xbal, apoCIII Sstl, apoE, and ACE genotypes on the levels of the blood basic lipids were analyzed using Statgraphics software. A marked effect of the apoE (E3/E4) genotype on the total and LDL-cholesterol variability was observed in group IV. The individuals carrying the E4 apoE allele had increased levels of total and LDL-cholesterol (p < 0.02 and p < 0.03, respectively). The level of triglycerides was higher in the subjects carrying the S2 apoCIII allele in the third group (p < 0.04). A statistically reliable difference was however observed only in girls (p < 0.01). We failed to detect reliable correlations between lipid levels and various apoB and ACE genotypes. Hence, the genetic variants of apoCIII and apoE genes affect the blood lipid levels as early as in adolescence.
...
PMID:[DNA polymorphism in the region of APOB100, APOCIII, APOE, and angiotensin-converting enzyme genes and indicators of the lipid spectrum in children and adolescents in St. Petersburg]. 941 Dec 20

Coronary heart disease (CHD) has been considered as a multifactorial disorder with the involvement of both environmental and genetic factors. The advent of tools to investigate individual variability of DNA has allowed us to perform the association studies of candidate genes. However, an association between genetic trait and phenotypic variations is not easy to demonstrate and several reported association between genetic markers and risk factors or overt CHD have gone unconfirmed. It should not be assumed that for a given genetic trait, the impact on risk will be similar in all populations. In particular, most studies of the molecular bases of CHD have involved Caucasian subjects, so much more work with the Korean population is needed before genetic testing for susceptibility to CHD can be offered to Koreans as a clinical service. In this review, we discuss two aspects of the molecular bases of CHD: i) Molecular bases of the candidate gene related to lipoprotein metabolism including apolipoprotein AI-CIII-AIV gene duster, apolipoprotein B, apolipoprotein E-CI-CII gene cluster, apolipoprotein(a), LDL receptors, lipoprotein lipase, cholesteryl ester transfer protein, and apo B editing protein; ii) Molecular bases of the candidate gene related to thrombotic and other factors including fibrinogen, factor VII, plasminogen activator inhibitor 1, homocysteine, stromelysin, paraoxonase, and angiotensin converting enzyme. Studies involving the Korean population, especially those performed by our teams, are also summarized.
...
PMID:Molecular bases of coronary heart disease in Koreans. 953 12

Recent developments in molecular biological techniques allowed us to examine the genetic risk factors responsible for essential hypertension. The candidate gene approach revealed that several gene polymorphisms increase the relative risk for hypertension. Most genetic studies, however, examined only young subjects but not elderly ones. To examine the importance of gene polymorphisms in elderly hypertension, we carried out a case-control study and compared the odds ratio for hypertension between young (< 60) and elderly (> or = 60) subjects. The participants of this study were recruited from the outpatients of Osaka University Medical School with informed consent. We examined the following polymorphisms as candidates: the angiotensinogen (AGT/M235T), angiotensin converting enzyme (ACE I/D), angiotensin II type 1 (AT1/A1166C) and type 2 (AT2/C3123A) receptors, alpha-adducin (adducin/Gly460Trp), methylenetetrahydrofolate reductase (MTHHR/C677T), and apolipoprotein (apoE/epsilon 4, apoE/T-491A). In young subjects, the AGT/T235 allele significantly increased the odds ratio for hypertension but not in elderly subjects. In young males, the AT2/A3123 allele was also associated with hypertension but not in females or in elderly subjects. Other associations between polymorphism and hypertension did not reach a significant level. To sum up, it was revealed that some polymorphisms increase the susceptibility for hypertension but others do not, which suggests that there is heterogeneity in the genetic involvement of polymorphism due to aging.
...
PMID:[Genetic analysis of candidate gene polymorphisms in elderly hypertension]. 1055 62

Cardiovascular disease is the leading cause of death in patients receiving dialysis. This is attributed in part to the shared risk factors of cardiovascular disease and end-stage renal disease. The risk factors for coronary artery disease include the classic cardiac risk factors of diabetes mellitus, hypertension, dyslipidemia, and smoking. Also in this population, hyperparathyroidism, hypoalbuminemia, hyperhomocysteinemia, elevated levels of apolipoprotein (a), and the type of dialysis membrane may play a role. Management begins with risk factor modification and medical therapy including aspirin, beta blockers, angiotensin converting enzyme (ACE) inhibitors, and lipid-lowering agents. Revascularization is often important, and coronary artery bypass grafting appears to be preferable to percutaneous transluminal coronary angioplasty. This is especially true for those with multivessel disease, impaired left ventricular function, severe symptoms, or ischemia. Congestive heart failure is another common problem in dialysis patients. The management includes correction of underlying abnormalities, optimal dialysis, and medical therapy. Data obtained from the general population indicate obvious benefits from ACE inhibitors and beta blockers, and these agents would be considered the therapies of choice. Erythropoetin is also an essential component of therapy, but the ideal hemoglobin concentration has yet to be determined. Peritoneal dialysis may be helpful in severe cases of heart failure. Pericarditis is seen in less than 10% of dialysis patients and is best diagnosed by clinical examination and echocardiography. Intensive dialysis is often the best initial therapy. Pericardiocentesis is reserved for the setting of pericardial tamponade, but a pericardial window is more definitive.
...
PMID:Cardiac complications of end-stage renal disease. 1092 9

Familial hypercholesterolemia (FH) is the most common genetic disorder leading to premature atherosclerosis. Typically, it is due to mutations in the LDL receptor gene resulting in elevated total and LDL cholesterol levels. The type of the LDL receptor gene mutations may affect the severity of hypercholesterolemia and consequently the incidence of coronary atherosclerosis. Furthermore, high-density lipoprotein (HDL) cholesterol levels have been recently shown to be an independent risk factor for coronary heart disease in this population. We examined the effect of the type of the LDL receptor gene mutations and of common gene polymorphisms possibly affecting HDL metabolism [cholesterol ester transfer protein (CETP), apolipoprotein A-IV (ApoA-IV), angiotensin converting enzyme (ACE), and apolipoprotein E (ApoE)] on HDL cholesterol levels in patients with molecularly defined heterozygous FH who were attending our lipid clinic (n=84). The nature of the LDL receptor gene mutation (81T>G, n=12; 858C>A, n=13; 1285G>A, n=12; 1646G>A, n=22; and 1775G>A, n=25) did not significantly influence HDL cholesterol levels. Unlike other gene polymorphisms, the apolipoprotein (apo) E gene polymorphism did significantly affect these levels. In fact, the presence of the E4 allele was associated with lower HDL cholesterol levels compared to patients not carrying this allele. We conclude that HDL cholesterol levels in heterozygous FH patients may be affected by the apoE gene polymorphism.
...
PMID:HDL cholesterol levels in patients with molecularly defined familial hypercholesterolemia. 1184 18

The following seven polymorphic marker loci of genes responsible for predisposition to coronary atherosclerosis (CAS) were studied: the ACE locus responsible for angiotensin-converting enzyme insertion/deletion polymorphism for the presence or absence of the Alu insertion in the gene; the F13, PLAT, and APOA1 loci, controlling the clotting factor 13, plasminogen-activating tissue factor, and apolipoprotein A, respectively; the MTHFR and AGT polymorphic loci responsible for point mutations in methylenetetrahydrofolate reductase and those in angiotensinogen, respectively, and the NOS3 locus controlling the number of tandem repeats in the nitric oxide synthase gene. These loci are located on different chromosomes and encode products involved into various metabolic pathways leading to CAS. In the populations studied, significant differences between healthy subjects and patients predisposed to cardiovascular diseases were revealed with regard to the above seven markers. The 174M allele (T174M polymorphism in the ACE gene) was significantly associated with coronary atherosclerosis. It was found that specific gene combinations are involved in the CAS development and determine variation in the pathogenetically important quantitative traits.
...
PMID:[Analysis of gene complexes predisposing to coronary atherosclerosis]. 1196 67

Distributions of alleles at three apolipoprotein loci (APO E, APO H, and APO A-IV) and an insertion/deletion (I/D) polymorphism at the angiotensin converting enzyme (ACE) locus among 274 American Samoans are described here. Genotypes at each locus are examined for associations with quantitative lipid (total cholesterol (total-c), LDL-cholesterol (LDL-c), HDL-cholesterol (HDL-c), and triglycerides) and apolipoprotein (APO AI, APO AII, APO E, and APO B) levels. Genotype frequencies at all four loci are in Hardy-Weinberg equilibrium. The most common APO A-IV genotype (1-1) was observed in 252 American Samoans (97%). The three most common APO E genotypes were 3-3 (47%), 3-4 (30%), and 2-3 (12%). The most frequent APO H genotype was 2-2 (86%). The most common ACE genotype (I/I) was observed in 75% of sampled individuals, and 23% were I/D heterozygotes. APO E genotypic variation was associated with total-c, HDL-c, LDL-c, and all four quantitative apolipoproteins (AI, AII, E, and B). APO A-IV genotypes were associated significantly with total cholesterol, LDL-c, and APO-B levels. APO H showed little association with any quantitative lipid or apolipoprotein. ACE D/D homozygotes had higher AII levels. ACE showed a consistent association with APO AII levels, with either APO A-IV or APO E as a covariate. The interaction term between ACE and APO E was also significantly associated with total-c and APO E levels, and the ACE genotype showed a significant main effect on APO AI levels in multivariate analyses.
...
PMID:Population genetics of apolipoproteins A-IV, E, and H, and the angiotensin converting enzyme (ACE): associations with lipids, and apolipoprotein levels in American Samoans. 1525 64


1 2 Next >>

---