PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17941464-12 2007 In carriers of DD ACE genotype blood pressure and HDL-cholesterol serum concentrations were higher than in patients with II polymorphism. Cholesterol 54-65 angiotensin I converting enzyme Homo sapiens 18-21 19456900-6 2009 CONCLUSION: Female ACE I/I homozygotes have higher liver fibrosis scores in comparison to D/* women and to men; moreover, they are leaner and have a lower LDL/HDL cholesterol ratio. Cholesterol 163-174 angiotensin I converting enzyme Homo sapiens 19-22 18516470-7 2008 In subjects with a family history of hypertension and presenting 90 kDa ACE, there were lower levels of HDL-cholesterol (P < 0.05) and higher levels of triglycerides (P < 0.05). Cholesterol 108-119 angiotensin I converting enzyme Homo sapiens 72-75 18516470-8 2008 Subjects with 90 kDa ACE irrespective of hypertensive history presented a trend for higher levels of triglycerides and HDL-cholesterol (P = 0.06) compared to subjects without 90 kDa ACE. Cholesterol 123-134 angiotensin I converting enzyme Homo sapiens 21-24 24026142-11 2014 Cholesterol level decreased by 0.95 mmol/L in the ACE-I group and 1.02 mmol/L in the ARB group (ns). Cholesterol 0-11 angiotensin I converting enzyme Homo sapiens 50-53 22307319-0 2012 Angiotensin converting enzyme gene polymorphism is associated with severity of coronary artery disease in men with high total cholesterol levels. Cholesterol 126-137 angiotensin I converting enzyme Homo sapiens 0-29 22307319-8 2012 These results suggest that men who carry ACE c.2306-117_404 DD genotype and have high total cholesterol, high LDL cholesterol and low HDL cholesterol levels may be predisposed to the development of more severe CAD. Cholesterol 92-103 angiotensin I converting enzyme Homo sapiens 41-44 22307319-8 2012 These results suggest that men who carry ACE c.2306-117_404 DD genotype and have high total cholesterol, high LDL cholesterol and low HDL cholesterol levels may be predisposed to the development of more severe CAD. Cholesterol 114-125 angiotensin I converting enzyme Homo sapiens 41-44 22307319-8 2012 These results suggest that men who carry ACE c.2306-117_404 DD genotype and have high total cholesterol, high LDL cholesterol and low HDL cholesterol levels may be predisposed to the development of more severe CAD. Cholesterol 114-125 angiotensin I converting enzyme Homo sapiens 41-44 22227126-4 2012 Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis [angiotensinogen, renin, angiotensin-converting enzyme (ACE)], degradation (ACE2), or responsiveness (angiotensin II type 1 receptors, Mas receptors) to angiotensin peptides in cell types (e.g., pancreatic islet cells, adipocytes, macrophages) that mediate specific disorders of the metabolic syndrome. Cholesterol 51-62 angiotensin I converting enzyme Homo sapiens 173-202 22227126-4 2012 Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis [angiotensinogen, renin, angiotensin-converting enzyme (ACE)], degradation (ACE2), or responsiveness (angiotensin II type 1 receptors, Mas receptors) to angiotensin peptides in cell types (e.g., pancreatic islet cells, adipocytes, macrophages) that mediate specific disorders of the metabolic syndrome. Cholesterol 51-62 angiotensin I converting enzyme Homo sapiens 204-207 21863747-1 2011 Statins and angiotensin-converting enzyme (ACE) inhibitors have beneficial impact on the serum cholesterol and blood pressure. Cholesterol 95-106 angiotensin I converting enzyme Homo sapiens 12-41 21863747-1 2011 Statins and angiotensin-converting enzyme (ACE) inhibitors have beneficial impact on the serum cholesterol and blood pressure. Cholesterol 95-106 angiotensin I converting enzyme Homo sapiens 43-46 21216861-9 2011 If abnormal UAE values are high and persist for >1 year, only long-lasting treatment with ACE inhibitors seems able to induce persistent remission, especially when associated with good metabolic control and high HDL cholesterol levels. Cholesterol 219-230 angiotensin I converting enzyme Homo sapiens 93-96 17168204-0 2006 [The relationship between ACE I/D polymorphism and HDL cholesterol]. Cholesterol 55-66 angiotensin I converting enzyme Homo sapiens 26-29 17168204-4 2006 RESULTS: Statistical differences in high-density lipoprotein (HDL) cholesterol levels according to ACE genotype were observed using ANOVA (p<0.05), but no differences were found in other cardiovascular risk factors. Cholesterol 67-78 angiotensin I converting enzyme Homo sapiens 99-102 17168204-6 2006 CONCLUSIONS: In men, the D-allele of the ACE I/D polymorphism was significantly associated with reduced HDL cholesterol levels. Cholesterol 108-119 angiotensin I converting enzyme Homo sapiens 41-44 17168204-7 2006 In the future, larger studies are needed to confirm this relationship between ACE I/D polymorphism and HDL cholesterol. Cholesterol 107-118 angiotensin I converting enzyme Homo sapiens 78-81 17044652-8 2006 Multivariate logistic regression analysis showed that the ACE DD genotype was a risk factor for T2DM, with the OR of 2.35 (95% CI 1.17-4.71) adjusted for age, sex, BMI, WHR, blood pressure, and serum cholesterol levels. Cholesterol 200-211 angiotensin I converting enzyme Homo sapiens 58-61 16490688-9 2006 The changes in glycohemoglobin A1 (GHbA1) levels and HDL cholesterol were significantly associated with the ACE I/D polymorphism. Cholesterol 57-68 angiotensin I converting enzyme Homo sapiens 108-111 15759455-7 2005 Serum ACE activity depends on concentration of total cholesterol (TC) and triglycerides. Cholesterol 53-64 angiotensin I converting enzyme Homo sapiens 6-9 16078597-5 2005 After administration of ACE inhibitors in doses lowering arterial pressure not higher than 130/80 mm Hg and statins reducing serum cholesterol nitric residues stopped accumulating while serum creatinine went down after 5 months of the combined treatment. Cholesterol 131-142 angiotensin I converting enzyme Homo sapiens 24-27 16415489-5 2005 Originally, ACE-I and statins were introduced to clinical medicine to lower arterial blood pressure or to lower blood LDL cholesterol levels, respectively. Cholesterol 122-133 angiotensin I converting enzyme Homo sapiens 12-17 12658909-10 2003 CONCLUSION: The present study showed that the interaction between the DD genotype of angiotensin-converting enzyme and chronic hyperglycaemia (expressed by HbA1c level) is related to higher plasma levels of atherogenic lipoproteins, such as apoB and cholesterol, in patients with Type 2 diabetes. Cholesterol 250-261 angiotensin I converting enzyme Homo sapiens 85-114 15646128-4 2004 The maximal ACE activity was observed at a concentration of total cholesterol of 9.41 mM/l and at a concentration of triglycerides of 3.05 mM/l. Cholesterol 66-77 angiotensin I converting enzyme Homo sapiens 12-15 12624008-5 2003 Bivariate analyses revealed that ACE activity was genetically correlated (rhoG) with LDLC response (LDLCRC) to a high-cholesterol diet (rhoG=0.30+/-0.13, P=0.01) but not to LDLC on a basal diet (rhoG=0.08+/-0.13). Cholesterol 118-129 angiotensin I converting enzyme Homo sapiens 33-36 15646128-3 2004 The ACE activity in blood serum was found to depend on a concentration of total cholesterol and of triglycerides. Cholesterol 80-91 angiotensin I converting enzyme Homo sapiens 4-7 11575216-15 2001 Conversely to BB and AAII, the use of ACE and non-DHP CA increases with presence of diabetes and cholesterol increase. Cholesterol 97-108 angiotensin I converting enzyme Homo sapiens 38-41 11896508-2 2002 ACE inhibitors and calcium channel blockers (CCBs) reduce MA and are neutral on total cholesterol and triglycerides. Cholesterol 86-97 angiotensin I converting enzyme Homo sapiens 0-3 11896508-12 2002 CONCLUSION: These data support the concept that ACE inhibition with B reduces the atherogenic profile by decreasing Lp(a) and increasing HDL-cholesterol, the latter being correlated with reductions in MA. Cholesterol 141-152 angiotensin I converting enzyme Homo sapiens 48-51 12032106-1 2002 OBJECTIVE: Because ACE insertion/deletion (I/D) polymorphism has been shown to be associated with diabetes, hypertension, coronary artery diseases, and diabetic nephropathy, and because plasma ACE concentration has been found to be associated with plasma triglyceride and total cholesterol levels in patients with type 2 diabetes, the goal of this study was to investigate whether ACE gene I/D polymorphism is associated with metabolic syndrome in Chinese subjects with type 2 diabetes. Cholesterol 278-289 angiotensin I converting enzyme Homo sapiens 19-22 12032106-1 2002 OBJECTIVE: Because ACE insertion/deletion (I/D) polymorphism has been shown to be associated with diabetes, hypertension, coronary artery diseases, and diabetic nephropathy, and because plasma ACE concentration has been found to be associated with plasma triglyceride and total cholesterol levels in patients with type 2 diabetes, the goal of this study was to investigate whether ACE gene I/D polymorphism is associated with metabolic syndrome in Chinese subjects with type 2 diabetes. Cholesterol 278-289 angiotensin I converting enzyme Homo sapiens 193-196 12032106-1 2002 OBJECTIVE: Because ACE insertion/deletion (I/D) polymorphism has been shown to be associated with diabetes, hypertension, coronary artery diseases, and diabetic nephropathy, and because plasma ACE concentration has been found to be associated with plasma triglyceride and total cholesterol levels in patients with type 2 diabetes, the goal of this study was to investigate whether ACE gene I/D polymorphism is associated with metabolic syndrome in Chinese subjects with type 2 diabetes. Cholesterol 278-289 angiotensin I converting enzyme Homo sapiens 193-196 12898814-3 2002 The goal of our research was to assess the association of ACE gene I/D polymorphism with myocardial infarction in Polish population regarding different variables related to the disease (smoking, concomitant hypertension, obesity, plasma cholesterol level and family history). Cholesterol 237-248 angiotensin I converting enzyme Homo sapiens 58-61 12020174-15 2002 It is possible that results from on-going trials such as Women"s Atovarstatin Trial on Cholesterol (WATCH) will shed more light on ACE inhibitor and aspirin interaction in the future. Cholesterol 87-98 angiotensin I converting enzyme Homo sapiens 131-134 7773733-1 1995 Recent reports have shown that the frequency of the homozygous deletion genotype (DD) of the angiotensin-converting enzyme (ACE) gene is highly associated with myocardial infarction and cardiomyopathy, particularly in those considered to be at low risk for coronary heart disease (CHD) on the basis of their apoB or LDL cholesterol concentrations. Cholesterol 320-331 angiotensin I converting enzyme Homo sapiens 93-122 10488952-0 1999 The D allele of the angiotensin-converting enzyme gene contributes towards blood LDL-cholesterol levels and the presence of hypertension. Cholesterol 85-96 angiotensin I converting enzyme Homo sapiens 20-49 8866203-0 1996 Angiotensin converting enzyme polymorphism is associated with severity of coronary heart disease and serum lipids (total cholesterol and triglycerides levels) in Japanese patients. Cholesterol 121-132 angiotensin I converting enzyme Homo sapiens 0-29 8761013-7 1996 In addition, multiple regression analysis with a forward elimination procedure showed that only the ACE genotype was associated with RI of arcuate arteries (R2 = 0.24, p < 0.01) among the parameters of sex, age, IDDM duration, body mass index, HbA1c, plasma glucose levels, serum levels of total cholesterol and creatinine, urinary albumin excretion index, mean blood pressure and ACE genotype. Cholesterol 299-310 angiotensin I converting enzyme Homo sapiens 100-103 11054622-10 2000 The ACE gene genotypes appeared to be significant predictors for plasma PAI-1 antigen, tPA antigen, fibrinogen, D -dimer, and vWF even after adjustment for age, sex, body mass index, triglyceride and cholesterol levels, and blood pressure. Cholesterol 200-211 angiotensin I converting enzyme Homo sapiens 4-7 10962519-7 2000 ACE inhibitors decreased total cholesterol, triglycerides, apoprotein B and LpE:B; and this effect remained after multivariate adjustment. Cholesterol 31-42 angiotensin I converting enzyme Homo sapiens 0-3 10962519-10 2000 Antihypertensive treatment with beta-blockers decreases HDL parameters, whereas treatment with ACE inhibitors appears to decrease total cholesterol and LDL-related parameters. Cholesterol 136-147 angiotensin I converting enzyme Homo sapiens 95-98 10642275-12 2000 Our results suggest that an increased plasma LDL cholesterol level may induce increased arterial chymase and ACE activity. Cholesterol 49-60 angiotensin I converting enzyme Homo sapiens 109-112 10948701-3 1999 Angiotensin converting enzyme gene DD genotype associated with type 2 diabetes in overweight and obese patients and patients with normal total plasma cholesterol. Cholesterol 150-161 angiotensin I converting enzyme Homo sapiens 0-29 10221351-7 1999 Angiotensin-converting enzyme (ACE) activity in the thoracic aorta in the high-cholesterol-diet group was significantly higher than that in the normal-diet group, and the ACE activities in the alacepril groups were lower than that in the high-cholesterol-diet group. Cholesterol 79-90 angiotensin I converting enzyme Homo sapiens 0-29 10221351-7 1999 Angiotensin-converting enzyme (ACE) activity in the thoracic aorta in the high-cholesterol-diet group was significantly higher than that in the normal-diet group, and the ACE activities in the alacepril groups were lower than that in the high-cholesterol-diet group. Cholesterol 79-90 angiotensin I converting enzyme Homo sapiens 31-34 10221351-7 1999 Angiotensin-converting enzyme (ACE) activity in the thoracic aorta in the high-cholesterol-diet group was significantly higher than that in the normal-diet group, and the ACE activities in the alacepril groups were lower than that in the high-cholesterol-diet group. Cholesterol 243-254 angiotensin I converting enzyme Homo sapiens 0-29 9920000-7 1998 CONCLUSION: We hypothesize that differences in the frequency of the ACE DD genotype in populations with low mean serum cholesterol concentrations may play some part in determining interethnic differences in CHD mortality rates. Cholesterol 119-130 angiotensin I converting enzyme Homo sapiens 68-71 9591757-11 1998 In all subjects, plasma ACE levels were associated weakly with plasma triglyceride (partial r=.20, P < .01) and total cholesterol (partial r=.13, P <.03) concentrations, but not with fasting plasma insulin or PAI-1 activity. Cholesterol 121-132 angiotensin I converting enzyme Homo sapiens 24-27 7773733-1 1995 Recent reports have shown that the frequency of the homozygous deletion genotype (DD) of the angiotensin-converting enzyme (ACE) gene is highly associated with myocardial infarction and cardiomyopathy, particularly in those considered to be at low risk for coronary heart disease (CHD) on the basis of their apoB or LDL cholesterol concentrations. Cholesterol 320-331 angiotensin I converting enzyme Homo sapiens 124-127 7752591-11 1995 ACE inhibitors may have a modest cholesterol lowering effect in diabetic patients mediated, in part, through the decline in albuminuria. Cholesterol 33-44 angiotensin I converting enzyme Homo sapiens 0-3 7479254-9 1995 In this last group, in addition, the positive correlation was present between ACE activity values and total cholesterol levels (r = 0.86, p < 0.001). Cholesterol 108-119 angiotensin I converting enzyme Homo sapiens 78-81 7479254-10 1995 Correlation between ACE activity and total cholesterol level was ascertained in patients with LDL hypercholesterolemia over 200 mg% too (r = 0.81, p < 0.01). Cholesterol 43-54 angiotensin I converting enzyme Homo sapiens 20-23 8907209-8 1995 The ACE genotype was only an independent predictor of the progression of CHD in patients whose LDL cholesterol had been substantially reduced with diet and cholestyramine. Cholesterol 99-110 angiotensin I converting enzyme Homo sapiens 4-7 7852538-8 1995 However, serum high density lipoprotein cholesterol, high density lipoprotein subfraction 3 cholesterol, and apolipoprotein-A-I and -A-II were inversely associated with ACE activity in women with syndrome X, but not in controls. Cholesterol 40-51 angiotensin I converting enzyme Homo sapiens 169-172 7965277-2 1994 EXPERIMENTAL STUDIES: In studies of experimental atherosclerosis involving hypertensive and normotensive hyperlipidemic animals, ACE inhibitors have had potent anti-atherogenic effects, reducing the total aortic intimal surface involved and the aortic cholesterol content. Cholesterol 252-263 angiotensin I converting enzyme Homo sapiens 129-132 8285181-2 1993 Our recent data show that in patients with proteinuric renal disease, serum levels of total cholesterol and lipoprotein(a) [Lp(a)] may be lowered during treatment with an ACE inhibitor, fosinopril sodium. Cholesterol 92-103 angiotensin I converting enzyme Homo sapiens 171-174 34421038-4 2021 There were also statistically significant monotonic increases in risk with worsening ACE score for all chronic diseases except hypertension, cancer, and high cholesterol. Cholesterol 158-169 angiotensin I converting enzyme Homo sapiens 85-88 8355471-10 1993 ACE inhibition resulted in a 40% reduction of proteinuria, a partial normalization of LCAT activity, and a decrease in VLDL and LDL cholesterol. Cholesterol 132-143 angiotensin I converting enzyme Homo sapiens 0-3 8449471-7 1993 Via an improvement in glucose tolerance, ACE-inhibitors can contribute to a lowering of triglyceride concentrations and an increase in the HDL cholesterol levels. Cholesterol 143-154 angiotensin I converting enzyme Homo sapiens 41-44 33790999-10 2021 The D allele of ACE I/D was associated with high levels of total cholesterol and low-density lipoprotein cholesterol (LDL-C). Cholesterol 65-76 angiotensin I converting enzyme Homo sapiens 16-19 2670218-3 1989 Angiotensin-converting enzyme (ACE) inhibitors are lipid neutral and associated with few metabolic side effects, and may be considered over agents that cause adverse effects on such parameters as serum cholesterol, glucose, potassium, and uric acid levels. Cholesterol 202-213 angiotensin I converting enzyme Homo sapiens 0-29 2670218-3 1989 Angiotensin-converting enzyme (ACE) inhibitors are lipid neutral and associated with few metabolic side effects, and may be considered over agents that cause adverse effects on such parameters as serum cholesterol, glucose, potassium, and uric acid levels. Cholesterol 202-213 angiotensin I converting enzyme Homo sapiens 31-34 32356512-7 2020 ACE I/D genotypes were associated with dyslipidemia; AGT M235T genotypes with dyslipidemia and total cholesterol. Cholesterol 101-112 angiotensin I converting enzyme Homo sapiens 0-3 33363465-8 2020 Notably, our results identified ACE/ACE2-ATR1-Cholesterol-HDAC axis signals that also matched with some available clinical data. Cholesterol 46-57 angiotensin I converting enzyme Homo sapiens 32-35 31430320-12 2019 The D allele of ACE showed association with altered levels of lipid profile variables on case group (VLDL-cholesterol, p = 0.01) and DD genotype in all individuals analysis (triglycerides, p = 0.01 and VLDL-cholesterol, p = 0.01). Cholesterol 106-117 angiotensin I converting enzyme Homo sapiens 16-19 31430320-12 2019 The D allele of ACE showed association with altered levels of lipid profile variables on case group (VLDL-cholesterol, p = 0.01) and DD genotype in all individuals analysis (triglycerides, p = 0.01 and VLDL-cholesterol, p = 0.01). Cholesterol 207-218 angiotensin I converting enzyme Homo sapiens 16-19 27050505-13 2016 Total and HDL cholesterol were statistically significant for DD genotype of ACE gene (OR = 1.42, 95% CI = 0.72-2.81). Cholesterol 14-25 angiotensin I converting enzyme Homo sapiens 76-79 26483160-8 2016 CONCLUSION: The children having both ACTN3 RR or RX genotype and ACE DD genotype showed high systolic blood pressure and low blood HDL cholesterol level, which may be considered a high-risk in metabolic syndrome. Cholesterol 135-146 angiotensin I converting enzyme Homo sapiens 65-68