Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate whether circulating endothelin-1 (Et-1) may be related to the increased incidence and severity of ischaemic heart disease in type 2 diabetes mellitus, we compared the concentrations in type 2 diabetic patients and in non-diabetic patients with coronary artery disease (CAD) angiographically documented. Plasma levels of Et-1 were determined in 34 type 2 diabetic patients with CAD (16 with stable angina, 6 with unstable angina, 12 with previous myocardial infarction) and in 19 nondiabetic patients with CAD (4 with stable angina, 5 with unstable angina, 10 with previous myocardial infarction). Fifteen diabetic patients without CAD and 9 healthy volunteers served as control subjects. In the type 2 diabetic patients, the mean Et-1 levels were 3.19 +/- 1.61 pmol/l in those with stable angina, 3.58 +/- 1.92 pmol/l in those with unstable angina, 4.24 +/- 2.53 pmol/l in those with myocardial infarction. These values were not significantly different one another, nor from the values obtained from type 2 diabetic controls (3.64 +/- 2.13 pmol/l). In the non-diabetic patients, the mean Et-1 levels were 3.92 +/- 0.73 pmol/l in those with stable angina, 4.35 +/- 1.67 pmol/l in those with unstable angina, 4.33 +/- 1.66 pmol/l in those with myocardial infarction. These values were not significantly different one another, but significantly higher than those obtained from healthy controls (2.07 +/- 0.67 pmol/l; P < 0.001). No significant differences were found in Et-1 levels between diabetic and non-diabetic patients with stable, unstable angina and previous myocardial infarction. In contrast, a statistically significant difference was found in Et-1 levels between diabetic and non-diabetic control subjects (P < 0.05). In conclusion, similar raised concentrations of Et-1 in diabetic and non-diabetic patients with stable, unstable angina and previous myocardial infarction do not support the hypothesis that higher levels of Et-1 in diabetic patients are responsible for the increased incidence of CAD in diabetes mellitus. However, the raised Et-1 levels found in diabetic patients in the absence of CAD strongly suggest that a generalised endothelial dysfunction, documented in our study by increased levels of Et-1, most probably precedes subsequent cardiovascular diseases.
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PMID:Circulating endothelin-1 levels in type 2 diabetic patients with ischaemic heart disease. 890 34

The prevalence of coronary heart disease (CHD) and its risk factors in first-generation Asian Indian immigrants to the United States of America (US) were compared with those of the native Caucasian population. A total of 1688 Asian Indian physicians and their family members (1131 men and 557 women, age > or = 20 years) completed a questionnaire and in 580 subjects serum lipoproteins were determined. The age-adjusted prevalence of myocardial infarction and/or angina was approximately three times more in Asian Indian men compared to the Framingham Offspring Study (7.2% versus 2.5%; P < 0.0001) but was similar in women (0.3% versus 1%; p = 0.64). Asian Indians had higher prevalence of noninsulin-dependent diabetes mellitus (NIDDM; 7.6% versus 1%; p < 0.0001) but markedly lower prevalence of cigarette smoking (1.3% versus 27%; p < 0.0001) and obesity (4.2% versus 22%; p < 0.0001). Hypertension was less prevalent in Asian Indian men 14.2% versus 19.1%, p < 0.008) but similar in women (11.3% versus 11.4%). The prevalence of elevated total a low-density lipoprotein (LDL) cholesterol levels was similar in men [17% versus 23.4% (p = 0.24) and 13.7% versus 22.3% (p = 0.22), respectively] but lower in women [15% versus 26.1% (p = 0.018) and 14.3% versus 19.6% (p = 0.047) respectively]. The mean levels of high-density lipoprotein (HDL) cholesterol were less in younger (30-39 years) Asian Indian men (mean: 0.98 versus 1.18 mmol/l; p < 0.001) and middle-aged (30-59 years) women (mean: 1.24 versus 1.45 mmol/l; p < 0.001). The prevalence of hypertriglyceridaemia was similar in men (18.5% versus 11.3%), but higher in Asian Indian women (8.3% versus 4.1%, p = 0.02). To conclude, immigrant Asian Indian men to the US have high prevalence of CHD, NIDDM, low HDL cholesterol levels and hypertriglyceridaemia. All these have "insulin resistance" as a common pathogenetic mechanism and seem to be the most important risk factors.
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PMID:Coronary heart disease and its risk factors in first-generation immigrant Asian Indians to the United States of America. 906 34

The Steno hypothesis suggests that albuminuria reflects widespread vascular damage (proliferative retinopathy and severe macroangiopathy) due to a generalized vascular (endothelial) dysfunction. We assessed this concept in NIDDM (non-insulin-dependent diabetic) patients with (13 female/ 39 male, age 60 +/- 7 years, group 1) and without (12 female /41 male, age 61 +/- 7 years, group 2) diabetic nephropathy compared to matched non-diabetic subjects (7 female/15 male, age 58 +/- 8 years, group 3). A 12-lead ECG was recorded and coded blindly using the Minnesota Rating Scale; the World Health Organization cardiovascular questionnaire was used to assess past and present evidence of myocardial infarction, angina pectoris, stroke, and peripheral vascular disease (digital systolic blood pressure determination). The degree of diabetic retinopathy was scored from fundus photography. The following variables were measured: transcapillary escape rate of albumin (initial disappearance of intravenously injected 125I-labelled human serum albumin), plasma concentrations of prorenin (radioimmunoassay) and serum concentrations of von Willebrand factor (enzyme-linked immunoadsorbent assay). Prevalence of ischaemic heart disease (ECG reading) (49/20/5)% and peripheral vascular disease as indicated by reduced systolic blood pressure on big toe (69/30/ 14)% was significantly higher in group 1 vs group 2 (p < 0.01) and in group 2 vs group 3 (p < 0.01), respectively. The prevalence and severity of retinopathy was higher in group 1 vs 2 (p < 0.01). Transcapillary escape rate of albumin (%/h) was elevated in group 1 and 2 as compared to control subjects: 7.9 (4.3-13.7); 7.4 (3.7-16.4) vs 6.0 (3.4-8.7), (p < 0.005), respectively. Plasma prorenin activity (IU/ml) was raised in group 1 and group 2 as compared to group 3: 272 (59-2405); 192 (18-813), and 85 (28-246), p < 0.001, respectively. Serum von Willebrand factor (IU/ ml) was elevated in group 1 as compared to group 2 and 3: 2.07 (0.83-4.34); 1.60 (0.30-2.99) and 1.50 (1.00-2.38), p < 0.001, respectively. Our study demonstrated that NIDDM patients with and without albuminuria had increased transcapillary escape of albumin and raised prorenin activity, whereas only those with albuminuria had increased von Willebrand factor. Patients with NIDDM may have abnormal endothelial function in the absence of albuminuria.
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PMID:Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy. 896 Aug 47

In NIDDM a clustering of established coronary risk factors, e.g. the metabolic syndrome is responsible for excessive incidence of myocardial infarction. The harmful effects of these risk factors are aggravated by poor glucose control. Hyperinsulinaemia is associated with a higher level of risk factors for coronary heart disease. Individuals with subsequent myocardial infarction exhibit higher levels of serum insulin at entry. However, insulin in multivariate analysis was no independent risk factor. Perfect control of blood glucose, triglycerides and blood pressure was associated with a lower incidence of coronary heart disease. By extrapolation an integrated approach to correct the anomalies of the metabolic syndrome seems to be necessary to prevent macroangiopathy and improve life expectancy.
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PMID:Determinants for coronary heart disease in non-insulin-dependent diabetes mellitus: lessons from the diabetes intervention study. 896 95

Microalbuminuria and proteinuria are strong independent predictors for increased cardiovascular mortality in non-insulin-dependent diabetic (NIDDM) patients. In such patients, angiotensin converting enzyme (ACE) inhibition improves the evolution of diabetic nephropathy; however, no data are currently available on the effects of such intervention on cardiovascular morbidity and mortality. The aim of the Diab-Hycar study is to test the hypothesis that ACE inhibition with a low daily dose of 1.25 mg ramipril, which has no significant effect on blood pressure, may reduce cardiovascular morbidity and/or mortality in normotensive or hypertensive NIDDM patients with persistent albuminuria. Selected and followed by general practitioners, 4000 patients will receive their usual oral antidiabetic treatment and if necessary antihypertensive treatment (ACE inhibitors excluded). In addition in a randomized, double-blind trial they will be given either a placebo or 1.25 mg ramipril daily. The follow-up is currently scheduled to last 3 years. The efficacy of ACE-inhibition will be assessed by the following major end-points: cardiovascular death, sudden death, myocardial infarction, stroke, renal replacement therapy. The Diab-Hycar study started on 3 February 1995. By 1 September 1995, 11,000 urine samples were tested. The prevalence of persistent albuminuria was 23%, 964 patients were initially included in the study, with 619 eligible patients included soon after. Different strategies have been developed to record cardiovascular events correctly and to minimize the number of patients lost to follow-up.
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PMID:The DIAB-HYCAR Study. 908 52

Elevated plasminogen activator inhibitor type 1 (PAI-1) activity has been shown to correlate with plasma insulin, proinsulin-like molecules, serum triglycerides and insulin sensitivity in both non-insulin dependent diabetic (NIDDM) subjects and subjects with coronary heart disease. We examined the relative roles of these variables in determining PAI-1 activity in four groups of male caucasian subjects: non-diabetic subjects with (n = 38) and without (n = 38) previous myocardial infarction (MI) and NIDDM subjects with (n = 26) and without (n = 30) previous MI. Insulin and proinsulin-like molecules were measured using specific two-site immunometric assays and insulin sensitivity estimated using the Homeostasis Model Assessment (HOMA) model. Subjects were comparable in age and body mass index. In univariate analysis, there were significant correlations of PAI-1 activity with intact and des-31,32-proinsulin and serum triglycerides in non-diabetic subjects with (r = 0.52, P = 0.001; r = 0.58, P < 0.001; r = 0.41, P = 0.010) and without (r = 0.31, P = 0.056; r = 0.46, P = 0.006; r = 0.41, P = 0.011) MI, but not with plasma insulin or insulin sensitivity. In NIDDM subjects, PAI-1 activity correlated significantly with intact and des-31,32-proinsulin and serum triglyceride (r = 0.47, P = 0.015; r = 0.58, P = 0.002; r = 0.44, P = 0.026) only in subjects with MI. In multiple regression analysis, MI was the most important determinant of PAI-1 activity levels (r2 = 0.31, F = 55.6, P < 0.001). In conclusion, concentrations of proinsulin-like molecules and serum triglycerides appear to be stronger determinants of PAI-1 activity than plasma insulin or insulin sensitivity in both NIDDM subjects and non-diabetic subjects with and without MI. However, the relationship of MI with PAI-1 activity is independent of these variables.
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PMID:Proinsulin-like molecules and plasminogen activator inhibitor type 1 (PAI-1) activity in diabetic and non-diabetic subjects with and without myocardial infarction. 912 61

This study examined the association between limited joint mobility (LJM) and diabetic control, atherosclerotic vascular disease and other diabetic complications in non-insulin-dependent diabetic (NIDDM) patients. LJM was studied in 139 [age (mean +/- SD) 61.3 +/- 12.3 years] NIDDM patients. Limitation of several joints was examined with a goniometer and LJM was classified by the Rosenbloom method. The NIDDM patients were examined for the following diseases: history of myocardial infarction, coronary heart, cerebrovascular and peripheral vascular diseases. The diabetic complications, background and proliferative retinopathy, nephropathy, and neuropathy, were also assessed. The metabolic control of the diabetes was evaluated by the average glycosylated hemoglobin Alc (GHbA kappa) concentration and lipid values were also measured. Mean levels of GHbAlc were 8.9 vs. 8.2% (p < 0.05) in NIDDM patients with and without LJM. NIDDM patients with LJM had a 3.1- (95% confidence interval, 1.2-7.7) and a 4.0-fold risk (95% confidence interval, 1.2-13.0) for coronary heart and cerebrovascular disease respectively, when the confounding effects of age, duration of diabetes and control of diabetes were controlled using stepwise logistic regression analysis. Patients with LJM had a 9.3- (95% confidence interval, 1.1-79.0) and a 3.3-fold risk (95% confidence interval, 1.0-10.5) of proliferative retinopathy and nephropathy respectively, when the confounding effects of age and duration of diabetes were controlled, but the correlation disappeared when control of diabetes was included in the model. In conclusion, the presence of LJM is associated with the control of diabetes and with the presence of coronary heart and cerebrovascular diseases in NIDDM patients.
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PMID:Limited joint mobility in non-insulin-dependent diabetic (NIDDM) patients: correlation to control of diabetes, atherosclerotic vascular disease, and other diabetic complications. 920 97

Patients with NIDDM are at increased risk for coronary heart disease (CHD). However, information on the predictive value of cardiovascular risk factors and the degree of hyperglycemia with respect to the risk for CHD in diabetic patients is still limited. Therefore, we carried out a prospective study on risk factors for CHD, including a large number of NIDDM patients. At baseline, risk factor levels of CHD were determined in 1,059 NIDDM patients (581 men and 478 women), aged from 45 to 64 years. These patients were followed up to 7 years with respect to CHD events. Altogether, 158 NIDDM patients (97 men [16.7%] and 61 women [12.8%]) died of CHD and 256 NIDDM patients (156 men [26.8%] and 100 women [20.9%]) had a serious CHD event (death from CHD or nonfatal myocardial infarction). A previous history of myocardial infarction, low HDL cholesterol level (<1.0 mmol/l), high non-HDL cholesterol (> or =5.2 mmol/l), high total triglyceride level (>2.3 mmol/l), and high fasting plasma glucose (>13.4 mmol/l) were associated with a twofold increase in the risk of CHD mortality or morbidity, independently of other cardiovascular risk factors. High calculated LDL cholesterol level (> or =4.1 mmol/l) was significantly associated with all CHD events. The simultaneous presence of high fasting glucose (>13.4 mmol/l) with low HDL cholesterol, low HDL-to-total cholesterol ratio, or high total triglycerides further increased the risk for CHD events up to threefold. Our 7-year follow-up study provides evidence that dyslipidemia and poor glycemic control predict CHD mortality and morbidity in patients with NIDDM.
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PMID:Dyslipidemia and hyperglycemia predict coronary heart disease events in middle-aged patients with NIDDM. 923 62

We analysed a well-characterized group of 83 patients (43 men, 40 women; mean age +/- SEM: 65.5 +/- 0.6 years at the 10-year examination) with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) and in 123 control subjects (56 men, 67 women; mean age +/- 0.9 years) retrospectively for the relationship of apolipoprotein E (apo E) genotypes (E2/3, E3/3 vs E3/4, E4/4) to the incidence of clinical macrovascular disease and its risk factors and the incidence of microvascular complications of diabetes during the first 10 years of NIDDM, as well as carotid intima-media thickness measured by B-mode ultrasound at the 10-year examination. In patients with NIDDM, apo E4 genotype showed no relationship to clinical events or carotid intima-media thickness. However, in the control subjects with apo E4, the incidence of non-fatal myocardial infarction during the follow-up was increased (apo E4 positivity: 17.1%; apo E4 negativity 5.1%; p = 0.035) and they had higher common carotid intima-media thickness than those with apo E2/3 or apo E3/3 (1.15 +/- 0.05 mm vs 1.01 +/- 0.03 mm, p = 0.008). Apo E genotype groups showed no relationship to microvascular complications of diabetes, although control subjects with apo E4 positivity showed a higher frequency of microalbuminuria than those lacking apo E4. We conclude that apo E4 was a marker of vascular disease and increased atherosclerosis in non-diabetic subjects, whereas in the diabetic patients these relationships were absent. It is likely that NIDDM per se influences the vascular risk so overwhelmingly that the effects of other risk factors are obscured.
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PMID:Divergent association of apolipoprotein E polymorphism with vascular disease in patients with NIDDM and control subjects. 930 Feb 24

Prostacyclin (PGI2) synthesis by vascular endothelial cells (ECs) decreases in diabetic subjects, possibly leading to the development of diabetic angiopathy, such as that seen in atherosclerosis. We recently found a novel bioactive peptide, prostacyclin-stimulating factor (PSF), which stimulates PGI2 synthesis by cultured aortic ECs. Our previous studies demonstrated that PSF is dominantly expressed by arterial smooth muscle cells (SMCs). In the present study, we found PSF to exist in the SMCs of human coronary arteries by means of immunohistochemical methods. Human coronary arteries obtained from autopsies were divided into four subgroups, with or without NIDDM and/or myocardial infarction. Immunostaining for PSF was performed by the avidin-biotin peroxidase complex method using a purified anti-PSF antibody, and the immunostaining for PSF was assessed semiquantitatively. PSF staining was markedly reduced in coronary arterial SMCs from patients with NIDDM and/or myocardial infarction. In addition, the effect of a high glucose culture on PSF mRNA expression and PSF production in bovine aortic SMCs was examined by immunocytochemical staining and both Western and Northern blot analyses. The immunostaining and immunoblot band for PSF also significantly decreased when bovine aortic SMCs were cultured with high concentrations of glucose. Furthermore, as compared with the SMCs cultured with a physiological glucose concentration, the density ratio of PSF mRNA to 28S rRNA expression significantly decreased when the SMCs were cultured with high concentrations of glucose. These results strongly suggest that the decreased PSF production may thus results in a decreased production of PGI2 in the coronary artery, thus leading to the development of both diabetic macroangiopathy and atherosclerosis.
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PMID:Immunohistochemical study of prostacyclin-stimulating factor (PSF) in the diabetic and atherosclerotic human coronary artery. 931 60


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