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)

A cohort of 447 subjects with Type 2 diabetes mellitus (208 male, 239 female; age range 30-82, median 62 years; and of predominantly European origin) was characterized in a clinic survey in 1989. Individual status (dead or alive) at 1 June 1995 was ascertained. Mortality rates were compared with the general New Zealand population by calculating standardized mortality ratios (SMR) and the hazard ratio (HR) of prognostic factors evaluated with Cox's proportional hazards model. At 6 years, 289 subjects were confirmed as alive and 133 as dead; only 25 were untraceable. Six-year survival for the cohort was 70% (95% CI 66-74). SMR was 2.53 (95% CI 1.99-2.68) for the female cohort and 2.03 (95% CI 1.60-2.59) for the male cohort. Factors assessed at baseline (1989) that were independently prognostic of total mortality included age, male sex, pre-existing coronary artery disease (CAD) (HR 2.2, 95% CI 1.5-3.3) and plasma cholesterol (HR for 1.4 mmol l(-1) change: 1.49, 95% CI 1.2-1.9). HDL-cholesterol was protective in women (HR for 0.4 mmol l(-1) change: 0.72, 95% CI 0.51-1.00) but not men. Glycated haemoglobin was not a significant predictor of total mortality. Predictors of CAD mortality (in those subjects free of CAD in 1989) included plasma cholesterol (HR for 1.4 mmol l(-1) change: 1.86 95% CI 1.20-2.89), glycated haemoglobin (HR for 1.8% change: 1.9 95% CI 1.04-3.47), male sex, peripheral vascular disease, and smoking. There is therefore increased mortality in Type 2 diabetic subjects in Canterbury, New Zealand. HDL-cholesterol is protective against total mortality in females.
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PMID:Lipid but not glycaemic parameters predict total mortality from type 2 diabetes mellitus in Canterbury, New Zealand. 960 55

Although low-density lipoprotein (LDL) cholesterol is a critically important factor in the development of atherosclerosis, nearly half the patients with coronary artery disease have LDL cholesterol levels within the National Cholesterol Education Program (NCEP) guidelines. Therefore, attention has focused on other modifiable risk factors that could strongly impact the development of coronary artery disease. Type 2 diabetics have a 3-fold increased risk of coronary artery disease; prediabetics, without chronic hyperglycemia, have a 2-fold increased risk compared with normal subjects. Insulin resistance has also been implicated as the cause of atherosclerosis. Insulin resistance is associated with hyperinsulinemia and a constellation of other factors, some of which are themselves independent risk factors for coronary artery disease. These include reduced levels of high-density lipoprotein (HDL) cholesterol, hypertriglyceridemia, increased small dense LDL particles, hypertension, visceral obesity, and increased levels of plasminogen activator inhibitor-1 (PAI-1). Hyperinsulinemia and insulin resistance at the vascular level also may contribute to vascular injury and the atherosclerotic process. Current studies suggest that controlling hyperglycemia, LDL cholesterol, and blood pressure are important to protect the diabetic from atherosclerosis. A key question, particularly in type 2 diabetes, is to define the best regimen for glucose control that will protect the vasculature. Sulfonylureas, metformin, and troglitazone have direct vascular actions. Metformin lowers LDL cholesterol and triglycerides, while troglitazone reverses many of the components associated with the insulin resistance syndrome. Clinical trials focusing on coronary artery disease outcomes are now warranted to prevent coronary artery disease, the major vascular complication and cause of mortality in diabetes.
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PMID:Cardiovascular risk continuum: implications of insulin resistance and diabetes. 970 62

There is a paucity of data regarding outcomes of Type 2 diabetes mellitus. A cohort of 447 Type 2 diabetic subjects (208 male, 239 female; age range 30-82 years, median 62 years; and of predominantly European origin) was characterised in a clinic survey in 1989. Individual status (dead or alive) at 1 June 1995 was ascertained. At 6 years, 289 subjects were confirmed as alive and 133 as dead--only 25 were untraceable. Of those subjects identified as alive, follow-up clinical and biochemical data were obtained for 253 (87.5%) individuals. In those subjects, glycated haemoglobin deteriorated from 63.1 +/- 18.7 mmol/mol haem in 1989 to 71.7 +/- 24.4 in 1995, P < 0.0001. An increased prevalence of retinopathy was evident at 6-year follow-up, 59.7% cases in 1995 compared with 39.5% in 1989, P < 0.001. Similarly there was an increased prevalence of coronary artery disease (CAD) (33.6 vs 18.2% of cases), albuminuria (26.5 vs 19% of cases; P < 0.001), and hypertension (71.5 vs 54.9% of cases; P < 0.001) in 1995 vs 1989, respectively. Multiple logistic regression analysis showed that glycated haemoglobin (odds ratio (OR) for 18 mmol/mol haem change, 1.78; 95% CI, 1.15-2.85), hypertension (OR, 3.33; 95% CI, 1.40-8.41) and known duration of diabetes (OR for 7 year change, 2.12; 95% CI, 1.24-3.80) were predictors for development of retinopathy. There is therefore a deterioration in glycaemic control in Type 2 diabetes over 6 years and an increased prevalence of complications that present strategies in a multidisciplinary specialist diabetes clinic are unable to prevent on a sustainable basis.
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PMID:Clinical and biochemical outcomes of type 2 diabetes mellitus in Canterbury, New Zealand: a 6-year cohort study. 971 20

Insulin resistance and hyperinsulinemia both in normal persons and those with non-insulin dependent diabetes mellitus (NIDDM) (type 2 diabetes) appears to be related to obesity. It seems also that insulin plays a role in modulating the obesity-related factors (eg, hyperinsulinemia, hyperglycemia, hypertension, hypertriglyceridemia, hypercholesterolemia, low concentrations of high-density lipoprotein cholesterol) and takes its place among the many risk factors for coronary artery disease (CAD) associated with obesity. Insulin resistance and hyperinsulinemia could play the same role in pathogenesis of CAD independently of obesity. The authors determined blood glucose and immunoreactive insulin and plasma triglyceride concentrations in the fasting state at 60 and 120 minutes after a glucose load of 75 g in 68 patients (54 men, 14 women) with angiographic evidence of CAD and in 65 healthy volunteers matched to the patients for age, gender, and body mass index (43 men and 22 women). Patients with CAD and the healthy volunteers were categorized as obese (body mass index > or = 26 kg/m2) and nonobese (body mass index < 26 kg/m2). Four groups of subjects were analyzed: Group A included 40 healthy (28 men and 12 women) nonobese volunteers; group B, 25 healthy (15 men and 10 women) obese volunteers; group C, 39 (30 men and 9 women) nonobese patients with CAD; and group D, 29 (24 men and 5 women) obese patients with CAD. Fasting and postchallenged 60- and 120-minute glucose values were similar in groups A and C. However, significantly higher insulin values (mU/L) were observed in group C than in group A during fasting (12.2+/-6.2 vs 91+/-3, p<0.05), and postchallenged at 60 minutes (103.1+/-53.2 vs 71.9+/-64.3, p<0.01) and 120 minutes (57.9+/-41.2 vs 44.9 +/-41.3, p<0.01). Fasting glucose and insulin values were similar in groups B and D. However, significantly higher glucose (mg/dL) and insulin values were observed in group D than in group B postchallenged at 60 and 120 minutes: glucose at 60 minutes (188.7 +/-45.1 vs 154.2+/-37.5, p<0.05); insulin at 60 minutes (127.5+/-98.5 vs 112.1+/-81.1, p<0.05); glucose at 120 minutes (124.2+/-46.1 vs 99.5+/-28.9, p<0.05); insulin at 120 minutes (86.1+/-57.6 vs 62.8+/-27.9, p<0.05). The glucose and insulin values during 60- and 120-minute fasting as well as postchallenged were similar in groups B and C. Significantly higher plasma triglyceride concentrations were observed in group C than in group A (149.0+/-64.1 vs 114.6+/-46.6, p<0.01) and in group D compared with group B (229.4+/-104.7 vs 144.9+/-65.1, p<0.001). Plasma triglyceride concentrations were similar in groups B and C. The authors conclude that patients with documented CAD are insulin resistant independently of obesity.
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PMID:Insulin resistance, hyperinsulinemia, and hypertriglyceridemia in patients with coronary artery disease independent of obesity. 971 89

The results of various studies suggest that hypertriglyceridaemia is associated with an increased risk of coronary artery disease. It is unclear, however, which particular triglyceride (TG)-rich lipoproteins contribute to the risk. Different types of TG-rich lipoprotein differ in function, composition, size and density. TG-rich lipoproteins in the range Svedberg flotation (Sf) 12-60 have been shown to be associated with angiographic severity in both diabetic and non-diabetic individuals. A study in people with type 2 diabetes found that those with moderate coronary artery disease had higher levels of both Sf 12 60 and Sf 60-400. Multivariate analysis showed that this association was independent of both low (LDL)- and high-density lipoprotein (HDL). The association was not seen in patients with severe coronary artery disease, suggesting that these lipoproteins may only be involved in the early stages of atherogenesis. Further research has indicated that the risk correlates positively to the postprandial levels of apolipoprotein B48 in the Sf 20-60 fraction. This suggests that elevated levels of chylomicron remnants are involved in progression of coronary artery disease.
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PMID:Intermediate-density lipoproteins, diabetes and coronary artery disease. 974 May

The increased risk of coronary artery disease in subjects with diabetes mellitus can be partially explained by the lipoprotein abnormalities associated with diabetes mellitus. Hypertriglyceridemia and low levels of high-density lipoprotein are the most common lipid abnormalities. In type 1 diabetes mellitus, these abnormalities can usually be reversed with glycemic control. In contrast, in type 2 diabetes mellitus, although lipid values improve, abnormalities commonly persist even after optimal glycemic control has been achieved. Screening for dyslipidemia is recommended in subjects with diabetes mellitus. A goal of low-density lipoprotein cholesterol of less than 130 mg/dL and triglycerides lower than 200 mg/dL should be sought. Several secondary prevention trials, which included subjects with diabetes, have demonstrated the effectiveness of lowering low-density lipoprotein cholesterol in preventing death from coronary artery disease. The benefit of lowering triglycerides is less clear. Initial approaches to lowering the levels of lipids in subjects with diabetes mellitus should include glycemic control, diet, weight loss, and exercise. When goals are not met, the most common drugs used are hydroxymethylglutaryl coenzyme A reductase inhibitors or fibrates.
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PMID:Hyperlipidemia and diabetes mellitus. 978 48

The missense mutation in the 677th nucleotide (C677T) of methylenetetrahydrofolate reductase gene causes substitution of valine (V) for alanine (A) resulting in three genotypes VV, VA and AA. The VV genotype causes hyperhomocysteinemia and may be a risk factor for coronary artery disease. We determined genotypes by polymerase chain reaction and subsequent restriction fragment length analysis and compared them in 84 patients with type 2 diabetes and in 115 non-diabetic subjects with and without coronary disease. Fractional urinary excretion rate of albumin was assessed by nephelometry. The VV, VA, and AA frequencies in the diabetic and in the control groups were 0.095, 0.357, 0.548 and 0.061, 0.417, 0.522, respectively (p = NS, diabetic vs. controls, chi2 test). Genotype frequencies did not differ in either diabetic or control subjects between those with or those without coronary disease (chi2 test). The fractional urinary excretion rate of albumin (mean +/-SD) in diabetic patients with the VV genotype i.e. 1.59 +/-0.71 was lower (Kruskall-Wallis test p = 0.002) than in the other genotypes i.e. VA 5.98 +/-9.75 and AA 3.75 +/-4.77, respectively (post-hoc Mann-Whitney test VV vs. VA p = 0.005 and VV vs. AA p = 0.054, respectively). We found that in patients with type 2 diabetes the methylenetetrahydrofolate reductase VV genotype was associated with a low urinary albumin excretion but not with coronary artery disease or diabetes per se.
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PMID:Mutation C677T of methylenetetrahydrofolate reductase gene is not associated with coronary artery disease, but possibly with albuminuria, in type 2 diabetic patients. 980 73

Management of major risk factors (smoking, hypercholesterolaemia, hypertension), in the context of secondary prevention, has an impact on recurrence and life expectancy. However, there is a delay between the publication of therapeutic trials and their diffusion within the medical community. The objective of this study was to evaluate the prevalence and management of the main risk factors in a sample of 500 men, with a mean age of 55.1 +/- 7.5 years, presenting with stable coronary artery disease. 11% of subjects had a family history of premature myocardial infarction. Smoking was frequent: 21% of smokers, 60% of ex-smokers. Hypercholesterolaemia (LDL-C > 3.4 mmole/l or treatment) was present in 82% of subjects. Only 45% of treated subjects had an LDL-C < 3.4 mmole/l. Hypertension (systolic blood pressure > or = 140 mmHg or diastolic blood pressure > or = 90 mmHg or treatment) was present in 61% of subjects. Only 33% of treated subjects were controlled. Non-insulin-dependent diabetes mellitus (blood glucose > or = 7.7 mmole/l or treatment) was present in 21% of subjects. Only 43% of treated subjects were controlled. Calculation of the distribution of major risk factors (smoking, pathological obesity, hypercholesterolaemia, hypertension, diabetes) showed that 90% of coronary patients presented at least two risk factors. Overall, the prevalence and management of risk factors in patients with stable coronary artery disease is far from optimal.
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PMID:[Prevalence and management of major risk factors in 500 men with stable coronary disease]. 980 37

Atherosclerosis/coronary artery disease (CAD) is largely a result of genetically linked dyslipidemias that can often be identified in clinical practice. Expression of these genetic traits is highly individual and can be affected by environmental factors such as diet and exercise. By understanding the heterogeneity of CAD, it becomes clear that all patients cannot be optimally managed with the same therapeutic regimen. Whereas elevated low-density lipoprotein (LDL) cholesterol is strongly correlated with CAD risk, reduction of LDL cholesterol alone is not an adequate strategy in many cases. Patients with the small, dense LDL of the atherogenic lipoprotein profile (pattern B) experience a 3-fold increased risk of CAD, and pattern B is also correlated with the development of type 2 diabetes. Likewise, elevated lipoprotein(a) increases atherosclerotic risk, particularly in the presence of other risk factors, and is predictive of CAD risk in both women and men. Recent data show that the routine lipid profile--total cholesterol, triglycerides, LDL cholesterol, and high-density lipoprotein (HDL) cholesterol--does not detect the most common inherited dyslipidemias. Newer, more sophisticated tests, such as gradient gel electrophoresis, can detect disease-relevant lipidemic details, e.g., LDL subclass pattern, LDL particle diameter, and LDL subregions. Although these testing procedures are more expensive, their cost must be weighed against the potential lifelong cost of sometimes expensive drug treatment that may be avoided based on the results of such tests. Thus, by attending to the implications of family history, the interactions of genetic, metabolic, and environmental factors, and utilizing more targeted testing procedures, physicians can match the patient's disorder with specifically effective therapy while maintaining a cost-effective approach to disease management.
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PMID:Did grandma give you heart disease? The new battle against coronary artery disease. 981 2

Death from myocardial infarction was a rare clinical entity at the beginning of this century, but with an ageing population it is poised to become the most common cause of death worldwide. Ample epidemiological evidence confirms the clinical impression that cardiovascular risk factors--hypertension, glucose intolerance, dyslipidaemia, obesity--tend to 'cluster' in individual patients. This metabolic syndrome, or 'Syndrome X', which is thought to be underpinned by decreased insulin sensitivity, was first described in 1966 by Camus and popularized by Reaven in 1988. The enthusiasm and interest generated have led to the elucidation of some details concerning the pathogenesis of insulin resistance and coronary artery disease but have done little to change treatments or outcomes. Meanwhile, a global epidemic of Type 2 diabetes mellitus is said to be on the horizon- and it has been calculated that by the year 2230, 100% of the adult United States population will be obese.
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PMID:The metabolic syndrome: overeating, inactivity, poor compliance or 'dud' advice? 982 66


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