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)

The incidence of atherosclerotic vascular disease is greatly increased in patients with non-insulin-dependent diabetes (NIDDM). The most frequent lipoprotein abnormalities in this type of diabetes are an increase in triglyceride-rich lipoproteins and a decrease in high-density lipoproteins. Hypertriglyceridaemia appears to be a stronger coronary heart disease risk factor in patients with NIDDM than in nondiabetic subjects. Plasma total and low-density lipoprotein cholesterol levels in NIDDM patients and nondiabetic subjects do not differ. Hypercholesterolaemia is, however, as powerful a predictor of coronary heart disease risk in diabetic patients as in nondiabetic subjects. In spite of this knowledge, there is to date no solid evidence to indicate whether correction of dyslipoproteinaemia in order to reduce coronary heart disease risk in patients with NIDDM is more, equally, or less beneficial than it is in nondiabetic subjects. The only available data come from post-hoc subgroup analyses of the Helsinki Heart Study and the Scandinavian Simvastatin Survival Study (4S). Other trials including patients with diabetes are in progress. Only one intervention trial (currently in its treatment phase), the Diabetes Atherosclerosis Intervention Study (DAIS), is specifically designed to examine the lipid hypothesis in patients with NIDDM.
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PMID:Will correction of dyslipoproteinaemia reduce coronary heart disease risk in patients with non-insulin-dependent diabetes? Need for trial evidence. 886 91

Hypercholesterolaemia is a strong risk factor of coronary artery disease (CAD). The importance of high triglyceride and low HDL cholesterol in predicting risk of CAD is less well-established. This review presents data showing that high triglyceride and low HDL cholesterol are important risk factors of CAD and suggests that combined lipid profiles of triglyceride, HDL cholesterol, and total cholesterol provide more information about risk of CAD than total cholesterol alone. High triglyceride and low HDL cholesterol is the characteristic dyslipidaemia seen in subjects with insulin resistance, a basic abnormality in glucose- and insulin metabolism. Since insulin resistance and raised triglyceride and decreased HDL cholesterol can be identified in children of patients with NIDDM, essential hypertension, and CAD, we suggest that efforts to prevent CAD should include interventions against all these associated abnormalities in glucose-, insulin-, and lipid metabolism and not only high cholesterol.
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PMID:[High triglyceride, low HDL-cholesterol and risk of coronary heart disease]. 898 51

To assess the effect of a high monounsaturated fatty acids (MFA) diet on serum lipids, 30 healthy adult normolipidemic volunteers and 37 adult patients with mild hypercholesterolemia (5.4-9.3 mmol/l), 15 of them also with hypertriglyceridemia (2.3-4.8 mmol/l), were studied. Fifteen healthy and 30 hypercholesterolemic subjects (15 of them with associated type 2 diabetes mellitus) received an avocado enriched diet (2000 Kcal, lipids 53% MFA 49 g saturated/unsaturated ratio 0.54), and seven non-diabetic hypercholesterolemic individuals received an isocaloric control diet (MFA 34 g, saturated/unsaturated ratio 0.7). Serum total cholesterol, LDL-cholesterol, HDL-cholesterol and triglyceride concentrations were measured before and after a 7-day diet period. In healthy individuals a 16% decrease of serum total cholesterol level followed the high MFA diet, while it rose after the control diet (p < 0.001 between diets). In hypercholesterolemic subjects a significant (p < 0.01) decrease of serum total cholesterol (17%), LDL-cholesterol (22%) and triglycerides (22%), and increase of HDL-cholesterol (11%) levels occurred with the avocado diet, while no significant changes were noticed with the control diet. High lipid, high MFA-avocado enriched diet can improve lipid profile in healthy and especially in mild hypercholesterolemic patients, even if hypertriglyceridemia (combined hyperlipidemia) is present.
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PMID:Monounsaturated fatty acid (avocado) rich diet for mild hypercholesterolemia. 898 88

Prednisone in combination with cyclosporine and/or azathioprine is commonly used after kidney transplantation to prevent graft rejection. Long-term use of prednisone can give rise to multiple side effects and morbidity. This randomized study was conducted to find out if prednisone could be withdrawn in recipients at least 1 yr after kidney transplantation. Eighty-four such recipients of a cadaveric kidney with stable renal function on cyclosporine and prednisone were randomized to continue prednisone (N = 42) or to withdraw prednisone in a 2-month period (N = 42). The main end point was the percentage of successful prednisone withdrawal. Both groups were compared for the incidence of infections and cardiovascular risk factors and for the incidence and cause of deterioration of renal function. All patients had a 14-month follow-up. In 67% (N = 28) of the patients, prednisone could be withdrawn successfully. Acute rejection was the main cause of withdrawal failure (N = 11, 26%). No grafts were lost due to rejection. In the prednisone withdrawal group, a tendency was noted for a lower incidence of infections (difference: 17%; 95% confidence interval [CI]: -4% to 37%). After withdrawal, less antihypertensive drugs were necessary to control hypertension (difference: 0.5 drugs/patient; 95% CI: -0.9 to -0.1) and 35% less patients (23 of 41 versus nine of 42) needed cholesterol-lowering drugs (95% CI: -54% to -15%). A reduction of the frequency of patients with Type II diabetes mellitus was found (difference 10%; 95% CI: -24% to 5%) with a decrease of glycosylated hemoglobin (difference: 0.4 mmol/L; 95% CI: 0.1 to 0.8). Disappearance of moonface was found in 25% of the patients. Elective withdrawal of prednisone > 1 yr after postmortal kidney transplantation can be accomplished safely provided that patients are controlled frequently. Beneficial effects were found regarding hypertension, hypercholesterolemia, hyperglycemia, and appearance.
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PMID:Late prednisone withdrawal in cyclosporine-treated kidney transplant patients: a randomized study. 904 49

Although persons with diabetes constitute only 3.1% of the US population, costs for their care account for 11.9% of total US health care expenditures. Approximately half of the expenditures for medical care for diabetes are for treatment of the metabolic condition and half for the treatment of chronic complications. Intensive therapy for persons with diabetes uses more resources and is more expensive than conventional therapy. On the other hand, intensive therapy is associated with a lower incidence of costly chronic complications. Formal economic analyses have demonstrated that intensive therapy is cost-effective for the treatment of diabetes. In IDDM, intensive therapy costs approximately $20,000 per QALY gained; in NIDDM, it costs approximately $16,000 per QALY gained. From an economic perspective, intensive therapy for persons with diabetes compares favorably with pharmacologic therapy for high-risk individuals with hypertension and hypercholesterolemia. Health policy should foster the use of such therapy for persons with diabetes mellitus.
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PMID:The cost-effectiveness of intensive therapy for diabetes mellitus. 931 22

Fatty acid (FA) profiles of total serum lipids were determined by capillary gas chromatography in Type 2 diabetic patients (NIDDM) with diverse types of hyperlipidemia. In patients with hypertriglyceridemia (DM-HTG) and combined hypertriglyceridemia and hypercholesterolemia (DM-HLP), a significantly different total FA composition was found compared with healthy controls or diabetics with normal serum lipids. In particular, the proportions of saturated and monounsaturated FA were increased and the proportions of n-6 polyunsaturated FA were decreased. In DM-HLP patients, PUFA n-6 metabolites and C20-C22 PUFA were also decreased. Thus, hyperlipidemia shifts significantly the serum FA composition in NIDDM patients into an atherogenic profile. More study is needed, however, to understand if serum FA changes may contribute to the increased atherogenesis commonly found in these patients.
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PMID:The effect of hyperlipidemia on serum fatty acid composition in type 2 diabetics. 932 91

The granulocytes from elderly patients were investigated, in previous studies, with FMLP and it was found that the postreceptor signal, the inositol phosphate production and inositol phosphate dependent calcium signal were markedly reduced. It was observed that the 125I LDL binding was slightly reduced while the intracellular degradation of the LDL and endogenous cholesterol synthesis inhibitory effect was significantly decreased on monocytes of patients with non insulin dependent diabetes mellitus. It was suggested that of in patients suffering from NIDDM with hypercholesterolemia the LDL receptor numbers of monocytes are close to normal, while the post receptor signal transmission is damaged. In this study the monocytes from 12 patients with hypercholesterolemia were investigated before and after LDL treatment and were compared to the 11 age-matched healthy volunteer control patients. The cells were stimulated with LDL and chemotactic peptide FMLP. The postreceptor signal mechanism in monocytes was investigated. According to the results the inositol phosphate level of the patient group decreased independently from the stimulus. The LDL induced IP3 and Ca2+ level elevation was PT resistant both in the control and in the patients group.
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PMID:[Biologic effect of LDL binding and intracellular degradation in monocytes from patients with hypercholesterolemia]. 934 May 72

Insulin resistance is characterized principally by impaired insulin-mediated glucose uptake which provokes a compensatory increase in pancreatic beta-cell secretory activity. For a time this may produce well-controlled plasma glucose levels but as the insulin resistance worsens the augmented insulin production becomes inadequate to keep plasma glucose at euglycemia leading to the development of non-insulin dependent diabetes mellitus (NIDDM), accompanied by hyperinsulinemia and hyperglycemia. A number of metabolic defects are associated with NIDDM including obesity, hypercoagulability, cardiovascular disease risk factors such as hypertension and dyslipidemia and these constitute the insulin resistance syndrome. The identity of the biochemical factor that might link all these defects is not yet known. We have hypothesized that platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) may be such a link. In this study, we measured plasma acetylhydrolase (EC.1.1.48), which degrades PAF to the inactive metabolise lyso-PAF, as a surrogate for PAF activity in three groups of hypercholesterolemic subjects: lean controls (n = 9), non-diabetic obese (n = 6) and NIDDM subjects (n = 6). The ages and body mass indices of the subjects were 46 +/- 3.1 and 24.2 +/- 2.2 for the lean controls, 52 +/- 2.5 and 28.7 +/- 0.9 for the NIDDM subjects and 60 +/- 2 and 27.6 +/- 2.1 for the obese, non-diabetic subjects (mean +/- S.E.M.). The measurements were made before and after therapy with the cholesterol-lowering drug lovastatin, a 3-hydroxy 3 methylglutaryl (HMG) coenzyme. A reductase inhibitor (40 mg/day) for 3 months. Fasting plasma glucose (FPG) levels were 91 +/- 11, 96 +/- 3 and 146 +/- 11 mg/dl, for the lean, obese and NIDDM subjects, respectively, before therapy began. Lovastatin did not affect FPG in any of the three subject groups. Before treatment, the fasting plasma insulin (FPI) levels were 6.1 +/- 0.92, 10.83 +/- 2.03 and 14.68 +/- 3.64 mU/l for the lean, non-diabetic obese and NIDDM subjects, respectively. After lovastatin therapy only the obese group exhibited a significant change in FPI (15.35 +/- 2.47 mU/l) (P < 0.05). Total cholesterol levels were similar in all three groups both before and after lovastatin therapy but within each group lovastatin therapy significantly reduced the total cholesterol by 32, 29 and 34% in the lean, obese and NIDDM subject groups respectively (P < 0.0001). Lovastatin therapy reduced LDL-cholesterol levels by 40, 32 and 46% in the lean, obese and NIDDM subjects, respectively, but produced no significant effect on HDL or triglyceride levels. Before therapy, the plasma acetylyhydrolase activities were 104 +/- 7, 164 +/- 7 and 179 +/- 7 nmol/ml per min in the lean, obese and NIDDM subjects, respectively. Lovastatin therapy reduced plasma acetylhydrolase levels to 70 +/- 7, 87 +/- 6 and 86 +/- 7 nmol/ml per min in the lean, obese and NIDDM subjects, respectively. Plasma acetylhydrolase activity was predominantly (> 80%) associated with LDL cholesterol both before and after lovastatin treatment. Also, plasma acetylhydrolase activity significantly correlated with fasting plasma insulin levels before lovastatin therapy but not after. Taken together, this study clearly implicates PAF metabolism in three defects associated with the insulin resistance syndrome: hypercholesterolemia, obesity and NIDDM. Additionally, we conclude that chronic hyperinsulinemia may play a significant role in the production of plasma acetylhydrolase.
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PMID:Plasma PAF acetylhydrolase in non-insulin dependent diabetes mellitus and obesity: effect of hyperinsulinemia and lovastatin treatment. 945 36

The objective of this study was to estimate the prevalence of poor glycaemic control and cardiovascular risk factors in an Italian population-based cohort of subjects with Type 2 diabetes mellitus (DM). Out of a cohort of 1967 subjects (estimated completeness of ascertainment 80%), 1574 (80%) were investigated, and adherence to targets for control of the European NIDDM Policy Group assessed. Prevalence of poor glycemic control (HbA1c > = 8) was 47.7%. Obesity was present in 23.4% of the cohort, hypertension in 83.4%, hypertriglyceridaemia (>2.26 mM) in 19.3%, hypercholesterolaemia (>6.46 mM) in 25.5%, and low HDL-cholesterol (<0.90 mM in men and <1.03 mM in women) in 13.7%. Only 153 (9.7%) subjects were free from other disorders. Subjects were treated as follows: 26.2% exclusively by general practitioners; 13.3%, 69.9%, 10.9%, and 5.9% with diet, oral hypoglycaemic drugs, insulin, and both, respectively. Multiple linear regression analysis showed associations between HbA1c and fibrinogen (p < 0.001), total cholesterol (p = 0.006), and triglycerides (p = 0.04), independent of age, sex, duration of diabetes, and antidiabetic treatment. Neither BMI nor blood pressure were associated with HbA1c. In conclusion, this Italian population-based cohort of subjects with Type 2 DM showed a high prevalence of poor glycaemic control, high consumption of oral hypoglycaemic drugs, and an independent association between glycaemic control and cardiovascular risk factors (fibrinogen, total cholesterol, and triglycerides). The presence of obesity or hypertension was not significantly associated with glycaemic control.
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PMID:Glycaemic control and cardiovascular risk factors in type 2 diabetes: a population-based study. 958 95

Acarbose is the first of a new class of antidiabetic agents, the alpha-glucosidase inhibitors. Acarbose has proven effectiveness as a first-line drug in type 2 diabetes insufficiently controlled by diet alone. In addition to providing short-term glycemic control, acarbose also reduces HbA1c levels. This effect is greatest when therapy is initiated early in the disease and when baseline HbA1c levels are high. Depending on the baseline HbA1c value, therapeutic doses of acarbose lead to a HbA1c reduction of 0.5%-1.2%. Acarbose may be safely combined with all oral hypoglycemic agents, and has been found to have utility as an adjunct to sulfonylurea and metformin therapy. It also improves control of insulin-treated type 2 diabetes and enables a reduction of exogenous insulin requirements of up to 30%. Acarbose also has beneficial effects on the coronary risk factors, e.g. postprandial triglyceride levels, elevated cholesterol, and hyperinsulinemia. The early phase of acarbose therapy may be associated with side effects such as meteorism, flatulence, and diarrhea. These result from the local effect of the drug and decline with time. To date, there have been no reports of systemic toxicity. Acarbose does not cause hypoglycemias or weight gain.
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PMID:The role of acarbose in the treatment of non-insulin-dependent diabetes mellitus. 964 42


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