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)

Low density lipoprotein (LDL-) particles can be subfractionated in large-buoyant (lb), intermediate-dense (id) and small-dense (sd) LDL-subtypes. Fibrates improve the LDL-subtype profile by reducing proatherogenic sd-LDL which are prominent in diabetic dyslipoproteinemia. We evaluated the effect of etofibrate on the LDL-subtype distribution in patients with type 2 diabetes mellitus (n = 13, 55 +/- 18 years, BMI 27.9 +/- 5.5 kg/m2, HbA1c 10.1 +/- 3.9 %) and diabetic dyslipoproteinemia (triglycerides 343 +/- 253 mg/dl, HDL-cholesterol 36 +/- 7 mg/dl, LDL-cholesterol 110 +/- 37 mg/dl). Plasma lipids (enzymatic methods) and LDL-subtypes (7 LDL-subfractions, density gradient ultracentrifugation) were measured before and during etofibrate therapy (500 mg/d, 7 - 16 weeks). Etofibrate significantly (p < 0.05, Wilcoxon-test) reduced triglycerides (- 31 +/- 60 %) and increased HDL-cholesterol (+ 24 +/- 22 %), whereas total cholesterol and LDL-cholesterol did not change. Cholesterol concentration decreased in sd-LDL by 12 % (p < 0.05), while it increased in id- and lb-LDL (+ 26 %,+ 39 %, respectively). Thus, the LDL-subtype profile showed a relative increase of the fraction of lb- (+ 13 +/- 32 %, n.s.) and id-LDL (+ 23 +/- 33 %, p < 0.05) and a relative decrease of the fraction of sd-LDL (- 19 +/- 18 %, p < 0.05). We conclude that etofibrate not only decreases triglycerides and increases HDL-cholesterol but also improves the LDL-subtype profile and thus may reduce the cardiovascular risk in patients with an abundance of sd-LDL such as diabetic patients.
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PMID:Influence of etofibrate on LDL-subtype distribution in patients with diabetic dyslipoproteinemia. 1452 May 96

Cardiovascular disease is responsible for 65 percent of deaths in persons with type 2 diabetes. However, awareness of cardiovascular disease risk factors among patients with diabetes remains low, resulting in missed opportunities to lower risks for coronary events and strokes. The National Diabetes Education Program has begun a campaign to increase patient participation in risk-reduction practice s by promoting the "ABCs" of diabetes care: A(1c) level, Blood pressure, and Cholesterol level. By increasing patient awareness of the link between diabetes and heart disease, family physicians can encourage patients to take medications (including aspirin), stop smoking, lower blood pressure, and lower cholesterol and blood glucose levels.
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PMID:Reducing cardiovascular disease risk in patients with type 2 diabetes: a message from the National Diabetes Education Program. 1459 38

We hypothesized that the administration of troglitazone (TGZ), an insulin-sensitizing agent of the thiazolidinedione class, would improve dyslipidemia associated with insulin resistance in polycystic ovary syndrome (PCOS). Three hundred and ninety-eight women with PCOS in a multicenter, double-blind trial were randomly assigned to 44 wk of treatment with: placebo or troglitazone (150, 300, or 600 mg/d). We examined the responses of circulating lipid and lipoproteins [total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and triglycerides (TTG)] by treatment arm, and the influence of glycemic parameters on baseline levels and response to treatment. There was a high prevalence of abnormal baseline lipid parameters, as defined by National Cholesterol Education Program guidelines [total cholesterol, > or = 200 mg/dl (35%); LDL-C, > or = 130 mg/dl (31%); HDL-C, <35 mg/dl (15%); TTG, >200 mg/dl (16%)]. Baseline models showed that parameters of insulin action had poor predictive power on lipid parameters. There was no significant response of any of the circulating lipids to treatment with either placebo or one of the troglitazone arms (after correction for multiple analyses). There were favorable, but nonsignificant, trends in HDL-C (increase) and LDL-C (decrease) and a trend toward decreased circulating TTG in the 300- and 600-mg TGZ dose treatment arms, both in an intention to treat analysis (n = 375) and in study completers (44 wk; n = 152). There also was a minimal treatment effect noted when only subjects with abnormal baseline levels were examined, and responders differed little from nonresponders in terms of indices of insulin action. There is a substantial prevalence of clinically recognized dyslipidemia in the population of women with unrecognized PCOS without type 2 diabetes. Treatment with an insulin-sensitizing agent may have minimal impact on circulating lipids. Further surveillance and treatment of abnormal lipid levels may be necessary in these women.
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PMID:Minimal response of circulating lipids in women with polycystic ovary syndrome to improvement in insulin sensitivity with troglitazone. 1460 40

The observed reduction in macrovascular outcomes in the United Kingdom Progressive Diabetes Study (UKPDS) trial in patients with type 2 diabetes mellitus (DM), treated intensively with insulin or sulfonylureas, was of borderline significance (p = 0.052). This may be because of the role of factors other than glycemic control in the etiology of macrovascular disease. The UKPDS and other studies have suggested that lipid parameters are potent predictors of adverse outcomes in patients with type 2 DM. In patients with DM, dyslipidemia is characterized by elevated serum triglycerides and low high density lipoprotein-cholesterol (HDL-C) with normal total serum cholesterol levels and usually accompanied by an elevation of atherogenic, small, dense low density lipoprotein-cholesterol (LDL-C) particles. Dyslipidemia is only partly corrected by dietary and lifestyle modifications and pharmacological glycemic control in patients with DM. Several guidelines, including those published by the New Zealand Heart Foundation, suggest that lipid-modifying therapies are appropriate in patients considered to be at high or very high risk of a cardiac event. This includes patients with established vascular disease. Some recent studies suggest that patients with type 2 DM have risk comparable to patients without DM, but have experienced previous myocardial infarction (MI). Subgroup analysis of trials including the Scandinavian Simvastatin Survival Study (4S) and Cholesterol and Recurrent Events (CARE), which included patients with DM, have shown a significant reduction in adverse outcomes, although many patients with DM and dyslipidemia were excluded. Of lipid-lowering drugs, fibric acid derivatives are probably the most appropriate for patients with DM and dyslipidemia and their role is being evaluated in large, long-term outcome studies such as Fenofibrate Intervention and Event Lowering in Diabetes (FIELD). Thiazolidinediones, a new class of compound for treating patients with type 2 DM, primarily exert their glucose-lowering effect by increasing insulin sensitivity at the level of skeletal muscle, and to a lesser extent, at the liver by decreasing hepatic glucose output. Some of their actions are mediated through binding and activation of the peroxisome proliferator-activated receptor-gamma, a nuclear receptor that has a regulatory role in differentiation of cells, especially adipocytes. The nonhypoglycemic effects of thiazolidinediones, therefore, offer additional potential mechanisms for benefit in patients with type 2 DM and insulin resistance. Thiazolidinediones increase serum HDL-C levels. Troglitazone and pioglitazone have been shown to decrease serum triglyceride levels. Rosiglitazone, conversely has no significant effect on serum triglyceride levels. All of the thiazolidinediones increase serum LDL-C levels (pioglitazone to a lesser extent), although changes in the size of the LDL fraction may render it less susceptible to oxidation and, therefore, less atherogenic. A randomized comparative trial needs to be undertaken to determine whether true differences exist between the thiazolidinediones. Longer studies need to be undertaken to assess their effect on cardiovascular outcomes.
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PMID:Management of co-existing diabetes mellitus and dyslipidemia: defining the role of thiazolidinediones. 1472 95

Cholesterol plays an important role in atherogenesis. Cholesterol-ester that has been carried by circulating low-density lipoprotein particles accumulates in the atherosclerotic plaque. Statins are considered the most potent and effective agents for reducing low-density lipoprotein cholesterol and the incidence of cardiovascular events. Total cholesterol and LDL cholesterol levels, however, are not always a useful marker for distinguishing patients with or without cardiovascular disease. Low levels of high-density lipoprotein cholesterol are the most predictive marker for cardiovascular disease. Low HDL cholesterol levels originate in some genetic and acquired diseases and conditions. Most cases of low HDL cholesterol associated with the development of atherosclerosis are of secondary origin, especially those associated with increasing triglyceride-rich lipoprotein. These conditions are present in insulin-resistant syndrome, namely metabolic syndrome. Type 2 diabetes mellitus and the closely related metabolic syndrome are associated with a significant risk for cardiovascular disease. Recent evidence suggests that both conditions are increasing in epidemic proportions. Dyslipidemia is characterized by increased triglyceride-rich lipoproteins; low high-density lipoprotein cholesterol; small, dense low-density lipoprotein particles; and increased postprandial lipemia. All these lipoprotein disturbances accelerate atherosclerosis. It is likely that many patients will need lipid-modifying therapy to help prevent cardiovascular disease.
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PMID:[Atherosclerosis and metabolic disease]. 1502 16

Cardiovascular disease is the major cause of morbidity and mortality in type 2 diabetes mellitus. Among the established risk factors, the lipid triad (elevated triglycerides, decreased high-density lipoprotein cholesterol, and small dense low-density lipoprotein cholesterol) is a powerful risk factor for atherosclerosis in type 2 diabetes. The prevalence of hypertriglyceridaemia (HTG) in type 2 diabetes is two to three times higher than in non-diabetics. The Copenhagen Male study, the AMORIS study, and several other trials showed hypertriglyceridaemia to be an independent predictor of coronary heart disease (CHD). HTG may promote risk both directly and indirectly through association with alterations of lipoprotein size and composition. The Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial (VA-HIT) demonstrated that raising high-density lipoprotein cholesterol (HDL-C) in patients with low (HDL-C) and low-density lipoprotein cholesterol (LDL-C) is associated with a significant reduction in CHD risk. It was shown in the Diabetes Intervention Study, AFCAPS/TexCAPS, and PROCAM studies that decreased HDL-C and elevated triglycerides are independent risk factors for atherosclerosis, particularly in patients with diabetes mellitus. Several epidemiological studies demonstrated that total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratios or low-density lipoprotein cholesterol/high-density lipoprotein cholesterol (LDL-C/HDL-C) ratios could be better predictors of atherosclerosis than any single lipid parameter. Intima-media thickness (IMT), a well established marker of early atherosclerosis, is associated with HTG/low HDL-cholesterol. In the Risk factors in IGT for Atherosclerosis and Diabetes (RIAD) study total and HDL-cholesterol were independent determinants of IMT in subjects at risk for type 2 diabetes. Postprandial HTG was also shown to be correlated with increased IMT in type 2 diabetic patients.
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PMID:The lipid triad in type 2 diabetes - prevalence and relevance of hypertriglyceridaemia/low high-density lipoprotein syndrome in type 2 diabetes. 1503 70

In order to investigate the effect of high carbohydrate/low fat diet on glucose tolerance and on lipid profiles, we performed a 4-week crossover study. Japanese subjects (30 patients with type 2 diabetes mellitus, 15 subjects with impaired glucose tolerance and 8 subjects with normal glucose tolerance) were allocated either 55% standard carbohydrate/30% fat (sc) or 70% high carbohydrate/15% low fat (hc) diet for four weeks, and evaluated by OGTT and various parameters. Then, the diet was crossed over to another diet, and identical parameters were re-evaluated after four weeks. Area under the glucose concentration-time curve (AUG) or triglyceride did not show significant changes between the two diets. HDL-Cholesterol and body mass index decreased significantly by hc diet. Free fatty acids and homeostasis model assessment insulin resistance index showed a tendency to be decreased by hc diet. AUG hc/sc ratio was inversely correlated with AUG or free fatty acids on standard carbohydrate diet. In conclusion, the present 4-week high carbohydrate/low fat diet may be useful to reduce body weight and insulin resistance. The 4-week high carbohydrate/low fat diet did not affect glucose tolerance as a whole. Although the 4-week high carbohydrate/low fat diet decreased HDL-Chol, it did not increase triglyceride.
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PMID:Effects of a 4-week 70% high carbohydrate/15% low fat diet on glucose tolerance and on lipid profiles. 1503 22

Elevated triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) levels, hallmarks of the atherogenic lipid profile found in the metabolic syndrome and type 2 diabetes, are commonly seen in Japanese patients with coronary heart disease (CHD). In the setting of mildly to moderately elevated plasma TG (150-500 mg/dl), very-low-density lipoprotein (VLDL) accumulates and so do high levels of atherogenic TG-rich, cholesterol-enriched remnant particles. Indeed, in hypertriglyceridemia, abnormalities are seen in the quantity and quality of all lipoprotein B-containing lipoproteins. Non-HDL-C (total cholesterol minus HDL-C) provides a convenient measure of the cholesterol content of all atherogenic lipoproteins, and thus incorporates the potential risk conferred by elevated levels of atherogenic TG-rich remnants that is additional to the risk associated with low-density lipoprotein cholesterol (LDL-C). Non-HDL-C level has been found to be a strong predictor of future cardiovascular risk among patients whether or not they exhibit symptoms of vascular disease, and was recently recommended as a secondary treatment target (after LDL-C) in patients with elevated TG by the National Cholesterol Education Program Adult Treatment Panel III. Adoption of this readily available measure to assess risk and response to treatment in patients with elevated TG would improve treatment of dyslipidemia in a substantial number at risk for CHD.
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PMID:Non-HDL cholesterol as a measure of atherosclerotic risk. 1506 93

African Americans have the highest overall coronary heart disease (CHD) mortality rate of any ethnic group in the United States. They also exhibit a greater prevalence of a number of individual CHD risk factors, especially hypertension and type 2 diabetes mellitus (a CHD risk equivalent) and greater clustering of risk factors. The African-American population is under-represented in lipid-lowering clinical end point trials and remains inadequately treated with lipid-lowering therapy in the clinical setting; this latter fact is of particular concern because, in the new National Cholesterol Education Program guidelines, many more black patients with hypercholesterolemia should be receiving more intensive lipid-lowering treatment. A number of steps must be taken to improve prospects of CHD risk reduction through lipid-lowering therapy in African Americans. These include improving the understanding of the relationship of risk factors to disease and improving the understanding of both lipid responses to and clinical benefits of lipid-lowering therapy. In addition, because African Americans have a higher prevalence of several modifiable CHD risk factors, this population should be rigorously targeted for risk-reduction strategies, including screening and treatment for hypertension, type 2 diabetes mellitus, and dyslipidemia. Educational outreach programs can provide a key role in raising community awareness of CHD risk factors and potential treatment options.
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PMID:Coronary heart disease and lipid-modifying treatment in African American patients. 1513 30

The most common alterations in lipid and lipoprotein metabolism in type 2 diabetes involve an elevation in both plasma triglyceride and VLDL concentrations, a dense LDL phenotype and low levels of HDL cholesterol. The inverse relationship between the level of HDL cholesterol and the risk of cardiovascular disease is commonly explained by the crucial role of HDL in reverse cholesterol transport. Cholesterol ester transfer protein (CETP) has a central role in the metabolism of HDL and may therefore alter the susceptibility to atherosclerotic vascular disease. To evaluate the effect of Taq1B polymorphism of intron 1 of CETP gene on serum lipid concentrations in Turkish type 2 diabetic patients, we investigated Taq1B polymorphism and serum lipid levels in 116 controls and in 164 diabetic patients. Polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP), and agarose gel electrophoresis techniques were used to determine the CETP Taq1B polymorphism. Serum lipid levels were measured enzymatically. Statistical analyses was performed by SPSS. In control group: subjects with B2B2 genotype have high HDL-cholesterol levels (p=0.029) and B1B1 genotypes have high triglyceride levels (p=0.07). Diabetic patients with and without MI with B2B2 genotype have high HDL-cholesterol levels. Taq B1B1 genotype has higher in diabetic patients with myocardial infarction (MI) than diabetic patients without myocardial infarction (42.1% and 32.7%; chi2=1.42, p=0.23). The present study demonstrates that the CETP Taq1B gene polymorphism is an association with low HDL cholesterol levels in patients with type II diabetes mellitus and healthy controls in Turkey. We also showed that CATE Taq1B gene polymorphism may be related to myocardial infarction in type II diabetic patients.
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PMID:Taq1B polymorphism of CETP gene on lipid abnormalities in patients with type II diabetes mellitus. 1513 31


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