Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of coronary artery disease (CAD) and peripheral artery disease (PAD) was studied in 280 (203 males, 77 females) patients with different types of primary hyperlipoproteinemia. In primary hyperbetalipoproteinemia the prevalence of CAD (45% for Type IIa and 47% for Type IIb) is significatly higher than that in the other types of hyperlipoproteinemia (38% for Type IV and 17% for Type V). On the other hand, PAD prevalence is much higher in hypertriglyceridemia (21% in Type IIb and 20% in Type V) than in hypercholesterolemia alone (9% in Type IIa). These results suggest ths atherosclerotic complications are concerned. Moreover, the high frequency of PAD found in hypertriglyceridemia can be related to the high occurrence of diabetes in these patients. The effects of other major risk factors of atherosclerosis (smoking and hypertension) were also evaluated. Our results indicate that the association of hypercholestolemia and hypertension is more dangerous than the co-occurence of hypercholesterolemia and smoking.
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PMID:Prevalence of coronary artery disease and peripheral artery disease in patients with different types of primary hyperlipidemia. 85 27

Platelet hypersensitivity has been documented in diabetes and angina pectoris and can be partially reversed in hyperbetalipoproteinemia by clofibrate. We therefore examined the effects of incubating another lipid-lowering agent, halofenate, with both normal platelets and platelets made hypersensitive in vitro by incorporation of 55 per cent excess cholesterol into their membranes. At therapeutic concentrations, halofenate caused a time- and dose-dependent inhibition of the aggregation of normal platelets by epinephrine. After 30 minutes' incubation at 37 degrees C., halofenate significantly inhibited the extent of aggregation by 88 per cent (p less than 0.01), whereas clofibrate inhibited aggregation by 44 per cent (p less than 0.01). Halofenate was a more potent inhibitor of platelets than clofibrate (p less than 0.01). The mean threshold concentration of epinephrine necessary for aggregation of normal platelets (4.2 muM) was not significatnly increased with clofibrate (10 muM) but was markedly elevated with halofenate (245 muM; p less than 0.001). Significant but less dramatic increases in threshold concentration of ADP and collagen were found with halofenate but no clofibrate. Cholesterol-rich platelets were 114-fold more sensitive to epinephrine and twofold more sensitive to ADP than normal platelets but after incubation with halofenate became even less sensitive than normal. Clofibrate inhibited the extent of aggregation of hypersensitive platelets but did not alter the threshold concentration of epinephrine necessary for aggregation. Thus, halofenate is more potent than clofibrate in reducing the sensitivity of normal platelets to aggregating agents in vitro and can completely reverse experimentally produced platelet hypersensitivity. These data suggest that halofenate might be useful in reversing increased platelet sensitivity in cardiovascular diseases.
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PMID:Halofenate: a potent inhibitor of normal and hypersensitive platelets. 95 86

Fasting levels of plasma cholersterol and triglyceride, lipoprotein patterns, and fasting and postintravenous glucose levels of blood glucose, serum insulin, serum growth hormone, and plasma free fatty acids in a genetic potential diabetic population were compared to those in a similar normal control population. THe potential diabetic population was further divided into groups of patients with a normal (prediabetic) or abnormal (chemical diabetic) glucose tolerance test. Although no clear-cut lipid differences were noted, certain trends appeared. More type IV hyperlipoproteinemia was seen in male prediabetic (21%) and male chemical diabetic patients (19%) than in normal male subjects (5%); in female subjects only a few type IV patterns were seen. Type II hyperlipoproteinemia was not seen in any normal subject, but was noted in nearly 9% of those with chemical diabetes. Fasting cholesterol levels correlated better with age than did fasting triglyceride levels in most of the patient groups. Fasting triglyceride levels showed a significant positive correlation with the serum insulin area of the oral glucose tolerance test in the normals wna prediabetic persons, and also showed a significant positive correlation with the blood glucose area of the prediabetic and chemical diabetic patients. It is suggested that a normal relationship between triglyceride concentration and insulin response to glucose is lost in chemical diabetes. Sex differences were also noted in the inslin response and the insulin-glucose relationships during the oral glucose tolerance test, with normal menstruation women showing a significantly lower insulin-glucose relationship than the age-related men.
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PMID:Lipid, glucose, and insulin interrelationships in normal, prediabetic, and chemical diabetic subjects. 95 89

The prevalence of mild and moderate hypercholesterolemia among the middle-aged population of the G.D.R. is about 30%. Thus, this is the most important risk factor for coronary heart diseases. Primary therapeutic techniques are elimination of overweight, low-fat diet, rich in monoenic and polyenic acids, and increase of physical activity. When by these measures a decrease of cholesterol to 5.2-5.5 mmol/l is not achieved the introduction of lipid drugs is to be considered in dependence on the individual risk (associated risk factors like smoking, hypertension, diabetes, low HDL-cholesterol). In case of mild to moderate polygenic hypercholesterolemia cholestyramine, nicotinic acid and modern fibrates have the priority. Familial hypercholesterolemia demands as a rule the introduction of statins (e.g. lovastatin) or combinations of the above mentioned lipid drugs or the combination of cholestyramine and lovastatin, resp. In this way the prognosis even of patients with severe familial hypercholesterolemia can be improved decisively. Considering the fact that this would be a life-accompanying therapy a thorough consideration of the risk/benefit ratio and an adequate medical supervision are necessary.
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PMID:[Guidelines for the treatment of hypercholesterolemia]. 224 95

In 3 groups of patients with high thrombotic risk (diabetes mellitus, hyperbetalipoproteinemia, hypertension) the platelet aggregation and the level of circulating platelet aggregates were found statistically higher than in normal controls. In addition, platelet aggregation in diabetic patients was found statistically higher than in the other 2 groups of patients. Therefore these 2 parameters of platelet function are useful for the screening of patients with potential risk for thrombosis allowing a more selective and defined prophylaxis, both of thrombosis and atherosclerotic complications.
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PMID:[Platelet hyperfunction in prethrombotic vascular disease]. 673 1

Atherosclerosis and its consequences account for most morbidity and mortality in Western countries. Atherosclerosis develops over a period of decades and has a complex pathogenesis. It is a disease of the intima and primarily involves four cell types, i.e. endothelial and vascular smooth muscle cells, monocytes and platelets. In recent years, elucidation of the cellular and molecular mechanisms of these cells, and their alterations by cardiovascular risk factors and in atherosclerosis, has markedly expanded knowledge of this disease. In particular, it became clear that endothelial cells play a crucial role in the regulation of platelet function and coagulation, as well as vascular tone and structure. Interestingly, endothelial dysfunction occurs early on in the presence of cardiovascular risk factors such as hyperlipidemia, hypertension and diabetes. This could lead to adhesion of circulating platelets and monocytes, increased accumulation of lipids in the subintima, increased contraction, migration and proliferation of vascular smooth muscle cells. The fact that atherosclerosis develops only in some but not in other parts of the circulation, however, has rarely been considered. With the development of molecular biology it has now become possible to clone differentially expressed genes in vessels with or without atherosclerosis; this in turn makes it possible to characterize better the molecular and cellular mechanisms of the disease. The search for such candidate genes could form the basis for future genetic interventions. This therapeutic approach is likely to assume clinical importance, particularly in monogenetic diseases (i.e. familial hypercholesteremia), while its use in complex polygenetic diseases such as atherosclerosis is more difficult. Restenosis, however, may be accessible to gene therapy earlier on as it is accessible to local gene transfection.
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PMID:[Molecular medicine and gene therapy as exemplified with arteriosclerosis and restenosis]. 750 10

Familial hypercholesterolemia (FH) is a genetic disease characterized by high serum cholesterol levels and premature coronary atherosclerosis. Hypercholesterolemia is one of the factors promoting the arteriosclerotic process and is a major cause of aortic aneurysm. Few data are available, however, about abdominal aortic aneurysms (AAAs) in patients with FH. In this study, the clinical and angiographic characteristics of AAAs found in patients with FH were investigated. Thirty-one cases (23 men, 8 women, aged fifty +/- fourteen years) were examined by coronary angiography, thoracic and abdominal aortography, and clinical data. Abdominal aortography detected abdominal aneurysms in 8 cases (26%), all of whom were men, including 4 cases (50%) that were complicated by diabetes mellitus. The abdominal aneurysm patients manifested severe coronary atherosclerosis, severe abdominal aortic irregularity, and higher blood pressure than the nonaneurysm FH patients. These findings suggest that AAAs are an important and prevalent feature in FH, especially in men with diabetes mellitus and high blood pressure.
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PMID:Abdominal aortic aneurysms in familial hypercholesterolemia--case reports. 850 16

The purpose of the present study was to elucidate the characteristic lipoprotein disorder in essential hypertension. Twenty-six patients with essential hypertension (HT) but without diabetes mellitus or obesity and 24 healthy subjects (control) were recruited into this study. Lipoproteins of HT and controls were separated by ultracentrifugation to very-low-density lipoprotein (VLDL), intermediate density lipoprotein (IDL), low-density liproprotein (LDL), and (HDL) fractions. Cholesterol and triglycerides were determined with enzyme assay, and apoB were determined by highly sensitive latex agglutination (Kyowa-hakko Co. LD). There was no difference in age (mean +/- SE; HT, 63 +/- 2 versus control, 60 +/- 2 years) or body-mass index (22.7 +/- 0.4 versus 21.7 +/- 0.5 kg/m2) between HT and controls. Blood pressure in HT and controls was 158 +/- 2/87 +/- 12 mm Hg and 123 +/- 3/72 +/- 2 mm Hg, respectively. Cholesterol did not change significantly in plasma (192.1 +/- 7.0 versus 176.4 +/- 4.2 mg/dL), VLDL (15.2 +/- 2.4 versus 11.8 +/- 1.7 mg/dL), IDL (14.8 +/- 2.4 versus 10.7 +/- 1.6 mg/dL), LDL (93.7 +/- 4.6 versus 83.1 +/- 3.9 mg/dL), nor in HDL (51.9 +/- 2.7 versus 58.1 +/- 3.2 mg/dL). Triglycerides (TG) increased in plasma (120.0 +/- 10.0 versus 87.5 +/- 9.3 mg/dL, p < 0.05), although TG did not change in all subfractions. ApoB increased in plasma (105.5 +/- 5.1 versus 85.6 +/- 3.6 mg/dL, p < 0.01), IDL (9.0 +/- 1.3 versus 5.4 +/- 0.6 mg/dL, p < 0.05), and LDL (76.3 +/- 4.3 versus 59.4 +/- 3.7 mg/dL, p < 0.01) in HT compared with controls. The ratio of cholesterol to apoB in LDL decreased (1.27 +/- 0.06 versus 1.48 +/- 0.08, p < 0.05). In essential HT, number of apoB containing lipoproteins (IDL, LDL) increased. Low ratio of cholesterol to apoB was noted in LDL, indicating the presence of small, dense LDL. As cholesterol in LDL was normal, hyperbetalipoproteinemia is also a characteristic disorder of essential HT.
J Diabetes Complications
PMID:Hyperbetalipoproteinemia with small low-density lipoprotein, a characteristic disorder of lipoprotein in essential hypertension. 857 33

Cholesterol, triglyceride (TG), and apolipoprotein (apo) B were determined in plasma and in lipoprotein subfractions (VLDL, intermediate-density lipoproteins [IDL], LDL, and HDL) in nonobese NIDDM subjects, who were classified into well-controlled, fairly controlled, or poorly controlled states with or without macrovascular complications (macroangiopathy [MA]). The same analyses were also performed on subjects who had coronary artery disease (CAD) with stable angina pectoris (SA) or unstable angina pectoris (UA) and acute myocardial infarction, cerebrovascular disease (CVD) with atherothrombotic or lacunar infarction, and arteriosclerosis obliterans (ASO). In nonobese NIDDM subjects, the number of apoB-containing lipoproteins (VLDL, IDL, and LDL) increased. This alteration was more prominent in subjects with poorly or fairly controlled disease as well as in subjects with MA, but not in those with well-controlled NIDDM. Cholesterol/apoB in LDL decreased in subjects with poorly or fairly controlled diabetes or with MA and was correlated with low HDL cholesterol. The disorder is characterized by hyperbetalipoproteinemia with elevated LDL cholesterol and small dense LDL. In obese NIDDM subjects, the similar disorder was more pronounced. Glycemic control had less effect and hyperinsulinemia, if present, aggravated the lipid disorder. In those with CAD, the number of IDLs increased and the LDL fraction had the properties of small dense LDL. HDL cholesterol decreased. In those with UA, the LDL number increased without elevation of LDL cholesterol, indicating typical hyperbetalipoproteinemia. The subjects with atherothrombotic brain infarction, an increased number of small-sized LDLs was noted. In those with ASO, the number of VLDL and IDL increased with small LDL. HDL cholesterol decreased in those with CAD, cerebrovascular disease, and ASO. Since similar quantitative and qualitative alterations of apoB-containing lipoprotein have been observed in NIDDM patients as well as in those with macrovascular diseases, diabetic patients are thought to be more susceptible to the initiation and progression of atheromatous lesions in coronary, brain, and peripheral arteries.
Diabetes 1996 Jul
PMID:Quantitative and qualitative derangement of apolipoprotein B-containing lipoproteins as a risk factor for diabetic macroangiopathy in nonobese NIDDM subjects. 867 86

Plasma lipoprotein cholesterol abnormalities, diabetes, hypertension and smoking have all been identified as independent predictors of cardiovascular events. Clustering of multiple risk factors suggests a common metabolic link among high blood pressure, insulin resistance, plasma lipoprotein abnormalities and obesity. New guidelines for the management of dyslipidemias target patients with established coronary artery disease (CAD), and high risk patients with multiple risk factors and severe genetic lipoprotein disorders, such as familial hypercholesterolemia. To determine the prevalence of lipoprotein, apolipoprotein and metabolic disorders in premature CAD, 243 men and 61 women with premature CAD (occurring before age 60 years) and 203 age- and sex-matched controls (152 men, 61 women) were studied. After correcting for beta-blocker use (40% of men and 54% of women), hypertension and diabetes were seen more frequently in CAD patients than in controls. In men and women, cholesterol, triglycerides, low density lipoprotein (LDL) cholesterol, apolipoprotein B and lipoprotein (a) were significantly higher, and high density lipoprotein (HDL) cholesterol was lower, in CAD patients than in controls. By stratifying patients according to LDL cholesterol: HDL cholesterol ratio (5 or less, or greater than 5) and by triglyceride levels (less than 2.3 mmol/L, or 2.3 mmol/L or greater), significantly more men and women with CAD were found to have an elevated LDL cholesterol:HDL cholesterol ratio and elevated triglycerides (13.8% versus 1.9%, men and women combined, CAD versus controls, P < 0.0001). A metabolic factor index was devised, assigning a score of 1 each for presence of hypertension, lipoprotein abnormalities, diabetes or fasting blood glucose above 7.0 mmol/L, and a body mass index of 27 or greater. The prevalence of a metabolic factor index of 3 or more was 29.2% in CAD men versus 6.7% in controls (P < 0.0001) and 38.3% in CAD women versus 11.7% in controls (P < 0.01). Familial hypercholesterolemia was seen in fewer than 5% of patients with premature CAD and type III dyslipoproteinemia in one of 343 CAD patients. The distribution of apolipoprotein E phenotypes was the same in CAD patients and controls. Multivariate analysis revealed that in men, HDL cholesterol, lipoprotein (a) levels and smoking were the best predictors of risk. In men, plasma levels of LDL cholesterol, triglycerides or body mass index did not enter the model at the P < 0.05 level. In women, low HDL cholesterol, lipoprotein (a), the presence of diabetes, smoking and apolipoprotein B levels were all predictors of risk (P < 0.05). However, the clustering of risk factors may be the best predictor of risk. In this selected population, HDL and lipoprotein (a) are the best metabolic markers of premature CAD; metabolic factor clustering is common in patients with premature CAD.
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PMID:Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians. 911 13


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