Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distal enzymatic step in the process of glucose output is catalyzed by the glucose-6-phosphatase (Glc-6-Pase) complex. The recently cloned catalytic unit of this complex has been shown to be regulated by insulin, dexamethasone, cAMP, and glucose. Using a combination of intralipid and/or nicotinic acid infusions and a pancreatic clamp technique, we maintained plasma free fatty acids (FFAs) at three different levels (0.26 +/- 0.07, 0.56 +/- 0.09, and 1.59 +/- 0.12 mmol/l) in the presence of well-controlled hormonal and metabolic conditions. An increase in the plasma FFA concentration within the physiological range caused a rapid, greater than threefold increase in the mRNA and protein levels of the catalytic subunit of Glc-6-Pase in the liver. These data indicate that the in vivo gene expression of Glc-6-Pase in the liver is regulated by circulating lipids independent of insulin and thus that prolonged hyperlipidemia may contribute to the increased production of glucose via increased expression of this protein.
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PMID:Induction of hepatic glucose-6-phosphatase gene expression by lipid infusion. 897 Oct 97

Atorvastatin is a synthetic HMG-CoA reductase inhibitor which lowers plasma cholesterol levels by inhibiting endogenous cholesterol synthesis. It also reduces triglyceride levels through an as yet unproven mechanism. Dose-dependent reductions in total cholesterol, low density lipoprotein (LDL)-cholesterol and triglyceride levels have been observed with atorvastatin in patients with hypercholesterolaemia and in patients with hypertriglyceridaemia. In large trials involving patients with hypercholesterolaemia, atorvastatin produced greater reductions in total cholesterol, LDL-cholesterol, apolipoprotein B and triglyceride levels than lovastatin, pravastatin and simvastatin. In patients with primary hypercholesterolaemia, the combination of atorvastatin and colestipol tended to produce larger reductions in LDL-cholesterol levels and smaller reductions in triglyceride levels than atorvastatin monotherapy. Although atorvastatin induced smaller reductions in triglyceride levels and more modest increases in high density lipoprotein (HDL)-cholesterol levels than either fenofibrate or nicotinic acid in patients with combined hyperlipidaemia, it produced larger reductions in total cholesterol and LDL-cholesterol. As with other HMG-CoA reductase inhibitors, the most frequently reported adverse events associated with atorvastatin are gastrointestinal effects. In comparative trials, atorvastatin had a similar adverse event profile to that of other HMG-CoA reductase inhibitors. Clinical data with atorvastatin are limited at present. However, with its ability to markedly reduce LDL-cholesterol levels, atorvastatin is likely to join other members of its class as a first-line agent for the treatment of patients with hypercholesterolaemia, if changes in lipid levels with atorvastatin convert to reductions in CHD mortality and morbidity. Atorvastatin may be particularly suitable for patients with heterozygous or homozygous familial hypercholesterolaemia because of the marked reductions in LDL-cholesterol experienced with the drug. Additionally, because of its triglyceride-lowering properties, atorvastatin appears to have the potential to become an appropriate treatment for patients with combined hyperlipidaemia or hypertriglyceridaemia.
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PMID:Atorvastatin. A review of its pharmacology and therapeutic potential in the management of hyperlipidaemias. 912 69

This review article examines the mode of action, the efficacy and the side effects of the various types of hypolipidemic agents (fibrates, bile acid sequestrants, statins, nicotinic acid and acipimox) currently available in Belgium. It also summarizes the recent guidelines recommended by the Belgian Lipid Club in the management of hyperlipidemia for the primary and secondary prevention of cardiovascular diseases as well as the therapeutic strategy.
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PMID:[Pharmacology of hypolipidemic agents]. 913 14

A 34-year-old male with a history of angina pectoris suddenly developed weakness in the right upper and lower limbs, and consulted our hospital. Computed tomography (CT) and magnetic resonance imaging (MRI) suggested cerebral infarction. Cerebral angiography revealed stenosis at the M1 portion of the left middle cerebral artery. Hypertension, diabetes, tobacco or hyperlipidemia were not considered as risk factors for cerebral infarction. The lipoprotein (a) [Lp(a)] level was high. In the present case, medication with a nicotinic acid agent, niceritrol, for hyperlipoproteinemia and low density lipoprotein (LDL) apheresis were performed. Concerning family history, the patient's mother and younger sister had hyperlipoproteinemia. Recent studies have reported that increased Lp(a) levels are an independent risk factor even in cerebral infarction and coronary artery disease. Measurement of Lp(a) levels and treatment for increased Lp (a) levels may be important.
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PMID:[Juvenile cerebral infarction with familial hyperlipoproteinemia (a)--case report]. 916 61

Pravastatin treatment of combined hyperlipidemia lowers low-density lipoprotein effectively; nicotinic acid lowers remnant cholesterol and raises high-density lipoprotein. A combination of these 2 drugs may be indicated for optimal treatment of lipoprotein abnormalities in combined hyperlipidemia.
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PMID:Comparison of pravastatin with crystalline nicotinic acid monotherapy in treatment of combined hyperlipidemia. 916 13

The aim of the treatment of dyslipidaemia is the primary and secondary prevention of coronary heart disease (CHD). Dietary therapy is the first line in the management of hyperlipidaemia. Lipid-lowering drugs should be used in patients with an inadequate dietary response, with CHD and/or multiple CHD risk factors. The choice of drug depends on the lipid disorder type, the desired plasma lipids reduction and presence of contraindications. Lipid-lowering drugs-anion-exchange resins, nicotinic acid and acipimox, fibrates, statins, probucol and two new classes used in experimental studies (ansamycins and ACAT inhibitors) are presented. Antiatherosclerotic properties of statins are characterized.
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PMID:[Pharmacologic treatment of lipid metabolism disorders]. 921 49

In all patients with coronary heart disease a fasting lipid profile (total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides) should be obtained. Hyperlipidemias can then be classified as hypercholesterolemia (LDL cholesterol elevated), mixed hyperlipidemia (LDL cholesterol elevated, triglycerides elevated) and hypertriglyceridemia (triglycerides elevated). Primary goal of lipid intervention is a LDL cholesterol < 100 mg/dl, secondary goals are HDL cholesterol > 35 mg/dl and triglycerides < 200 mg/dl. These goals can be reached by dietary intervention alone (reduction in fat and modification of fat intake) or in combination with lipid lowering drugs. Monotherapy with HMG-CoA reductase inhibitors or combined therapy with bile acid sequestrants will allow a reduction in LDL cholesterol by more than 50%; in predominant hypertriglyceridemia fibrates or nicotinic acid will lower triglycerides and elevate HDL cholesterol.
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PMID:[Goals and practical implementation of lipid therapy in coronary heart disease]. 930 97

Subjects with diabetes have a greatly increased risk of CHD, which is only partially related to their elevated glucose. Other factors such as insulin resistance and dyslipidemia are likely to be important. The type of dyslipidemia that is most characteristic of type 2 diabetic subjects is elevated triglycerides and decreased HDL cholesterol levels, although all lipoproteins have compositional abnormalities. Surprisingly few good prospective studies of lipoprotein levels in relation to CHD have been done in diabetic subjects. Available studies suggest that low HDL cholesterol may be the most important risk factor for CHD in observational studies. In studies in which total cholesterol and triglyceride were done, cholesterol and triglycerides were risk factors for CHD, although triglycerides were often a stronger predictor. However, the strength of triglyceride as a risk factor for CHD may depend partially on its association with other variables (e.g., hypertension, plasminogen activator inhibitor 1 [PAI-1], etc.). In clinical trials in diabetic subjects, LDL reduction with statins has led to significant reductions in CHD incidence. In addition, overall mortality was reduced with statin therapy, although the results were not statistically significant. Gemfibrozil has led to reductions in CHD incidence in diabetic subjects, although the results were not statistically significant perhaps because of low sample size. Regarding lipoproteins and CHD risk in diabetic patients, the very positive results of statin trials point to LDL cholesterol being more important than previous realized. Apparently, having a borderline high LDL cholesterol (between 130 and 160 mg/dl) in a diabetic patient is equivalent to a much higher LDL cholesterol in terms of CHD risk for a nondiabetic subject. Therefore, the primary target of therapy in diabetic patients is lowering LDL cholesterol (or possibly, non-HDL cholesterol). Statins are the preferred pharmacological agent in this situation. Once LDL cholesterol levels have been lowered, attention can be given to treatment of residual hypertriglyceridemia and low HDL. The goal here is weight reduction and increased exercise. However, for selected patients, combining a fibric acid (or low-dose nicotinic acid) with a statin also can be considered. Reduction of LDL levels should take priority over reduction of triglycerides in combined hyperlipidemia because of the proven safety of the statin class of drugs as well as greater reduction in CHD incidence.
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PMID:Management of dyslipidemia in adults with diabetes. 953 88

The aim of the study was to compare efficacy and safety of one-year therapy with slow-release nicotinic acid (KN-SR) and with ordinary form of the acid (KN). The examination was performed in the group of 136 patients with hyperlipidemia-type II. KN-SR had satisfactory effectiveness and was much better tolerated than KN. During one-year treatment with KN-SR there were observed the decrease of total cholesterol (TC) by 18%, LDL-C by 22%, triglycerides by 36%, Lp(a) by 56%, and the increase of HDL-C by 12%. The percentage of skin unwanted signs differed significantly between KN-group (90.2%) and KN-SR group (24%). Hepatotoxic effects were not observed and antipyrine kinetics did not change during one-year treatment with slow-release nicotinic acid.
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PMID:[Prolonged treatment with slow release nicotinic acid in patients with type II hyperlipidemia]. 959 56

The importance of treating dyslipidemias based on cardiovascular risk factors is highlighted by the National Cholesterol Education Program guidelines. The first step in evaluation is to exclude secondary causes of hyperlipidemia. Assessment of the patient's risk for coronary heart disease helps determine which treatment should be initiated and how often lipid analysis should be performed. For primary prevention of coronary heart disease, the treatment goal is to achieve a low-density lipoprotein (LDL) cholesterol level of less than 160 mg per dL (4.15 mmol per L) in patients with only one risk factor. The target LDL level in patients with two or more risk factors is 130 mg per dL (3.35 mmol per L) or less. For patients with documented coronary heart disease, the LDL cholesterol level should be reduced to less than 100 mg per dL (2.60 mmol per L). A step II diet, in which the total fat content is less than 30 percent of total calories and saturated fat is 8 to 10 percent of total calories, may help reduce LDL cholesterol levels to the target range in some patients. A high-fiber diet is also therapeutic. The most commonly used options for pharmacologic treatment of dyslipidemia include bile acid-binding resins, HMG-CoA reductase inhibitors, nicotinic acid and fibric acid derivatives. Other possibilities in selected cases are estrogen replacement therapy, plasmapheresis and even surgery in severe, refractory cases.
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PMID:Management of dyslipidemia in adults. 960 9


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