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)

As hypercholesterolemia is an essential risk factor of atherosclerosis, a strategy for diagnosis and treatment of hyperlipidemia is indispensable. Differences in mortality from coronary heart disease in different cultures seem to be due to environmental, not to genetic factors. Trials in Finland and the United States have shown that cholesterol levels and smoking can be reduced by information and education with an ensuing drop in cardiovascular mortality. This experience warrants national programmes for cholesterol-lowering in high risk countries. Programmes should be directed to doctors and health officials as well as legislators and the public. Within any given population individual differences of lipid levels are due to both nutritional habits and genetic variations concerning e.g. LDL-receptors and lipase activity. At present the only means of identifying subjects at risk is to measure their lipid levels and to scrutinize their family history. Measurements should be repeated to exclude biologic and laboratory variability. Drugs currently available include HMG CoA reductase inhibitors, bile acid binding resins, clofibrate derivatives and nicotinic acid. Formerly defined age groups with regard to therapeutic measures have meanwhile been abandoned.
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PMID:Strategy for diagnosis and treatment of hyperlipidemia. 219 53

Lipid metabolism was evaluated in patients with chronic enteritis, celiac disease, general variable immunodeficiency (GVI), short-bowel syndrome. In chronic enteritis with malabsorption syndrome degree I and II changes in metabolism were characterized by hyperlipidemia due to high lipid fractions, mainly triglycerides; in malabsorption syndrome degree III (celiac disease, general variable immunodeficiency, short-bowel syndrome) by a drop of serum total lipids, phospholipids, cholesterol, beta-lipoproteins, free fatty acids, elevated concentrations of triglycerides. Changes in fatty acid composition of blood serum in patients with malabsorption syndrome degree III manifested by derangement of polyunsaturated fatty acids ratio. Arachidonic acid concentration was reduced in 100% of cases, linolenic acid in 45%. In all the patients with celiac disease and malabsorption syndrome degree III there was hypoactivity of lipolytic blood enzymes lipase and tributyrinase.
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PMID:[Disorders of lipid metabolism in patients with chronic diseases of the small intestine]. 228 16

We have studied the lipoproteins, apolipoproteins, and postheparin lipase activities in an extended pedigree with familial hepatic lipase deficiency. A deficiency of hepatic lipase was found in three of five brothers and in one of their children. Triglyceride enrichment of low density and high density lipoproteins was identified as the constitutive phenotype. beta-very low density lipoprotein was observed in hepatic lipase-deficient subjects, but it was absent when the plasma triglyceride concentration was less than 1 mM/l. The hepatic lipase-deficient subjects had normal or elevated low density lipoprotein cholesterol and high density lipoprotein cholesterol concentrations. Hyperprebetalipoproteinemia, hyperbetalipoproteinemia, and hyperalphalipoproteinemia were observed in both affected and unaffected family members. Compared with the unaffected family members, the hepatic lipase-deficient subjects had no significant differences in very low density lipoprotein cholesterol, very low density lipoprotein triglyceride, or low density lipoprotein cholesterol. These observations are consistent with the presence of additional genes causing hyperlipidemia in this family, independent of the deficiency of hepatic lipase.
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PMID:Plasma lipoproteins in familial hepatic lipase deficiency. 229 46

An infection of golden hamsters with Ancylostoma ceylanicum, a hookworm parasite, induced profound hyperlipidemia, particularly hypertriglyceridemia, and the effect was directly related to the degree of infection. A significant increase was also noticed in serum cholesterol and phospholipid levels. The appearance of lipoprotein-X, an abnormal low density lipoprotein, was detected in the serum of hookworm-infected animals. The hyperlipidemia was further characterized by an increase in very low density lipoproteins (VLDL) and low density lipoproteins (LDL) with a concomitant decline in high density lipoproteins (HDL). Decreased lipolytic activities, especially triglyceride lipase, in hepatic tissue and induction of lipolytic activities in intestine and adipose tissues indicated mobilization of fats from adipose and jejunum with a defective removal of triglyceride-rich lipoproteins in hepatic tissues. Accumulation of lipids in liver and depletion in adipose tissue supported these results. The derangement may have a significant effect on host parasite interaction and is an important pathophysiological feature occurring during experimental ancylostomiasis.
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PMID:Molecular basis of hyperlipidemia in golden hamsters during experimental infection with Ancylostoma ceylanicum (Nematoda:Strongylidae). 233 80

A monoclonal antibody-based direct binding enzyme-linked immunosorbent assay (ELISA) for apoprotein (apo) B-100 has been developed for use as a reference method. The assay uses the two well-characterized monoclonal antibodies, MB24 and MB47. MB47, which recognizes an epitope at the low density lipoprotein (LDL) receptor-binding domain of apoB and is specific for apoB-100, is bound to the microtiter plate as the capture antibody. MB24, which binds an epitope in the amino terminal half of the apoB-100 and identifies both apoB-100 and apoB-48, is conjugated to horseradish peroxidase and is utilized as the indicating antibody. The assay was calibrated with LDL (d 1.030-1.050 g/ml) and the LDL protein was determined by a sodium dodecyl sulfate (SDS) Lowry procedure. The working range of the assay is 0.25-1.25 micrograms/ml. Optimal dilution of whole plasma was found to be 1:2000. In the assay, MB47 bound approximately 97% of the apoB in all low density lipoprotein, and greater than 90% of the apoB in the majority of very low density lipoprotein preparations. Small dense LDL from subjects with familial combined hyperlipidemia (FCHL) and large bouyant LDL from subjects with familial hypercholesterolemia (FH) exhibited binding properties similar to LDL from healthy normolipidemic subjects when tested in the reference ELISA. The intra- and interassay coefficients of variation averaged 2.5% and 6.0%, respectively. Plasma B-100 levels were not influenced by freezing and thawing or storage at 4 degrees C for up to 3 weeks or storage at -70 degrees C for up to 11 months. Excellent agreement was obtained between the reference ELISA and a polyclonal RIA which measures total apoB (r = 0.93, n = 105, mean ELISA B-100 value = 100 mg/dl, mean RIA value = 101 mg/dl, Sy = 9.6). Reference ELISA B-100 values of samples pretreated with bacterial lipase were not significantly increased in most samples with plasma triglyceride levels below 600 mg/dl. To help reduce the large among-laboratories variability of apoB measurements, we recommend that this candidate reference direct binding ELISA be used to assign apoB target values to apoB reference pools.
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PMID:Evaluation of a monoclonal antibody-based enzyme-linked immunosorbent assay as a candidate reference method for the measurement of apolipoprotein B-100. 260 May 45

Hyperlipidemia of initially Type V and finally of Type III was observed in a patient with Weber-Christian disease. The lipoprotein lipase (LpL) and hepatic triglyceride lipase (HTGL) activities of the post-heparin plasma were low, but detectable. Both lipase activities were higher when assayed with 20 microliters of post-heparin plasma than with more than 30 microliters, indicating the presence of some inhibitory factor in the plasma. This plasma inhibited purified LpL and HTGL from human post-heparin plasma. Zonal ultracentrifugation studies showed that the inhibitor of hepatic lipase was associated with the middle fraction of intermediate lipoprotein and low density lipoproteins (1.020 less than d less than 1.040). These results are consistent with the idea that dyslipoproteinemia in this patient was partially due to dysfunction of the catabolic system caused with an inhibitor of lipolytic enzymes.
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PMID:Dyslipoproteinemia and an inhibitor of lipolytic enzymes in Weber-Christian disease. 273 46

Salmon (Oncorhynchus kisutch) somatostatin (sSS; 4 or 8 ng/g body wt) or synthetic Gillichthys urotensin II (UII; 2 or 4 ng/g body wt) were injected intraperitoneally into juvenile freshwater coho salmon. Both sSS and UII caused a dose-dependent increase in plasma free fatty acids (FFA) which diminished with time. sSS induced an initial (1 hr) transient hyperglycemia. By contrast, UII tended to induce hypoglycemia, this effect being significant 5 hr after injection of the higher dose. Both sSS and UII depressed plasma insulin titers 1 hr after injection. By 3 hr, the sSS-associated insulin depression was no longer observed. UII treatment induced a hyperinsulinemia which was present 3 and 5 hr after peptide administration. Although no decreases in liver total lipid concentration or in mesenteric fat total tissue mass were observed, lipolytic enzyme activity within each depot was significantly enhanced by both peptides. Neither sSS nor UII altered 3H2O incorporation into fatty acids or neutral lipids. However, enhanced lipogenesis, particularly by UII, was indicated by increased NADPH production resulting from glucose-6-phosphate dehydrogenase activity. Both sSS and UII enhanced glucose mobilization, as indicated by decreased liver glycogen content and increased liver glucose-6-phosphatase activity. UII, but not sSS, stimulated glycogen synthetase activity. These results suggest that both sSS and UII stimulate hyperlipidemia by enhancing depot lipase activity and that although both factors are potentially gluconeogenetic, sSS seems to be glycogenolytic and hyperglycemic, whereas UII may channel glucose to FFA synthesis.
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PMID:Effects of somatostatin-25 and urotensin II on lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 288 97

Fourteen male patients (mean age +/- SD, 52 +/- 11 years) with a history of hypertension (systolic blood pressure, 148 +/- 10 mm Hg; diastolic blood pressure, 99 +/- 2 mm Hg) were enrolled in a cross-over trial of prazosin and atenolol, with a minimum of eight weeks of treatment with each drug. Measures of lipoprotein metabolism included levels of: total plasma cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and high-density lipoprotein2 cholesterol. Lipoprotein mass was measured by analytical ultracentrifugation in low-density to very low-density lipoprotein flotation rate intervals of 0 to 12, 12 to 20, and 20 to 400, and high-density lipoprotein flotation rate intervals of 0 to 3.5 and 3.5 to 9.0. Apolipoproteins A1 and B, postheparin lipoprotein and hepatic lipase activities, and magnitude of postprandial lipemia also were determined. Mass of intermediate-density lipoproteins (flotation rate, 12 to 20) was significantly lower (p = 0.05) following prazosin therapy compared with atenolol therapy. Other lipid parameters, including triglycerides and low- and high-density lipoprotein cholesterol, were not significantly different for the two drug treatments.
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PMID:Effect of alpha- and selective beta-blockade for hypertension control on plasma lipoproteins, apoproteins, lipoprotein subclasses, and postprandial lipemia. 291 69

We examined 56 French Canadians, aged 1 week to 54 years, from eastern Quebec who were referred to the Laval University Lipid Research Centre and in whom coincidental finding (in 46% of the cases), abdominal pain (in 32%) or family screening (in 22%) led to the diagnosis of primary lipoprotein-lipase-activity deficiency (familial hyperchylomicronemia). Half of the patients had one or more of the following signs: lipemia retinalis, eruptive xanthomas, splenomegaly and hepatomegaly; the plasma triglyceride concentrations were significantly higher (greater than 40 mmol/L) among these patients than among those without clinical signs (mean 21.7 [standard deviation 13.5] mmol/L). The prevalence rate of this disorder was 30 times higher than the previously published rate and was highest in the counties of Charlevoix and Saguenay-Lac-St-Jean (200 and 100 cases per million respectively) because of the distinct demographic history of these areas. Because of a founder effect an autosomal recessive gene involved in lipoprotein-lipase expression or activation has probably been disseminated among this isolated French Canadian population.
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PMID:Primary lipoprotein-lipase-activity deficiency: clinical investigation of a French Canadian population. 291 62

Apoprotein, lipoprotein and lipid parameters of 36 normolipidemic subjects (23 males, mean age 22.7 +/- 7.6 years; 13 females, mean age 26.2 +/- 9.8 years) receiving oral isotretinoin (mean daily dose 0.73 +/- 0.26 mg/kg body weight) for nodulocystic acne (n = 18), severe acne papulopustulosa (n = 15), gram-negative folliculitis (n = 2) and papulopustular rosacea (n = 1) were monitored before and during isotretinoin therapy at biweekly intervals over a period of 14.6 +/- 5.6 weeks. Pretreatment values of mean plasma triglycerides increased significantly (p less than 0.001) from 81.8 +/- 31.9 mg/dl to 112.4 +/- 38.7 mg/dl (47.4%) during isotretinoin treatment. With respect to the mean percent increase of plasma triglycerides from pretreatment levels, patients were classified as nonresponders (less than 10% triglyceride increase), responders (greater than 10% less than 50% triglyceride increase) and hyperresponders (greater than 50% triglyceride increase), revealing a distribution of 25.0, 36.1 and 38.9%, respectively. Isotretinoin treatment had no influence on the isoelectric focusing pattern of apoprotein E isoforms and C apoproteins. In particular, apoprotein C-II, the cofactor of lipoprotein lipase, was not affected. No correlation between apoprotein E phenotypes (2/3, 3/3, 3/4) and the mean plasma triglyceride increase could be demonstrated. Apoprotein B-48, a marker of chylomicrons and atherogenic chylomicron remnants, could not be detected by SDS-PAGE. On the other hand in 21.0% of patients with preexisting mean lipoprotein Lp(a) levels of 18.1 +/- 12.9 mg/dl a moderate increase of atherogenic Lp(a) to mean levels of 37.0 +/- 22.0 mg/dl was observed. Pretreatment values of very-low-density lipoprotein (VLDL) apoprotein (apo) B (7.5 +/- 2.0 mg/dl), low-density lipoprotein apo B (67.3 +/- 17.5 mg/dl) and total plasma apo B (76.6 +/- 19.0 mg/dl) increased significantly to levels of 10.3 +/- 2.4 mg/dl (p less than 0.001), 75.7 +/- 15.8 mg/dl (p less than 0.10) and 85.9 +/- 17.7 mg/dl (p less than 0.05), respectively. As lipoprotein lipase and hepatic lipase activities have been shown to be unaffected by isotretinoin treatment, our data support the hypothesis that isotretinoin induces hepatic oversecretion of VLDL, a condition resembling type IV hyperlipidemia in diabetics, familial hypertriglyceridemia of familial combined hyperlipidemia.
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PMID:Characterization of apoprotein metabolism and atherogenic lipoproteins during oral isotretinoin treatment. 296 29


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