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)

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

An important function of endothelium is to release PGI2, a prostaglandin produced from arachidonic acid that prevents platelet aggregation and causes arterial relaxation. Small amounts of other eicosanoids also are produced, but their role in endothelial function has not been elucidated. Much of the arachidonic acid present in the endothelium is obtained preformed from the plasma, either as FFA or from lipoproteins. Arachidonic acid is efficiently incorporated into endothelial lipids even when only relatively small amounts are available. In response to agonists, arachidonic acid is rapidly released from the endothelial phospholipids and converted to eicosanoids. Small amounts of eicosanoids also are continuously formed due to exposure of the endothelium to free fatty acid and lipoproteins containing arachidonic acid, without the need for any additional stimulus. Although the role of plasma lipid abnormalities has not been systematically investigated, there presently is little indication that hyperlipidemia interferes with endothelial arachidonic acid metabolism or the capacity of the endothelium to produce eicosanoids.
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PMID:Lipid and lipoprotein effects on endothelial eicosanoid formation. 306 Oct 5

We investigated the effect of 12 months' HMG-CoA reductase inhibitor treatment on plasma polyunsaturated fatty acid concentrations in 19 patients with hyperlipidemia. Arachidonic acid concentrations were significantly increased following treatment (from 110.1 +/- 20.4 mg/l to 129.2 +/- 31.6 mg/l, P < 0.05). The ratio of eicosapentaenoic acid to arachidonic acid was significantly decreased at the end of 12 months' treatment (from 0.702 +/- 0.370 to 0.541 +/- 0.204, P < 0.05). These results suggest that HMG-CoA reductase inhibitors may increase the synthesis of metabolites from arachidonic acid in patients with hyperlipidemia, and that the addition of fish oil is more effective for the prevention of coronary heart disease than HMG-CoA reductase inhibitors alone.
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PMID:Effect of HMG-CoA reductase inhibitors on plasma polyunsaturated fatty acid concentrations in patients with hyperlipidemia. 980 32

Acute pancreatitis (AP) is a progressive systemic inflammatory response with high morbidity and high mortality, which is mainly caused by alcohol, bulimia, gallstones and hyperlipidemia. The early diagnosis of different types of AP and further explore potential pathophysiological mechanism of each type of AP is beneficial for optimized treatment strategies and better patient's care. In this study, a metabolomics approach based on gas chromatography-mass spectrometry (GC-MS), and random forests algorithm was established to distinguish biliary acute pancreatitis (BAP), Hyperlipidemia acute pancreatitis (HLAP), and alcoholic acute pancreatitis (AAP), from healthy controls. The classification accuracies for BAP, HLAP, and AAP patients compared with healthy control, were 0.886, 0.906 and 0.857, respectively, by using 5-fold cross-validation method. And some special metabolites for each type of AP were discovered, such as l-Lactic acid, (R)-3-Hydroxybutyric acid, Phosphoric acid, Glycine, Erythronic acid, l-Phenylalanine, d-Galactose, l-Tyrosine, Arachidonic acid, Glycerol 1-hexadecanoate. Furthermore, associations between these metabolites with the metabolism of amino acids, fatty acids were identified. Our studies have illuminated the biomarkers and physiological mechanism of disease in a clinical setting, which suggested that metabolomics is a valuable tool for identifying the molecular mechanisms that are involved in the etiology of BAP, AAP, HLAP and thus novel therapeutic targets.
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PMID:GC-MS based metabolomics strategy to distinguish three types of acute pancreatitis. 3126 99