Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The beneficial effects obtained with dehydroisoandrosterone (DHA) feeding in the treatment of murine systemic lupus erythematosus are similar to those obtained with caloric restriction or with dietary manipulation of essential fatty acid availability. In this study, the fatty acid composition of selected tissues was examined in NZB/W F1 mice fed a diet containing 0.4% DHA. The effect of the DHA diet on liver composition and the activity of key hepatic enzymes involved in fatty acid synthesis and glucose metabolism was also investigated. The content of the essential fatty acid, arachidonate, was decreased in plasma cholesteryl esters and liver and kidney phospholipids in mice fed the DHA diet, yet no significant decrease in arachidonate content was observed in plasma phospholipid. The most striking change in both plasma and liver phospholipid was an increase in palmitic acid and a decrease in stearic acid, which could result from a decreased ability for fatty acid elongation. The liver mass was dramatically increased in the mice fed DHA, primarily from parenchymal cell hypertrophy, and contained little lipid. Significant changes in the activities of malic enzyme, glucose-6-phosphate dehydrogenase and pyruvate kinase, similar to those changes which occur with fasting, were observed during the initial adaptation to the DHA diet. The pyruvate kinase activity remained low, suggesting a decrease in liver glycolysis. These results are consistent with the concept that diets containing DHA result in an altered metabolism with a decreased dependence on carbohydrate metabolism and an increased metabolism of lipids.
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PMID:Liver composition and lipid metabolism in NZB/W F1 female mice fed dehydroisoandrosterone. 297 Aug 67

To test the hypothesis that T-cells which exhibit abnormal immunological behavior manifest derangements in the de novo synthesis of phospholipids, the utilization of [3H]palmitic acid in B220+ T-cells from autoimmune MRL-lpr/lpr mice was investigated. The rate of incorporation of [3H]palmitic acid into membrane phospholipids was markedly increased in intact B220+ T-cells compared to that in T-cells from immunologically normal mice. The activities of two key enzymes involved in the de novo synthesis of palmitoyl-phospholipids, acyl-coenzyme (CoA) ligase and acyl-CoA; sn-glycerol-3-phosphate acyl transferase, were significantly higher in homogenates from B220+ T-cell membranes compared with those in controls. Despite these findings, the molar concentration of individual palmitoyl glycerolipids was equivalent in the membranes of B220+ T-cells and control lymph node T-cells. The results indicate that T-cells from lupus mice exhibit complex defects in the biosynthesis and turnover of membrane phospholipids and suggest the possibility that these aberrations contribute to T-cell dysfunction in autoimmune diseases.
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PMID:Long chain fatty acid utilization of T-cells from autoimmune MRL-lpr/lpr mice. 809 30

Lysophosphatidylcholine (LPC) is present in oxidized low density lipoprotein (oxLDL), which is implicated in atherosclerosis. Antibodies to cardiolipin (aCL) and oxLDL (aoxLDL) have been shown to crossreact. LPC is formed by hydrolysis of phosphatidylcholine (PC) in LDL and cell membranes, induced by phospholipase A2 or by oxidation. We here demonstrate the presence of enhanced antibody levels to LPC in 184 patients with SLE as compared to 85 healthy, age-matched controls. The antibody reactivity to LPC was not specifically related to oxidation of the fatty acid moiety in LPC, since LPC containing only the saturated fatty acid palmitic acid showed equivalent antibody levels as LPC containing unsaturated fatty acids. aPC were significantly lower as compared to aLPC, indicating that hydrolysis of PC at the sn-2 position increases the antigenic potential of the molecule. Beta-glycoprotein 1 was a cofactor for aCL, but not for aoxLDL or aLPC, and the antigenicity of these compounds is therefore not directly related to beta2GP1. There was a close correlation between aoxLDL, aCL and aLPC and both LPC and oxLDL competitively inhibited aCL-binding to CL. LPC, oxLDL and CL thus display a common antigenic site, which could be formed by removal of a fatty acid at the sn-2 position, possibly due to the activity to phospholipase A2 and/or oxidation. This study indicates the potential role of LDL-oxidation and phospholipase A2 in SLE.
Lupus 1999
PMID:Antibodies against lysophosphatidylcholine and oxidized LDL in patients with SLE. 1019 9