Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanisms for hypercholesterolemia and hypertriglyceridemia and the effects of KCD-232, a new hypolipidemic agent, on them were studied in male Wistar rats with daunorubicin (DR)-induced nephrosis. Single intravenous injection of DR dose-dependently increased urinary protein loss and serum lipid levels (0,3,6 and 12 mg/kg). Twenty-four days after the injection of DR (6 mg/kg), serum cholesterol (Ch) and triglyceride (TG) levels markedly increased and free fatty acid level tended to decrease with no effects on liver lipid levels. Hepatic Ch synthesis from [14C]acetate in vitro increased by 2.1-fold, while exogenous Ch absorption slightly decreased. The clearance of intravenously injected [3H]Ch from the circulation was delayed. Hepatic fatty acid (FA) synthesis also increased by 2.7-fold, and hepatic TG lipase activity tended to decrease. KCD-232 improved the hypercholesterolemia and hypertriglyceridemia of DR-treated rats. The drug inhibited the elevated hepatic Ch synthesis and exogenous Ch absorption and thus improved the delayed Ch clearance from the circulation. KCD-232 markedly inhibited the elevated hepatic FA synthesis and stimulated both hepatic FA oxidation and lipoprotein lipase activity from the epididymal adipose tissue of the nephrotic rats. These results suggest that 1. DR-induced hypercholesterolemia is due to both an increased Ch synthesis in the liver and delayed clearance of Ch from the circulation; 2. DR-induced hypertriglyceridemia is caused by both an increased hepatic FA synthesis and depressed TG hydrolysis in the circulation; 3. KCD-232 improves the hypercholesterolemia by inhibiting the elevated Ch synthesis and Ch absorption from the gut; and 4. KCD-232 improves the hypertriglyceridemia by inhibiting the elevated hepatic FA synthesis and by stimulating both hepatic FA oxidation and TG hydrolysis activity in the circulation.
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PMID:[Experimental nephrotic hyperlipidemia induced in rats by daunorubicin and effects of KCD-232[4-(4'-chlorobenzyloxy)benzyl nicotinate] on lipid metabolism]. 402 7

The pathogenicity of highly purified brush border membrane (BBM) antigens in Heymann Nephritis was compared to that of a crude renal tubular Fx1A preparation and was found to be equally pathogenic. Both antigen preparations induced formation of autologous antisera. Double immunodiffusion studies demonstrated a reaction of identity between anti-BBM and anti-Fx1A antisera. Both antisera detected the same number of antigenic components when reacted against BBM or Fx1A preparations. When antibody was eluted from the kidneys of rats with Heymann nephritis it reacted in vitro with the renal BBM as shown by indirect immunofluorescence. Eluted antibody also cross reacted with epididymal tubules, but not with other epithelia, showing that the pathogenic antigens have a restricted tissue distribution. Heymann nephritis was readily induced in rats, but could not be induced in dogs, suggesting a species difference in susceptibility to this form of nephritis. Injection of heterologous anti-BBM or anti-Fx1A antisera resulted in rapid localization to the GBM in a granular pattern, suggesting reaction with circulating antigen or in situ immune complex formation with native or planted glomerular components. Rats with aminonucleoside nephrosis showed BBM localization of injected heterologous antisera, demonstrating their specificity in vivo. Our data provide a rationale for using purified BBM antigens for the production of a homogeneous model of Heymann nephritis.
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PMID:Pathogenicity of a highly purified brush border membrane preparation in Heymann nephritis. 645 9