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 induction of nephrotoxic nephritis in rats with rabbit antibodies preparation results in proteinuria, hypoproteinemia and hyperlipidemia with little glomerular lesions. A study of some hydrolases in cortex and medulla on one hand and glomerular and tubules on the other, showed changes in the activities of following enzymes. 1) A 20-30 % decrease in Na+, K+ dependent ATP-ase in whole kidney. 2) A 20 % decrease in beta-galactosidase activity in glomerular and medulla. 3) A 20 % increase of arylsulphatase A activity in tubules. These results are discussed in the light of the present knowledge of sulphatide metabolism in kidney.
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PMID:[Experimental nephrotic syndrome in the rat. Biologic parameters and study of several hydrolases in different purified kidney fractions]. 20 50

This is a kinetic assay for measuring serum Na+ concentration based on determination of Na+-dependent beta-galactosidase (EC 3.2.1.23) activity. The method, sufficiently sensitive to measure sub-millimolar concentrations of Na+, was modified by including a Na+-binding agent (cryptand) to provide a linear assay for serum Na+ concentrations between 110 and 160 mmol/L. The assay was developed with and evaluated in the Cobas Fara centrifugal analyzer (and has been used in other kinetic analyzers). Within-run and between-run CVs were less than 1%. The reaction rate for normal serum samples (0.20 delta A/min) is about 10-fold that of the reagent blank. Results correlated well with flame photometry. Interference from bilirubin, hemoglobin, lipemia, heparin, and other cations was negligible. The method offers a practical alternative to the use of ion-selective electrodes and flame photometry for measuring serum Na+ in high-throughput or "stat" biochemical analyzers.
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PMID:Enzymatic determination of sodium in serum. 314 Oct 85

We evaluated the effect of hemolysis, icteric discoloration, lipemia, paraproteinemia, and uremia on enzymatic methods for determining sodium, potassium, and chloride, according to the National Committee for Clinical Laboratory Standards EP7-P proposals for testing interference from endogenous substances. The sodium, potassium, and chloride assays (reagent kits supplied by Boehringer Mannheim) were based on electrolyte-dependent beta-galactosidase, pyruvate kinase, and alpha-amylase, respectively. The results were compared with those obtained by indirect ion-selective electrodes (ISE), which in turn had been validated by flame photometry. We analyzed the samples with Hitachi 717, 737, and 911 chemistry analyzers and with an IL943 flame photometer. The enzymatic results were in good agreement with those by ISE, the interference-related differences generally being without clinical significance; however, none of the enzymatic methods could analyze grossly lipemic samples.
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PMID:Enzymatic determination of sodium, potassium, and chloride in abnormal (hemolyzed, icteric, lipemic, paraproteinemic, or uremic) serum samples compared with indirect determination with ion-selective electrodes. 804 91

To determine whether the antilipogenic actions of insulin-induced gene 1 (insig-1) demonstrated in cultured preadipocytes also occur in vivo, we infected Zucker diabetic fatty (ZDF) (fa/fa) rats, with recombinant adenovirus containing insig-1 or -2 cDNA. An increase of both proteins appeared in their livers. In control ZDF (fa/fa) rats infected with adenovirus containing the beta-galactosidase (beta-gal) cDNA, triacylglycerols in the liver and plasma rose steeply whereas the insig-infected rats exhibited substantial attenuation of the increase in hepatic steatosis and hyperlipidemia. Insig overexpression was associated with a striking reduction in the elevated level of nuclear sterol regulatory element-binding protein (SREBP)-1c, the activated form of the transcription factor. The mRNA of SREBP-1c lipogenic target enzymes also fell. The mRNA of endogenous insig-1, but not -2a and -2b, was higher in the fatty livers of untreated obese ZDF (fa/fa) rats compared with controls, but the elevation was not sufficient to block the approximately 3-fold increase in SREBP-1c expression and activity. In normal animals, adenovirus-induced overexpression of the insigs reduced the increase in SREBP-1c mRNA and its target enzymes caused by refeeding. The findings demonstrated that both insigs have antilipogenic action when transgenically overexpressed in livers with increased SREBP-1c-mediated lipogenesis. However, the increase in endogenous insig-1 expression associated with augmented lipogenesis may limit it, but is insufficient to prevent it.
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PMID:Hepatic insig-1 or -2 overexpression reduces lipogenesis in obese Zucker diabetic fatty rats and in fasted/refed normal rats. 1509 98