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  • 1
    ISSN: 1432-1440
    Keywords: Lipoproteidlipase ; Lipoproteide ; Hyperlipoproteinämie Typ V ; Lipoprotein lipase ; Lipoproteins ; Type V Hyperlipoproteinemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effects of the main lipoprotein density classes on the human adipose tissue lipoprotein lipase activity were studied. A dose-dependent stimulation of lipoprotein lipase activity was obtained for HDL and, to a lesser extent, for VLDL on a constant weight basis. LDL exerted virtually no effect. At higher concentrations, HDL as well as VLDL inhibited the stimulated lipolytic activity. In type V hyperlipoproteinemia, the stimulating effect of VLDL and of HDL was significantly lower, whereas the inhibiting action of HDL was markedly increased.
    Notes: Zusammenfassung Die Effekte der einzelnen Lipoproteidfraktionen des Plasmas auf die Aktivität der Lipoproteidlipase des menschlichen Fettgewebes wurden untersucht. HDL (high density lipoproteins) und, in geringerem Ausmaß, VLDL (very low density lipoproteins) bewirkten eine dosisabhängige Stimulierung der Aktivität der Lipoproteidlipase. LDL (low density lipoproteins) übten praktisch keinen Effekt aus. In höheren Konzentrationen hemmten sowohl HDL als auch VLDL die stimulierte lipolytische Aktivität. Bei Patienten mit Hyperlipoproteinämie Typ V war der stimulierende Effekt der VLDL und HDL viel geringer, die Hemmwirkung der HDL jedoch deutlich stärker ausgeprägt.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Liver cirrhosis ; Lipoproteins ; LCAT ; Hepatic lipase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 12 patients with unequivocal post-alcoholic end-stage liver cirrhosis were compared with 12 healthy controls with regard to the plasma concentrations of lipids, lipoproteins (by rate zonal ultra-centrifugation) and apolipoproteins of high-density-lipoproteins (HDL) (by disc electrophoresis), as well as to the activities of lecithin-cholesterol acyltransferase (LCAT) in plasma and of hepatic lipase (HL) in post-heparin plasma. The cirrhotic group showed the following differences (all significant at thep〈0.01 level) from the control group: Total cholesterol, HDL-cholesterol, very-low-density-lipoproteins (VLDL), HDL, and HL were decreased. Intermediate-density-lipoproteins (IDL) were not detectable in the cirrhotic group. Low-density-lipoproteins (LDL) did not differ significantly from controls. However, LDL from cirrhotic patients contained more triglycerides but less esterified and free cholesterol (allp〈0.01). The percentage apolipoprotein composition of HDL did not differ significantly between controls and cirrhotics. Surprisingly, LCAT acivity in plasma as well as the ratios between esterified and free cholesterol in plasma, LDL, and HDL were nearly identical in both groups. It seems likely that LCAT activity decreases only in the states of acute or subacute liver injury or of biliary obstruction. Severe chronic liver damage as in our cases of end-stage liver cirrhosis without any signs of acute liver injury exhibits apparently no defect in cholesterol esterification.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Hepatic lipase ; Lipoproteins ; Hyperlipemia ; Intermediate-density lipoproteins (IDL)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The main lipoprotein density classes, namely very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3 were investigated with respect to their influence on hepatic lipase (HTGL) activity in vitro. Lipoproteins from pooled normal plasma (NP) and from pooled hyperlipemic plasma (HP) were prepared by means of sequential ultracentrifugation. Hepatic lipase was determined radioenzymatically after preincubation with protamine sulfate. It could be demonstrated that IDL from HP were able to stimulate HTGL activity by approximately 100% above the baseline value. HDL3 from both NP and HP revealed an inhibiting effect on HTGL activity. VLDL, LDL, and HDL2 exhibited no significant effect on HTGL activity. It is speculated that HTGL could possibly represent a second pathophysiological pathway for the catabolism of IDL in hyperlipemia but this presumption is supported by only a few investigations in vivo.
    Type of Medium: Electronic Resource
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