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  • Blood-pH in vivo  (1)
  • Hepatic lipase  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 62 (1984), S. 593-594 
    ISSN: 1432-1440
    Keywords: Lipoprotein lipase ; Blood-pH in vivo ; Acidosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show a marked impairment of lipoprotein lipase. Therefore we influenced blood-pH in 3 healthy subjects by infusions to get alkalotic, neutral and acidotic blood-pH on three days in series. On each day blood-pH from capillary blood and post-heparin lipoprotein lipase from fasting plasma was determined. In comparison to neutral blood-pH in vivo, alkalosis did not influence lipoprotein lipase. In contrast, during artificial acidosis, lipoprotein lipase was impaired significantly (p〈0.01). Therefore, it seems, that acidosis inhibits lipoprotein lipase in vivo.
    Type of Medium: Electronic Resource
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  • 2
    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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