Key result
Severity of liver dysfunction was associated with decreased total post-heparin lipolytic activity, primarily due to low hepatic triglyceride lipase (H-TGL) activity.
Observational (n=120)
Impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic triglyceride lipase activity.
Reduced H-TGL may underlie triglyceride accumulation in liver dysfunction; hypothesis-generating for targeted interventions in cirrhosis.
Hypertriglyceridaemia occurring in patients with liver disease has been studied by measuring hepatic triglyceride lipase (H-TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H-TGL with specific antibodies. Lipid analysis, determination of lecithin-cholesterol-acyltransferase (LCAT) activity, and liver function tests were performed in parallel in fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty with cirrhosis of the liver. Total post-heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H-TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridaemia disappeared with a concomitant increase of H-TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.
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Klose et al. (1977) conducted an observational in Parenchymal liver disease (n=120). Liver dysfunction severity was evaluated on Total post-heparin lipolytic activity (PHLA), hepatic triglyceride lipase (H-TGL), and plasma lipoprotein lipase (LPL) activity. Severity of liver dysfunction was associated with decreased total post-heparin lipolytic activity, primarily due to low hepatic triglyceride lipase (H-TGL) activity.
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