Elsevier

Metabolism

Volume 42, Issue 1, January 1993, Pages 19-23
Metabolism

Lecithin-cholesterol acyltransferase and lipid transfer protein activities in liver disease

https://doi.org/10.1016/0026-0495(93)90166-LGet rights and content

Abstract

The activities of lecithin-cholesterol acyltransferase (LCAT) and lipid transfer protein (LTP) were assayed using sensitive radioassay methods in controls (n = 113) and in patients with various liver diseases (n = 72). Plasma LCAT activity decreased with progression of hepatocellular damage. Plasma LTP activity in controls was 216 ± 68 nmol/mL/h, and there were no significant differences between controls and patients withchronic hepatitis ([CH], 193 ± 70), compensated liver cirrhosis (LC) with or without hepatocellular carcinoma ([HCC], 197 ± 48 and 193 ± 62, respectively), or decompensated liver cirrhosis ([dLC], 182 ± 65). In acute viral hepatitis, LTP activity decreased significantly; however, the degree of reduction was not as dramatic as that for LCAT. There was no correlation between LCAT and LTP activity both in controls and patients with various liver diseases. LCAT activity was positively correlated with serum albumin (r = .52, P < .01) and cholinesterase (r = .37, P < .01) levels, and inversely correlated with serum bilirubin level (r = −.38, P < .01); there was no correlation between plasma LTP activity and these parameters of liver function. That plasma LTP activity did not change with hepatocellular damage may indicate that the liver in humans may not be the primary site of LTP production.

References (42)

Cited by (34)

  • Role of lipids in pathophysiology, diagnosis and therapy of hepatocellular carcinoma

    2020, Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
    Citation Excerpt :

    Lecithin-cholesterol acyltransferase (LCAT), which is a key enzyme for cholesterol esterification in plasma, showed a progressive decline with hepatocellular damage [77]. Serum cholesterol and LCAT activity were low in liver cirrhosis patients and HCC [77]. Thus, total cholesterol and cholesteryl ester levels seem to decline in serum of liver cirrhosis patients.

  • Associations of systemic sphingolipids with measures of hepatic function in liver cirrhosis are related to cholesterol

    2017, Prostaglandins and Other Lipid Mediators
    Citation Excerpt :

    PUFA CEs are markedly low in the patients with more advanced liver injury analyzed in the present study [9]. LCAT is the major enzyme for esterification of cholesterol with PUFAs in serum, and is found reduced in patients with liver cirrhosis [25,26,35]. CE species formed by LCAT [27] are, however, mostly not related to Child-Pugh or MELD score.

  • Cardiovascular risk, lipidemic phenotype and steatosis. A comparative analysis of cirrhotic and non-cirrhotic liver disease due to varying etiology

    2014, Atherosclerosis
    Citation Excerpt :

    Therefore it may often be depressed in advanced cirrhosis with paralleling increased values of free CH and lecithin and corresponding decreases in CH ester and lysolecithin [129,143]. As a further consequence of reduced activities of LCAT and hepatic lipase [129,134], remodeling of VLDL to LDL is impaired, esterified/free CH ratio is reduced, HDL and LDL are poor in CH ester and proportionally enriched in TG and PL [15,129,143,144]. In vitro studies in cirrhotic patients have shown low HTGL activity, which account for impaired hepatic removal of TG and PL from lipoproteins [15].

View all citing articles on Scopus
View full text