The Cholesterol-Esterifying Enzyme of Human Serum. I. In Liver Disease 1

149

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bile salts and cholesterol in the pathogenesis of target cells in obstructive jaundice

Cooper¹,

Jandl²

1968

149

“…Simple retention of bile, increased plasma cholate (20), alteration in serum cholesterol esterifying enzyme activity (21,22) and increased hepatic cholesterol synthesis (23) have been suggested in explanation. While as much as 50 per cent of the cholesterol absorbed from the intestinal tract is present as cholesterol ester in the thoracic duct lymph (24), animal studies by Friedman and Byers (25) The metabolic significance of these correlations is not evident from this study.…”

Section: Discussionmentioning

confidence: 99%

Ultracentrifugal Characterization of the Lipoprotein Spectrum in Obstructive Jaundice: Studies of Serum Lipid Relationships in Intra- And Extrahepatic Biliary Obstruction 1

Furman¹,

Conrad²,

Fryer³

et al. 1957

The alterations in serum lipids accompanying obstructive jaundice have long been a matter of considerable interest. In the absence of significant hepatic failure, biliary obstruction of either intraor extrahepatic type often results in markedly increased serum total cholesterol and phospholipid levels. The increase in serum phospholipid concentration may be relatively greater, resulting in an increased phospholipid: total cholesterol ratio. Since the increment in serum total cholesterol is due mainly to increase in the unesterified cholesterol fraction, the ratio phospholipid: free cholesterol may be more meaningful. This ratio, according to Jackson, Wilkinson, Hand, Waldron, and Vogel (1), has a minimal limiting value (by weight) of 2, suggesting a homeostatic mechanism operating to maintain a molar ratio of at least one phospholipid molecule per molecule of unesterified plasma cholesterol.With the development of techniques such as ultracentrifugal flotation, paper and zone electrophoresis and plasma protein fractionation, the serum lipids and lipoproteins in biliary obstruction have again come under scrutiny. The serum lipid distribution in biliary obstruction has been studied by Barr, Russ, Eder, and their co-workers (2-4) employing Cohn method-10 (5) for lipoprotein fractionation. They found increased amounts of cholesterol in fractions IV + V + VI ("alpha lipoproteins"), mostly in the free form, and increased amounts of phospholipids in fractions I +

“…Patients who congenitally lack this enzyme have target-shaped red cells rich in clholesterol and lecithin (22). Since this enzyme deficiency exists in many patients with liver disease it has been proposed that LCAT may play a role in the red cell lipid abnormalities observed in cirrhosis (12,(23)(24)(25). Third, bile acids have been shown to influence membrane lipid composition under experimental conditions in vitro (12) and in vivo (26).…”

mentioning

confidence: 99%

An Analysis of Lipoproteins, Bile Acids, and Red Cell Membranes Associated with Target Cells and Spur Cells in Patients with Liver Disease

Cooper¹,

Diloy-Puray²,

Lando³

et al. 1972

190

A B S T R A C T MNlost p)atiellts witlh stable cirrhosis of the alcoholic have "target" red cells; however, a minoritv have "spur" cells and severe hemolytic anemia. These two syndromes were studied in 27 patients with target cells and 17 patients with spur cells, all of whom had advanced cirrhosis. The cholesterol and phospholipi(d content of red cell membranes effectively distinguished target cells from spur cells. Target cells alone were rich in lecithin, and both the cholesterol/phospholipid and cholesterol/lecithin mole ratios were greater in spur cells. The cholesterol/phospholipid mole ratio of both types of red cells correlated closely with the free cholesterol saturation of serum lipoproteins, as defined by the anmount of free clholesterol relative to phospholipid and protein in these lipoproteins. Lecithin: cholesterol acyltransferase (LCAT) activity was decreased in most patients with target cells and spur cells; however, the relationship between this activity and the lipid abnormiialities observed was weak. Serum bile acid levels also correlated poorly witlh serum and cell lipids. However, in patients with target cells the amount of cholic and (leoxycholic acids in serumi was approximately equal to the amount of chenodeoxycholic acid, whereas in patients with spur cells chenodeoxycholic acid (the precursor of lithocholic acid) pre(lominatedl.