Advances in lipid research. Volume 11 by Rodolfo Paoletti; David Kritchevsky

By Rodolfo Paoletti; David Kritchevsky

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11. Analytical ultracentrifugation of HDL subfractions from a patient with familial LeAT deRciency. Large and small n10lecular weight subfractions from patient A. A. (see also Fig. 10) compared with normal HDL. Fron1 N orUID et ale (1971a). fat" (140-155 gm fat/50-60 gm carbohydrate, or 125-145 gm fat/50-60 gm carbohydrate); and (3) "high carbohydrate" (40-50 gm fat/325-350 gm carbohydrate, or 40-55 gm fat/220-300 gm carbohydrate). ) in the top portion of a polyvinylpyrrolidone gradient, whereas high carbohydrate diets had the opposite effect.

Detailed descriptions of plasn1a lipoprotein abnormalities during this initial stage of biliary obstruction would be of great value in distinguishing between the direct effects of cholestasis and effects caused by hepatocellular injury. 47 Lecithin: Cholesterol Acyltransferase V. Discussion Although several of the abnorn1alities in fan1ilial LCAT deficiency appear to be "explained" by what ,ve now know about the LCAT reaction, the fact that sin1ilar abnorn1alities occur in cholesterol-fed guinea pigs and in cholestasis suggests that the n1etabolic role of the LCAT reaction should be considered in a broader context.

A, lipoproteins fronl a control guinea pig. B, lipoproteins from a cholesterol-fed guinea pig. From Puppione et ale (1971). 21 gm/fill control diet cholesterol diet a PL TG Protein (% of total weight) 6 31 52 17 16 32 2 2 24 18 9 24 25 15 25 31 2 2 39 28 Data from Sardet et ale (1972a). ) in particular. Several important differences between the abnormalities of cholesterolfed guinea pigs and patients with familial LCAT deficiency must be mentioned. First, LCAT appears to be present in normal guinea pig serum (Felt, 1971), although no measurements of the enzyme activity in the serun1 of cholesterol-fed guinea pigs have been reported.

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