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This material was taken in part from the thesis submitted by Carolyn D. Mitchell in partial fulfillment of the requirements for the degree of Doctor of Philosophy, University of Washington, 1965. 1 "Stroma" refers to the post-hemolytic residue or "ghosts," usually considered to be representative of the surface structure of the erythrocyte. ments have been formed. Ultracentrifugation of the

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Plasma Lipoproteins in Familial Lecithin:Cholesterol Acyltransferase Deficiency: Effects of Incubation with Lecithin:Cholesterol Acyltransfera in vitro. Scand. J. Clin. Lab. Invest.To study the effect of lecithin: cholesterol acyltransferase (LCAT) on the plasma lipoproteins of patients with familial LCAT deficiency, whole plasma or the lipoprotein fraction of d < 1.006 g/ml (VLDL) was incubated in the presence of LCAT and subsequently examined by chemical, physical, and immunological techniques. The following occurred upon incubating either hyperlipemic or nonlipemic plasma: The concentrations of polar lipids decreased, particularly in the large molecular weight lipoprotein subfraction of d 1.019-1.063 g/ml (LDLp) and in the lipoprotein fraction of d 1.063-1.25 g/ml (HDL). The concentration of cholesteryl ester (CE) increased, particularly in the VLDL and in the lipoprotein fractions of d 1.006-1.019 g/ml (LDL,) and LDL2. The concentration of arginine-rich. apolipoprotein decreased in the HDL and increased in the VLDL and LDL1. The concentrations of the C-apoliproteins appeared to change in the opposite direction. The concentration of apolipoprotein B in the LDL increased concomitantly with an increase in the concentration and flotation rate of the small LDL2. The concentration of apolipoprotein A-I in the HDL increased; and a major component in the HDL fraction became identical in appearance to normal HDL. Upon incubating a patient's isolated VLDL in the presence of LCAT, lipoproteins with properties similar to normal LDLz were formed. These experiments show that the LCAT reaction can alter the apolipoprotein content and physical properties as well as the lipid content of the patients' lipoproteins. Patients with familial 1ecithin:cholesterol acyl-implications of the abnormalities with respect transferase (LCAT)* deficiency have many to the metabolism of normal lipoproteins are plasma lipoprotein abnormalities (1) presum-not yet clear. In order to obtain information ably caused by the LCAT deficiency. How-relevant t o these questions we have been ever, the metabolic basis of these abnormali-attempting t o perturb the patients' lipoproteins ties remains to be fully established, and the in vivo and in vitro. In previous experiments -~ (2) we altered the patients' intake of dietary * For abreviations and definitions see page 54. fat land examined the effects on the plasma 31 Scand J Clin Lab Invest Downloaded from informahealthcare.com by McMaster University on 11/20/14 For personal use only.