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Lecithin:cholesterol acyl transfer (LCAT) rate in plasma and lipid concentrations in total plasma and high density lipoproteins (HDL) were determined before and after oral fat loads in healthy human subjects. The changes of LCAT rate after fat loading were compared to the effect of chylomicrons or lipid emulsions added in vitro to fasting plasma. After the fat loads there was an increase of mean molar LCAT rate simultaneous with an increase of mean phospholipid (PL) and HDL-PL concentration but not simultaneous with the increase of mean triglyceride (TG) concentration. Individual changes of molar LCAT rate correlated positively with changes of PL, HDL-PL, and unesterified cholesterol (UC) concentration but not with changes of TG concentration in the separate plasma samples after the fat loads. If only the maximal changes in each subject in any sample at any time after the loads were taken into account, the maximal increase of molar LCAT rate correlated positively with the maximal increase of TG concentration. Molar LCAT rate was not influenced by addition of chylomicrons in vitro but increased after addition of a PL emulsion. It is suggested that LCAT rate is stimulated by an excess of PL in plasma and substrate lipoproteins. This excess of PL may be created in vivo temporarily during chylomicron catabolism. The stimulation of LCAT rate by fat ingestion emphasizes the importance of LCAT as a connecting link between triglyceride and cholesterol metabolism.

Information concerning variation in the lecithin:cholesterol acyl transfer (LCAT) rate in normal persons is scanty. We have therefore analyzed the LCAT rate and the lipid and lipoprotein concentrations in the plasma of healthy normolipidemic persons 20-60 years of age, 40 men and 40 women. 10 per decade and sex. Interindividual variation in molar LCAT rate was 57-130 mumol-u(-1)-h-1 (mean +/- 2 S.D.) with no sex difference. Intraindividual variation of molar LCAT rate studied in 8 women and 9 men was shown to be greater than expected from methodological error and was not explainable by the small changes in plasma lipid concentration during the observation period. In the women the molar LCAT rat was lower during the preovulatory phase of the menstrual cycle than during the postovulatory phase. There was positive correlations between the molar LCAT rate and most of the lipid parameters in plasma. By partial correlation analysis a positive correlation was shown between LCAT rate and triglyceride concentration irrespective of other lipid parameters. Keeping triglyceride concentration constant, there was a positive correlation between molar LCAT rate and total phospholipid, unesterified cholesterol, esterified cholesterol, or low-density lipoprotein (LDL) cholesterol concentration. No correlation was found between high-density lipoprotein (HDL) lipid concentration and LCAT rate. Thus in normal subjects there seems to be a direct relation between very low density lipoprotein and LDL lipid concentration and molar LCAT rate but no relation between HDL lipid concentration and LCAT rate.

Concentrations of various plasma lipids were determined in 38 healthy women before and during the first year of treatment with either a combined or low-dose progestogen oral contraceptive. The combined pills taken cyclically were Anconcene (3 mg chlormadinone acetate .1 mg mestranol; 9 women) and Conluton (2 mg norethindrone .1 mg mestranol; 10 women). The low-dose progestogens were norethindrone (.4 mg daily 10 women) and chlormadinone acetate (.5 mg daily 9 women). Blood was drawn before treatment andusually 4-5 times during the first year of treatment. In the Anconcene group free fatty acids significantly (p less than .001) decreased. Triglycerides increased significantly in the Anconcene (p less than .001) Conluten (p less than .01) and norethindrone (p less than .05) groups. Total cholesterol was increased significantly among Anconcene (p less than .01) and Conluten (p less than .05) users. Total phospholipids were increased significantly in the Anconcene and Conluten groups (p less than .001) and in the chlormadinone acetate group (p less than .05). Changes in lysolecithin sphingomyelin lecithin and cephalin were similar to changes during pregnancy; the pattern was most exaggerated in the Anconcene group. The estrogenic component in the combined pills may bring about many of the changes. Norethindrone may exert an antiestrogenic effect. The low-dose progestogens were less active in causing alterations than were the combined pills. This difference gains importance when viewed in light of possible connections with vascular disease and thrombogenesis but frequency of bleeding irregularities and pregnancy rate are higher with low-dose progestogens.