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UCHIDA et al. December 1970 Endocrinol. Japon. initial half of pregnancy is sustained by hypophyseal factors, but that the one in the latter half of it by placental or uterine luteotrophic substances. Two peaks of progesterone secretion during pregnancy noted by Fajor and Barraclough (1967) may represent the actions of both luteotrophins from different origins. In the present experiments, ovarian progesterone and 20ƒ¿-OH-P secretions were measured in detail during pregnancy and pseudopregnancy in relation to the changes in corpora lutea weight, 20ƒ¿-hydroxysteroid dehydrogenase (20ƒ¿-OH-SDH) activity, cholesterol and both progestin concentrations in corpora lutea, since cholesterol (Everett, 1947) and 20ƒ¿-OH-SDH activity (Wiest et al., 1968) in corpora lutea are known to be related to luteal function. Meterials and Methods Animals Wistar strain female rats weighing 170 to 200g were reared with an ordinary rat chow and water ad

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Abstract-Effect of dietary cholesterol on biliary and fecal excretion of cholesterol and bile acids was examined in rats. Cholesterol supplemented diet (2%) caused almost no change in plasma lipid levels, but produced an increase of pre F3-lipoprotein and a de crease of a-lipoprotein.Dietary cholesterol increased bile secretion and biliary ex cretion of total bile acids but not of cholesterol. Biliary cholic and deoxycholic acids were not greatly changed but chenodeoxycholic acid was significantly increased. Dietary cholesterol also increased fecal excretion of sterols and bile acids. The excretion of coprostanol was increased about 10-fold and that of cholesterol was over 50-fold. Rat fecal bile acids consisted of lithocholic, deoxycholic, hyodeoxycholic or its 6,3-isomer, a-muricholic, ,3-muricholic and some keto bile acids. Dietary cholesterol increased fecal excretion of mostly the secondary bile acids from chenodeoxycholic acid, and also deoxycholic acid. When a cholesterol supplemented fat-free diet was provided, no increase was found in either plasma or liver lipid levels, or in biliary excretion of bile acids, but a marked increase was produced in fecal excretion of sterols and bile acids. It is concluded that dietary cholesterol increases the formation and excretion of cheno deoxycholic acid, and also that of cholic acid but to a lesser extent. The increase of bile acids, particularly chenodeoxycholic acid, is responsible for the diminution of tissue and blood cholesterol, though only a minor amount of dietary cholesterol is absorbed in rats.Excess feeding of cholesterol causes a marked hypercholesterolemia in the rabbit, chicken or hamster while in the rat the increase is almost nil. The mouse, dog, monkey and man are also reported to be less responsive to dietary cholesterol (1, 2, 3). The reason for the species difference is not clear, but an interesting event related to the difference has been reported. The excess feeding of cholesterol markedly increases the conversion of cholesterol to bile acids in rats (4, 5), or in dogs (6), but not in rabbits (7) or in hamsters (8). These response patterns of bile acid metabolism to dietary cholesterol are consistent with changes in blood cholesterol levels in various species. Species of animals which show a good re sponse in bile acid formation show no rise in blood cholesterol level and in cases where the response is poor, hypercholesterolemia results. In addition, Beher et al. (8,9) have shown that cholesterol feeding decreases cholic acid pool but increases chenodeoxycholic acid pool in rats. This qualitative change niay also be related to the poor response in blood