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    v. 24, 27, 29, 39, 1955, 1958, 1960, 1970.
    Call number varies. Search for James Arthur lecture on the evolution of the human brain to find individual volumes of this title.
  • Article
    Mibayashi Y.
    Nihon Naibunpi Gakkai Zasshi. 1978 Mar 20;54(3):203-18.
    In order to elucidate the mechanisms of glucocorticoid-induced hypertriglyceridemia, 3mg or 10mg/kg of cortisone acetate were administered daily intramuscularly for 8 days to male albino rabbits which were fed 150g/day of a complete commercial diet. Plasma triglyceride (TG), cholesterol (Chol), free fatty acid (FFA), glucose, IRI, very low density lipoprotein (VLDL)-TG, and post-heparin lipolytic activity (PHLA) were determined. PHLA was measured 10 minutes after a heparin (Novo Co., Denmark; 10 units/kg) injection, and then 30, 60, 120 and 180 minutes after pulse injections of heparin (100 units/kg) at 30 minute intervals up to 120 minutes. In another experiment, following 1 week of daily intramuscular injections of 3mg/kg of cortisone acetate, triglyceride secretion rates (TGSR) were estimated, using intravenous injections of Triton WR-1339 (750mg/kg). Also, plasma glucose, IRI, and FFA responses were measured after an intravenous glucose administration test (1.Og/kg) which was performed before and after cortisone acetate treatment. The results were the following: (1) Significant increase (p less than 0.001) in plasma TG and VLDL-TG without any rise of plasma Chol. (2) Increased plasma IRI, glucose and FFA levels at fasting and after intravenous glucose load. (3) No change in PHLA. (4) Highly significant increments (p less than 0.001) in TGSR. Plasma TG and VLDL-TG showed a significant correlation with fasting plasma IRI and sigma glucose (summation of each time glucose level in intravenous glucose load). These findings suggest that glucocorticoid-induced hypertiglyceridemia is primarily a consequence of increased hepatic TG production rates, through elevated plasma FFA, IRI and glucose levels.
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