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  • Title: Oral contraceptives stimulate the excretion of clofibric acid glucuronide in women and female rats.
    Author: Liu HF, Magdalou J, Nicolas A, Lafaurie C, Siest G.
    Journal: Gen Pharmacol; 1991; 22(2):393-7. PubMed ID: 1905251.
    Abstract:
    1. Glucuronidation of clofibric acid, the pharmacologically active form of the hypolipidemic drug clofibrate was investigated in a human population, either in vitro with liver homogenates from biopsies, or after ingestion of the drug and determination of the urinary metabolite. No difference in the glucuronidation rate according to age of the patients was observed. Bilirubin but not clofibric acid glucuronidation was significantly higher in women (106% increase), when expressed per gram of tissue. 2. The excretion of clofibryl glucuronide in women who took oral contraceptives was significantly enhanced by 25%. 3. In female rats, treatment with the contraceptive agent norethindrone also stimulated by 48% the formation of clofibrylglucuronide in liver microsomes. The effect of oral contraceptive (OC) intake on the glucuronidation of clofibric acid was investigated both in vivo, by measuring the excretion of urinary clofibrylglucuronide in female Wistar rats, or in vitro, with liver biopsy homogenates from 69 health female volunteers. In both study groups norethindrone markedly enhanced glucuronidation of clofibric acid while the situation was modulated by the administration of ethinyl estradiol. Excretion of clofibric acid into urine averaged 142.1 + or - 38.4 mg in OC users compared to only 105.8 + or - 31.5 mg in non-users. When expressed per gram of tissue, bilirubin but not clofibric acid glucuronidation was significantly greater in human liver biopsies from OC users compared to non-users. In rats treated with norethindrone, the liver microsomal protein content was increased 28% over the average control value and formation of clofibylglucoride was stimulated by 48%. It is hypothesized that the stimulation of clofibylglucuronide in OC users results from the selective stimulation in the liver of the isoenzyme involved in the process of the glucuronidation of clofibric acid.
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