Regulation of somatotrophic and lactogenic binding sites in mouse liver membranes
| Autor: | Toshio Tsushima, Fukashi Matsuzaki, Yasuo Imai, N. Sasaki |
|---|---|
| Rok vydání: | 1982 |
| Předmět: |
Male
endocrine system medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Mice Inbred Strains Biology Hysterectomy Mice Radioligand Assay chemistry.chemical_compound Fetus Endocrinology Pregnancy Corticosterone Internal medicine medicine Animals Testosterone Castration Binding site Placental lactogen Binding Sites Estradiol Adrenal gland Adrenalectomy Cell Membrane General Medicine Metabolism Placental Lactogen Prolactin medicine.anatomical_structure Liver chemistry Growth Hormone Female hormones hormone substitutes and hormone antagonists Hormone |
| Zdroj: | Acta Endocrinologica. 101:574-579 |
| ISSN: | 1479-683X 0804-4643 |
| Popis: | Both somatotrophic and lactogenic binding sites increase markedly in pregnant mouse liver membranes. The regulatory mechanisms of these binding sites involved in pregnancy are studied. The study of the effects of various hormone administration to female mice reveals that oestradiol increases and testosterone decreases lactogenic binding sites, and that other hormones affect neither somatotrophic nor lactogenic binding sites. Hysterectomy, adrenalectomy or foetectomy of pregnant mice cause a remarkable reduction of somatotrophic binding sites to the level observed in non-pregnant or post-partum animals. In contrast, the lactogenic binding sites are not influenced by these treatments. Replacement with corticosterone after adrenalectomy does not prevent the decrease of somatotrophic binding sites. The contents of placental lactogen from both adrenalectomized and foetectomized pregnant mice are similar to those of the normal pregnant group. These observations indicate that the regulatory mechanisms modulating somatotrophic and lactogenic binding activities are quite different and that increased somatotrophic binding sites during pregnancy are supported by the factor(s) generated in the foeto-placental unit and maternal adrenal gland. |
| Databáze: | OpenAIRE |
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