Regulation of serum insulin-like growth factor-I (IGF-I), hepatic growth hormone binding and IGF-I gene expression in the rat during pregnancy and lactation

• Published in: Journal of endocrinology Vol. 139; no. 1; pp. 89 - 95
• Main Authors: TRAVERS, M. T, MADON, R. J, FLINT, D. J
• Format: Journal Article
• Language: English
• Published: Colchester BioScientifica 01.10.1993; Portland Press
• Subjects: Animals; Biological and medical sciences; Female; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - physiology; Growth Hormone - metabolism; Hormone metabolism and regulation; Insulin-Like Growth Factor I - genetics; Insulin-Like Growth Factor I - metabolism; Lactation - metabolism; Liver - anatomy & histology; Liver - metabolism; Organ Size - physiology; Pregnancy; Pregnancy, Animal - metabolism; Pregnancy. Parturition. Lactation; Protein Binding; Rats; Rats, Wistar; RNA, Messenger - analysis; Vertebrates: reproduction; Lactation; Rat; Somatomedin C; Liver; STH; Rodentia; Gene expression; Pregnancy; Vertebrata; Mammalia; Adenohypophyseal hormone; Growth factor; Hormonal receptor
• ISSN: 0022-0795; 1479-6805
• DOI: 10.1677/joe.0.1390089

ABSTRACT An apparent GH resistance occurs in pregnancy, since GH concentrations in serum are reported to be normal or elevated, whereas serum IGF-I falls to very low levels. To determine whether this GH resistance is manifest at the level of the hepatic GH receptor or in the ability of GH to initiate IGF-I gene expression, we have determined hepatic IGF-I mRNA expression, circulating IGF-I and hepatic GH binding during various stages of pregnancy and lactation in the rat. The concentration of IGF-I in serum fell from 37 ± 5 nmol/l (means ± s.e.m.) in virgin rats to 17 ± 1 nmol/l in rats in late pregnancy, recovered in early lactation (31 ± 3 nmol/l) but was again significantly lower than in virgin animals by mid-lactation (22 ± 3 nmol/l). Hepatic GH binding did not vary significantly during pregnancy but showed a small significant decrease in early lactation when expressed per mg membrane protein. When expressed as GH binding per liver, however, there were no significant changes in GH binding at any stage. Liver weight increased significantly between virgin and early pregnant animals (7·1 ± 0·2 g compared with 9·2 ± 0·5 g respectively, P<0·01) and continued to increase up to late lactation (14·3 ± 0·4 g). Similarly, although the amount of IGF-I gene expression/unit RNA declined in late pregnant when compared with virgin animals (6·0 ± 0·6 versus 3·4 ± 0·4 arbitrary optical density units respectively, P<0·05), when the increase in liver weight and RNA content during pregnancy was taken into account there was actually a steady increase in IGF-I gene expression per total liver throughout both pregnancy and lactation, the difference becoming significant by mid-lactation (P<0·05). Thus, when the changes in liver weight which take place during pregnancy and lactation are taken into account we conclude that any hepatic resistance to GH in late pregnancy and lactation must be a post-receptor event which is mitigated in large part by increase in liver size, cell number and RNA content. Journal of Endocrinology (1993) 139, 89–95