Regulation of hepatic expression of IGF I and fetal IGF binding protein mRNA in streptozotocin-diabetic rats

• Published in: FEBS letters Vol. 251; no. 1; pp. 253 - 256
• Main Authors: Böni-Schnetzler, M., Binz, K., Mary, J.-L., Schmid, C., Schwander, J., Froesch, E.R.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 17-07-1989; Elsevier
• Subjects: Animals; Biological and medical sciences; Blood Glucose - metabolism; Diabetes Mellitus, Experimental - metabolism; Fetus - metabolism; Fundamental and applied biological sciences. Psychology; Gene expression; Gene Expression Regulation - drug effects; Insulin - pharmacology; Insulin-like growth factor I; Insulin-Like Growth Factor I - genetics; Liver - metabolism; Molecular and cellular biology; Molecular genetics; mRNA; Protein, IGF-binding; Rats; Rats, Inbred Strains; Receptors, Cell Surface - genetics; Receptors, Somatomedin; RNA, Messenger - genetics; RNA, Messenger - metabolism; Somatomedins - genetics; Streptozotocin-diabetic rat; Streptozotocin-diabetic rat; mRNA; Protein, IGF-binding; Insulin-like growth factor I; Somatomedin C; Gene expression
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/0014-5793(89)81465-6

Hepatic mRNA levels of insulin-like growth factor I (IGF I) and of the fetal, nonglycosylated 32 kDa IGF-binding protein (BP) were analysed in diabetic, diabetic insulin- and IGF I-treated rats as well as in age-matched, healthy control animals. IGF I mRNA levels are reduced in diabetic rats and increased by insulin treatment. In contrast, the infusion of IGF I does not significantly upregulate IGF I mRNA levels. Fetal IGF BP mRNA expression is very low in healthy control animals, but high levels are found in diabetic rats. Insulin therapy lowers fetal IGF BP mRNA levels, whereas IGF I has no efrect. We propose that insulin is a major regulator of the 32 kDa IGF BP levels in adult rats.