Growth Enhancement of Transgenic Mice Expressing Human Insulin-Like Growth Factor I*

TLDR

The authors generated a transgenic mouse line with chronically elevated IGF‑I to investigate its systemic effects. This was achieved by inserting a chimeric human IGF‑I gene driven by the mouse metallothionein I promoter into the mouse genome. The mice overexpress IGF‑I, showing 1.5‑fold higher circulating levels, a 1.3‑fold weight gain due to selective organomegaly, no skeletal growth increase, and down‑regulation of endogenous GH and IGF‑I genes, underscoring IGF‑I’s role in somatic growth. Endocrinology 123: 2827–2833, 1988.

Abstract

A line of transgenic mice carrying a chimeric gene composed of human insulin-like growth factor I (IGF-I) coding sequences fused to the mouse metallothionein I promoter was generated to study the effects of chronically elevated exposure to IGF-I. Mice in this line overexpress IGF-I in most tissues studied and have circulating IGF-I levels 1.5 times the normal value. This results in a growth response manifested by a 1.3-fold increase in weight as a result of selective organomegaly without an apparent increase in skeletal growth. In addition, expression of the endogenous GH and IGF-I genes is inhibited. These results are consistent with IGF-I playing an important role in the control of somatic growth. (Endocrinology123: 2827–2833, 1988)