SummaryEffects of a recessive gene causing high growth (hg) were studied on two major components of the growth axis in mice. Plasma and pituitary levels of growth hormone and plasma levels of insulin-like growth factor I (IGF-I) were measured in three lines homozygous for hg, each compared with a control line of alike genetic background but wild type for the hg locus (Hg). Line Gh (hghg) and line GH (HgHg) are from a line which had undergone long-term selection for high postweaning weight gain; line Ch (hghg) and line CH (HgHg) were extracted from the second backcross of Gh to C57BL/6J; line L54 (hghg) was from the sixth backcross to C57BL/6J (B6) (HgHg). Pituitary GH levels and plasma IGF-I levels were measured in both sexes at 3, 4·5, 6 and 9 wk of age. Plasma growth hormone was measured in 8- to 12-wk-old males at hourly intervals from 08.00 to 17.00. Body weight in lines homozygous for hg at 6 and 9 wk of age was 10–30% greater than in control lines. The ontogeny of this increased growth depended on genetic background. Pituitary growth hormone content was 52% lower in the two hghg lines measured (lines Ch and Gh) than in control lines at 4·5, 6 and 9 wk. Plasma growth hormone levels were also much lower in hg mice, with values only 20–30% of those in their respective controls, hg lines showed consistently low plasma growth hormone levels throughout the 9 hr sampling period, while control lines expressed the characteristic pulsatile hormone secretion. In contrast, plasma IGF-I levels were greater in line Ch (hghg) than in line CH (HgHg) at 3, 4·5 and 9 wk, and were also greater in line Gh (hghg) vs. line GH (HgHg) at 6 wk of age. The results suggest that the growth enhancing effect of the hg gene occurs through an IGF-I-mediated process. In addition, the genetic background itself is also a factor in the phenotypic expression of the gene.
Decreased circulating growth hormone levels following centrally administered insulin-like growth factor-1 is not mediated by somatostatin in the pig fetus
