Expression of insulin-like growth factor binding proteins (IGFBPs) before and during the hormone sensitive period of adipose tissue development in the fetal pig

The present study examined the influence of fetal age and thyroxine (T-4) a nd growth hormone (GH) treatment, on the expression of insulinlike growth f actor binding proteins (IGFBPs) in fetal pigs. On day 70 of gestation fetus es were either hypophysectomized (hypox), hyper and implanted with T-4 pell ets, or left intact, and were recovered 5, 10, 15 and 20 days following hyp er and T-4 pellet placement. Intact fetuses were also recovered from severa l dams at 50 days of gestation. In additional dams, hyper fetuses (day 70) were implanted with GH loaded Alzet mini-pumps on day 90, and control, untr eated, and GH-treated hyper fetuses were recovered on day 105 of developmen t. Subcutaneous adipose tissue, serum and other fetal tissues were collecte d at the time of recovery and prepared for subsequent ligand blot analysis with I-125-IGF-1 and immunoblot analysis with IGFBP antibodies. The main ef fect of IGFBP was significant (P <0.01) for age associated changes in serum IGFBP percentages. Between 50 and 75 days of fetal development the levels of 29 kDa IGFBPs in adipose tissue and serum markedly increased. In contras t, IGFBP-2 levels decreased and IGFBP-4 levels increased in adipose tissue while IGFBP-2 levels increased and levels of IGFBP-4 and -3 decreased in se rum. Fetal hyper decreased adipose tissue IGFBP levels in a time and IGFBP- dependent manner. For instance, IGFBP-2 and 29 kDa IGFBP levels decreased m uch faster after fetal hyper than did IGFBP-3 levels whereas IGFBP-4 levels did not decrease. The main effect of IGFBP was significant (P<0.01) for T- 4-induced changes in adipose tissue IGFBP levels. T-4 treatment increased a dipose tissue levels of 29 kDa IGFBPs but did not influence IGFBP-2,-3 and -4 levels. GH treatment had no influence on adipose tissue or serum IGFBP l evels. These studies indicate that IGFBP-1 (one of the 29 kDa IGFBPs) may b e the major IGFBP mediator of the influence of T-4 On fetal development.