make embryos more susceptible to apoptosis. In addition, IGF-1 reduced abundance of

the Bax gene transcript in porcine embryos (Kim et al., 2006). The increased abundance

of Bax coupled with no effect of IGF-1 treatment on the abundance of the anti-apoptotic

gene Bcl may help to explain why IGF-1 treated embryos in the present study did not

have reduced levels of apoptosis.

 The IGFBPs regulate the activity of IGF-1 in several ways, including extending

the half-life of IGF-1, transporting and localizing IGF-1 to specific cell types and tissues,

and stimulating and/or inhibiting IGF-1 actions at the cellular level (Jones and

Clemmons, 1995; Clemmons, 1997; Cohick, 1998; Mohan and Baylink, 2002). While

the precise role of IGFBPs in early embryo development is not fully understood, IGF-1

can alter the expression of IGFBPs by the early embryo (Prelle et al., 2001) and IGFBPs

can modulate the effects of IGF-1 on early embryo development (Lin et al,. 2003). In the

present study, IGF-1 treatment increased the abundance of IGFBP3 transcripts. The

majority of IGF-1 in the circulation is bound by IGFBP3 (Jones and Clemmons, 1995)

and IGF-1 has been reported to increase circulating levels of IGFBP3 in vivo (Zapf et al.,

1989; Camancho-Hubner et al., 1991a; Liao et al., 2006) as well as mRNA and protein

levels in vitro (Bale and Conover, 1992; Camancho-Hubner et al., 1991b; Fleming et al.,

2005). Treatment with IGF-1 also reduced transcripts for IGF1R, as has been found

previously for bovine embryos (Prelle et al., 2001) and other cells (Hernandez-Sanchez et

al., 1997). Taken together, it appears that one of the embryonic responses to IGF-1 is to

dampen embryonic responses to IGF-1 through increased sequestration (via IGFBP3) and

receptor downregulation.