The relationship between porcine growth hormone (pGH) and insulin-like growth factor-I (IGF-I) in swine was investigated. IGF-I levels were measured by radioimmunoassay (RIA) with an antisera specific for human IGF-I after ultrafiltration of acidified samples. Ultrafiltration quantitatively separated carrier proteins and IGF-I. Failure to separate these species interfered with the RIA. Using this assay, swine chronically treated with pGH had 2.6-fold higher sera levels of IGF-I than controls, whereas, serum IGF-I from a hypophysectomized animal was only 4% that of normal animals.

The ultrafiltration procedure was incorporated into a protocol to measure IGF-I in sera from neonatal swine treated with pGH (5O ug •kg BWt⁻¹•d⁻¹). Treatment of neonatal pigs with pGH for one or two weeks elevated pGH in sera, but did not significantly affect either growth or serum IGF-I concentrations. Preliminary studies were performed to determine if neonatal swine hepatocytes secreted IGF-I in vitro. Results indicated that neonatal hepatocytes synthesized limited quantities of IGF-I that approached the detection limits of the RIA. Furthermore, pGH did not stimulate hepatocyte IGF-I synthesis in vitro or in vivo. Neonatal hepatocytes synthesized a protein species that bound labeled IGF-I and had a molecular weight similar to a carrier protein in swine serum. Estimation of the rate of carrier protein synthesis suggested that IGF-I and carrier proteins are coordinately regulated in isolated neonatal hepatocytes. These results suggest that IGF-I is not inducible in the neonatal pig by GH therapy and that growth in neonatal swine is either maximal or GR-independent.