Small intestinal type i and ii insulin-like growth factor receptor expression in piglets fed formula supplemented with insulin-like growth factor-1 (IGF-I)

Piglets fed formula+IGF-I have enhanced intestinal mucosal growth and enzyme activity compared to piglets fed formula. The current study studied if oral IGF-1 affected intestinal type I and type II receptor number or binding affinities. Colostrum-deprived piglets received formula ±500 |ig/L IGF-I for 14 d. Piglets were killed, the intestine removed, flushed, and duodenal, jejunal and ileal mucosa samples were obtained. Microsomal membranes were isolated by differential centrifugation and purity was confirmed by enrichment of 5'-nucleotidase activity. Type I and type II receptors were identified by affinity crosslinking of membranes with [¹²⁵I]-IGF-I and [¹²⁵I]-IGF-II, respectively, and autoradiography. In competitive binding studies, [¹²⁵I]-IGF-I was displaced by excess unlabelled peptide in the following order IGF-I>IGF-II≫insulin. [¹²⁵I]-IGF-II binding was only inhibited by IGF-II. Dissociation constants for the type I (0.85 nM) and type II (4 nM) receptors were unaffected by oral IGF-I. The number of jejunal binding sites determined by Scatchard analysis for IGF-II (1.5 × 10⁸/mg prot) was greater than IGF-I (3.4 × 10⁷/mg prot), however, no difference between the treatment groups were noted. In contrast, binding studies showed that total binding of jejunal [¹²⁵I]-IGF-I and [¹²⁵I]-IGF-II in duodenum and jejunum were lower in IGF-I piglets than control (p<0.05). IGF-I action is associated with a decrease in membrane receptors due to internalization, these data suggest that the action of IGF-I within the intestine is receptor-mediated.