Intestinal glucose transport in suckling rats fed artificial milk with and without added epidermal growth factor

Epidermal growth factor (EGF), a potent mitogen present in milk, is postulated to play an important physiological role in the ontogeny of the intestine. An artificial rat milk, free of EGF, was developed and fed to newborn rats in an effort to evaluate the physiologic role of EGF on intestinal glucose transport. Comparisons were made between mother-fed (group 1) and artificial fed pups (group 2). Group 1 was divided into two subgroups to receive either the EGF vehicle (group 1-A) or twice daily subcutaneous injections (0.1 μg/g body weight/day) of EGF (group 1-B). Group 2 was divided into four subgroups: formula without EGF (group 2-A), formula with 62 ng/ml of EGF (group 2-B), formula with 200 ng/ml EGF (group 2-C), and formula without EGF but added anti-EGF IgG (40 ng/ml) plus subcutaneous injections of 1 μg anti-EGF twice daily (group 2-D). Treatment regimens were initiated on day 3 and assays performed on day 11 of life. Glucose transport was measured using gut 'sheet' preparations in all but group 2-C, which utilized brush border membrane preparations. Group 1-B showed a significant (p < 0.03) increase in gut length (47.5 ± 1.2 versus 42 ± 0.9 cm) and an increase (p < 0.03) in both V(max) (10.2 ± 0.5 versus 7.2 ± 0.3 nM/mg tissue) and K(m) (2.74 ± 0.49 versus 1.20 ± 0.19 mM) compared to group 1-A. All pups in group 2 showed a significant (p < 0.03) increase in intestinal length compared to group 1-A, but no differences was seen between group 1-B and all subsets of group 2. Glucose uptake was similarly affected with the exception that only the V(max) was significantly increased by the feeding. The suggested increase in glucose carriers resulting from EGF was further supported by the finding that only the large oral or systemic dose of EGF (groups 1-B and 2-C) caused a significant (p < 0.01) increase in the 1-minute accumulation ('over-shoot') of glucose in the brush border membrane. Whereas pharmacologic doses of EGF caused premature development of intestinal glucose transport and increased gut length, artificial feeding alone caused a similar increase in intestinal length and V(max) for glucose transport.