Relationship between Plasma Somatomedin-C and Liver Somatogenic Binding Sites in Neonatal Rats during Malnutrition and after Short and Long Term Refeeding*

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Abstract
To determine the mechanism(s) for the growth retardation associated with malnutrition early in life, the relationships among plasma somatomedin-C (SM-C), plasma GH, and hepatic bovine GH-binding sites were assessed in rat pups that were milk-deprived from birth until weaning (21 days). After this period of malnutrition, body weight, tail length, plasma SM-C, and liver GH-binding capacity of the malnourished animals were significantly (P < 0.001) reduced below those of control, well fed rats [SM-C at 21 days, 0.06 ± 0.01 vs. 0.30 ± 0.04 U/ml (mean ± SE); GH binding, 2.96 ± 0.39 vs. 7.19 ± 0.80 pmol/liver]. The number of GH-binding sites per mg DNA was also reduced (0.59 ± 0.06 vs. 1.08 ± 0.11 pmol/mg DNA; P < 0.001). After 1 week of ad libitum refeeding (days 21–28), body weight and tail length of malnourished pups increased significantly but showed no signs of catching up with that of control pups. Plasma SM-C and liver GH-binding capacity in the malnourished rats also rose significantly (P < 0.005) after refeeding, but remained as far below controls as at 21 days [SM-C on day 28, 0.19 ± 0.02 vs. 0.53 ± 0.02 U/ml (P < 0.001); GH binding, 6.59 ± 0.99 vs. 12.94 ± 1.60 pmol/liver (P < 0.005)]. After 7 weeks of refeeding (days 21–70), tail length but not body weight recovered, while plasma SM-C levels were normalized. The mean number of GH binding sites per mg DNA in the malnourished rats was not significantly different from that in controls and reached for the males and the females, respectively, 79% and 86% of control binding. When expressed per liver, GH binding followed a similar pattern; for the males, binding capacity returned to 73% of the control value (20.45 ± 1.82 vs. 27.93 ± 3.49 pmol/liver; P = NS), and for the females, it returned to 77% of the control value (36.42 ± 1.76 vs. 47.42 ± 4.13 pmol/liver; P < 0.01). In the young rats up to day 28, liver GH-binding capacities correlated with plasma SM-C concentrations (r = 0.81; P < 0.01), while in the adult rats no correlation was present. During malnutrition and refeeding, there were no changes in the affinity constants of the hepatic GH-binding sites or in plasma GH concentrations. The results suggest that in neonatal malnutrition, reduced liver GH-binding capacity could be one of the mechanisms whereby plasma SM-C concentrations are reduced. Prolonged, but not short term, refeeding leads to tail length catch-up growth, normalization of plasma SM-C concentrations, and restoration of near-normal liver GH-binding capacities. (Endocrinology115: 786–792, 1984)