Abstract
SM and inhibitors were estimated by the porcine bio-assay in acutely fasted, marasmic (M) and marasmic-kwas-hiorkor (MK) rats. In vitro endogenous activity and responsiveness to SM was measured in their costal cartilage using s35-Sulfate and H3-thymidine. Acute fasting for 3-4 days resulted in complete loss of SM activity, partly caused by a heat-labile, non-dialysable inhibitor. Cartilage endogenous activity and responsiveness were depressed. M-rats (pairfed with MK, normal food, ± 4 g/day, from 25 days age) after 1, 2 and 5 weeks had SM potency ratios compared to controls of 0.8, 0, 0.15, with diminished cartilage endogenous activity. MK rats (ad lib. isocaloric 0,5% casein food) showed a profounder depression of growth and cartilage endogenous activity despite SM ratios (tos controls) of 0.34, 0.75 and 0.45 after 1, 2, and 5 weeks. Evidence for a circulating inhibitor was found. On refeeding M rats, SM and cartilage responsiveness increased by 24 hrs and cartilage endogenous activity by 48 hrs. However catch-up growth in length seen after 1 and 2 weeks was best reflected by H3-thymidine uptake. Clearly differences in SM activity and target organ metabolism follow different nutritional insults. Further studies of these models may clarify the relative roles of SM and inhibitors in malnutrition.
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