Mosier H D, Jansons R A
Department of Pediatrics, University of California, Irvine 92717.
Pediatr Res. 1989 Apr;25(4):373-6. doi: 10.1203/00006450-198904000-00013.
Experiments were carried out to test the hypothesis that permanent growth retardation after glucocorticoid-induced growth suppression is due to an alteration of a central set point for target size rather than an inability of peripheral tissues to carry out catch-up growth. Rats were injected subcutaneously with saline, as controls, or with cortisone acetate, 1 mg/25 g body wt/d, for 4 d, beginning at 37 d of age. The treated animals were submitted to acute fasting for 48 h, beginning at 47 d of age, after which they were allowed to feed ad libitum. Cortisone treatment significantly stunted body wt, tail length, and tibia length. During recovery after fasting, both the cortisone-treated and the saline-injected rats exhibited catch-up growth in body wt and tibial length. In other rats killed at different time intervals during recovery after cortisone treatment, only, there was no pattern of catch-up growth in tibia length. There was no difference in tibial epiphyseal width between fasted and nonfasted rats within the saline- or cortisone-treated group. The findings demonstrate that rats that are permanently stunted by high-dose glucocorticoid treatment retain the capability for catch-up growth in both soft and skeletal tissues. The data support the hypothesis that catch-up growth is regulated by a central control with a mechanism (set point) for setting target size of the body. Stunting resulting from glucocorticoid treatment may be the result of a reset of the putative set point.
