Hormonal Control of Postnatal Development of Heal Neuraminidase and Acid Beta-Galactosidase

Abstract

This study examines the effect of changes of thyroid and glucocorticoid status on the development of ileal neuraminidase and acid beta-galactosidase. Thyroxine (T4) administration on postnatal days 6-13 had no effect on the activity of either enzyme. In contrast, a single injection of cortisone acetate on day 6 caused a precocious reduction of the activities of both enzymes. Hypothyroidism delayed the usual developmental decline of neuraminidase activity and prevented the decline of acid beta-galactosidase activity. This was probably due to an effect of T4 on endogenous glucocorticoids because cortisone acetate was just as effective as T4 in restoring enzyme activities to control levels. Adrenalectomy delayed the decline of both enzyme activities whereas glucocorticoid replacement in these same animals depressed enzyme activities to, or below, control levels. It is likely that glucocorticoids act as the primary cue in the maturation of these enzymes, but with T4 interaction necessary for the normal pattern to be elicited.