Intestinal glucose metabolism during development. II. The role of glucocorticoids and weaning.
Prolonged suckling, until 25 postnatal days, delays the increase in jejunal oxidation of glucose both to lactate and to CO2 that occurs after artificial weaning at 20 days of age. The cortisone-mediated increase in intestinal sucrase activity which normally occurs by 20 days is not effected by prolonged suckling. Following precocious weaning at 16 days, the rate of jejunal glucose oxidation to lactate and to CO2 increases, over a 48-h period, to adult rates. Exogenous cortisone treatment at 10-13 postnatal days, before the endogenous steroid burst, does not change the rate of glucose oxidation in suckling animals. After weaning, both at 20 days of age and precociously at 16 days, the rate of glucose oxidation to lactate and to CO2 increases within 24 h in those animals who received early steroid treatment, in comparison to 48-72 h in untreated controls. After prolonged suckling until 25 days, there is no effect of early steroid treatment. We conclude that neither endogenous glucocorticoid secretion nor exogenous cortisone treatment alters the rate of glucose oxidation in jejunum of suckling animals despite the induction of jejunal sucrase activity. After early cortisone treatment, glucose oxidation increases within 24 h of normal of precocious weaning.[1]References
- Intestinal glucose metabolism during development. II. The role of glucocorticoids and weaning. Kimura, R.E., Reinersman, G.T. Pediatr. Res. (1985) [Pubmed]
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