Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The control of weaning was studied in rat pups aged 17-24 days. The influence of two hormones, thyroxine (T4) and corticosterone, and the effect of declining intestinal lactase activity were evaluated. Hypothyroidism was induced by administration of n-propylthiouracil and hyperthyroidism was induced by injection of T4. Hypothyroid pups failed to begin nibbling chow while littermates injected with T4 weaned normally. Two abnormalities resulting from hypothyroidism, hypothermia and stunted incisors, were not responsible for the lack of weaning in hypothyroid pups. Hyperthyroidism did not cause precocious weaning. Glucocorticoid levels were manipulated by both adrenalectomy (ADX) and administration of corticosterone. ADX pups exhibited a delayed pattern of weaning while both ADX pups injected with corticosterone and sham-operated pups weaned normally. Corticosterone injected before its normal developmental surge did not cause precocious weaning. Lactase activity, measured throughout these experiments, did not consistently reflect the degree of weaning progression. We conclude that 1) the hormones, T4 and corticosterone, are necessary for the onset of weaning, but neither is a sufficient stimulus to initiate weaning, and 2) low lactase activity does not initiate weaning.
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PMID:Weaning in the rat: a study of hormonal influences. 640 84

Jejunal sucrase is known to display glucocorticoid responsiveness from birth through day 17 but not beyond that age. The aim of the current study was to determine whether this abrupt loss of responsiveness was shared by maltase, lactase, and acid beta-galactosidase. Glucocorticoid concentrations were manipulated by both adrenalectomy (ADX) and by administration of cortisone acetate (CA). Surgery or treatment was performed on each day from 16--22 days of age. Maltase activity was reduced by ADX at day 18 and earlier and was increased by CA at days 16 and 17. There were no effects at later ages. Acid beta-galactosidase was increased by ADX only at day 18 and earlier and was decreased by CA only at day 16. Lactase activity was increased by ADX at all ages up to and including day 20 but was reduced by CA only at days 16 and 17. Thus, we conclude that loss of glucocorticoid responsiveness at a relatively early stage of development is a common feature of both brush-border and lysosomal enzymes of the small intestine.
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PMID:Coordinate loss of glucocorticoid responsiveness by intestinal enzymes during postnatal development. 680 95