Disaccharidases in the small intestine of the mouse: Normal development and influence of cortisone, actinomycin D, and cycloheximide

Florence Moog, Alex E. Denes, Patricia M. Powell

Research output: Contribution to journalArticlepeer-review

68 Scopus citations

Abstract

The development of maltase, sucrase, and lactase activity has been examined in the small intestine of the mouse. After increasing during 2 days before birth, maltase remains unchanged for 14 days, after which activity surges up throughout the intestine. Sucrase is absent during the first 14 days, but then rises in a pattern similar to, but distinct from, that for maltase. Both enzymes rise faster in the proximal third of the intestine than in the terminal third. Lactase, which is high in the infant intestine, falls after 12 days in the proximal segment, but only after 16 days in the more posterior segments. Cortisone administered at 8 days causes a rise of maltase activity that continues for at least 72 hours. At 4 days the same treatment causes an increase that ceases after 48 hours. Sucrase activity is elicited by cortisone at 8 days but not at 4 days. Between 10 and 13 days both actinomycin D and cycloheximide evoke significant increases of both maltase and sucrase activity in all regions of the intestine. When administered in concert with cortisone, actinomycin D inhibits, but does not prevent, the stimulatory influence of the hormone on sucrase; with maltase activity, significant inhibition occurs only in the middle third of the intestine. Cycloheximide does not interfere with the effects of cortisone. No additive effects between hormone and antibiotics were obtained. These results are discussed in relation to results of similar studies on intestinal alkaline phosphatase and leucylnaphthylamidase.

Original languageEnglish (US)
Pages (from-to)143-159
Number of pages17
JournalDevelopmental Biology
Volume35
Issue number1
DOIs
StatePublished - Nov 1973
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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