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Precocious and reversible expression of sucrase-isomaltase unrelated to intestinal cell turnover

E Nsi-Emvo1, C Foltzer-Jourdainne, F Raul

  • 1Institut National de la Santé et de la Recherche Médicale, Université Louis Pasteur, Strasbourg, France.

Insights

Starvation in young rats triggers early intestinal sucrase-isomaltase (SI) production. Refeeding normalizes SI levels, with previously induced cells continuing production while new cells do not.

Area of Science:

  • Gastroenterology
  • Developmental Biology
  • Molecular Biology

Background:

  • Intestinal disaccharidase development is crucial for nutrient absorption.
  • The regulation of sucrase-isomaltase (SI) during early life stages is not fully understood.

Purpose of the Study:

  • To investigate the impact of starvation and refeeding on intestinal sucrase-isomaltase (SI) expression in preweaned rats.

Main Methods:

  • Analysis of SI activity and mRNA levels.
  • Immunostaining for SI localization.
  • Measurement of other enzyme activities (alkaline phosphatase, aminopeptidase, lactase).
  • Assessment of c-fos protooncogene expression and cell proliferation.

Main Results:

  • Starvation induced precocious SI activity and mRNA expression, localized to basal villus cells.
  • Refeeding decreased SI activity and mRNA to control levels, with newly formed cells not synthesizing SI.
  • Starvation-induced SI expression occurred without increased cell proliferation, preceded by c-fos expression.
  • SI expression patterns correlated with serum glucocorticoid levels.

Conclusions:

  • Starvation can prematurely induce SI expression in developing rat intestines.
  • Glucocorticoids and c-fos may play roles in mediating starvation-induced SI expression.
  • SI regulation during starvation and refeeding involves distinct cellular responses compared to normal development.

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