
Altered controls of proliferation in proximal small intestine of the senescent rat.
Author(s) -
Peter R. Holt,
KwoYih Yeh,
Donald P. Kotler
Publication year - 1988
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.85.8.2771
Subject(s) - crypt , basal (medicine) , 1,2 dimethylhydrazine , cell growth , biology , starvation , small intestine , medicine , intestinal villus , aberrant crypt foci , dna synthesis , endocrinology , intestinal mucosa , carcinogen , concomitant , cell , dna , microbiology and biotechnology , carcinogenesis , biochemistry , colorectal cancer , genetics , azoxymethane , colonic disease , cancer , gene , insulin
The proximal small intestine responds to starvation by rapidly reducing crypt cell proliferation rate and villus cellularity and to resumption of food intake (refeeding) by abruptly increasing proliferation and the number of villus epithelial cells. We show that villus cellularity responds to starvation and refeeding similarly in young and aging animals. However, as compared to young animals, senescent rats showed increased basal DNA synthetic activity, starvation resulted in a smaller decrease in DNA labeling of crypt cells, and refeeding produced an abrupt broadening of the proliferative zone in older animals without concomitant increased numbers of villus cells. Such altered crypt proliferative responses resemble precancerous changes seen in the colon and the aberrant proliferation found in both small and large intestine after administration of the carcinogen dimethylhydrazine.