Restriction of nutrition in utero selectively inhibits gastrointestinal growth in fetal sheep

Trahair, Jeffrey F., DeBarro, Tania M., Robinson, Jeffrey S. and Owens, Julie A. 1997, Restriction of nutrition in utero selectively inhibits gastrointestinal growth in fetal sheep, Journal of nutrition, vol. 127, no. 4, pp. 637-641, doi: 10.1093/jn/127.4.637.

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Title Restriction of nutrition in utero selectively inhibits gastrointestinal growth in fetal sheep
Author(s) Trahair, Jeffrey F.
DeBarro, Tania M.
Robinson, Jeffrey S.
Owens, Julie A.ORCID iD for Owens, Julie A.
Journal name Journal of nutrition
Volume number 127
Issue number 4
Start page 637
End page 641
Total pages 5
Publisher Oxford University Press
Place of publication Oxford, Eng.
Publication date 1997-04
ISSN 0022-3166
Keyword(s) Animal Nutritional Physiological Phenomena
Digestive System
Fetal Organ Maturity
Food Deprivation
Intestine, Large
Intestine, Small
Microscopy, Electron
Science & Technology
Life Sciences & Biomedicine
Nutrition & Dietetics
growth retardation
small intestine
Summary This study examined the effects of reduced nutrition on fetal growth over the first half of gestation. Reduced nutrition was achieved by a combination of reduced maternal food intake and carunclectomy, a procedure which restricts the development of the placenta. There were no major effects of restriction on fetal body, tissue or organ growth, except for the gastrointestinal tract (GIT). Total GIT weight was lower in restricted fetuses than in controls. More specifically, it was growth of the small and large intestine which was compromised. Small intestinal weight was significantly lower, both in absolute terms and relative to body weight. The intestinal diameter and mucosal area were significantly lower in both small and large intestine of restricted fetuses. Maturation of enterocytes was also delayed in nutrient-restricted fetuses. In addition, there were focal lesions of the brush border present, indicating abnormal epithelial differentiation. By term, in growth-retarded fetuses, growth deficits in many organs were present, including the GIT. The present study suggests that GIT growth deficits may have a long-term etiology, including at their onset, abnormal cellular differentiation. These results could explain why GIT function in intrauterine growth-retarded infants is more likely to be compromised than in premature or term infants.
Language eng
DOI 10.1093/jn/127.4.637
Field of Research 1111 Nutrition And Dietetics
0702 Animal Production
0908 Food Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©1997, American Society for Nutritional Sciences
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Document type: Journal Article
Collection: Office of the Deputy Vice-Chancellor (Research)
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