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PMID: 9754832 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat.

Diabetologia ·Vol. 41 ·No. 9 ·1998-09-00 ·Pages 1114-20

Garofano A, Czernichow P, Bréant B

Abstract

We have recently shown that maternal food restriction during late pregnancy in rats decreased beta-cell mass in the offspring at birth, without altering beta-cell proliferation. The aim of the present work was to determine: 1) whether sustained maternal undernutrition until weaning (R group) more dramatically alters beta-cell mass in the offspring and if normal food supply from weaning until adulthood could reverse the deleterious effects and; 2) if altered beta-cell proliferation was responsible for the decreased beta-cell mass. Beta-cell fraction and proliferative capacity were determined during the suckling period and at adult age after ad libitum feeding from weaning in the R animals and in age-matched controls (C group). At day 21, the offspring born and nursed by food-restricted mothers (R animals) showed a 66% reduction in beta-cell mass and number, which did not increase from birth to weaning, although beta-cell proliferation remained normal. At 3 months of age, R animals had 35% decreased beta-cell fraction, with a 50% decrease in the head of the pancreas. In that area, beta-cell proliferation was similar to that of the controls. In the tail of the pancreas, beta-cell fraction was only slightly impaired but beta-cell proliferation was increased by 37%, as compared with the controls. This increase was associated with a shift in islet size distribution towards medium and large islets compared with the head of pancreas from these R animals. No regional variations of beta-cell fraction, proliferation or islet size distribution were observed in adult control animals. In conclusion, prolonged malnutrition until weaning impairs beta-cell development but not beta-cell proliferation. Subsequent re-nutrition is followed by increased beta-cell proliferation but this is insufficient to fully restore beta-cell mass.

MeSH Terms
Animals Animals, Newborn Bromodeoxyuridine/metabolism Cell Division Female Fetal Growth Retardation/pathology Food Deprivation Insulin/metabolism Islets of Langerhans/cytology,growth & development,pathology Placental Insufficiency/pathology Pregnancy Rats Rats, Wistar Starvation/pathology
Chemicals
Insulin Bromodeoxyuridine
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Garofano A
INSERM U 457, Hôpital Robert Debré, Paris, France.
Czernichow P
Bréant B
Article Info
Journal
Diabetologia
Abbr.
Diabetologia
ISSN
0012-186X
Published
1998-09-00
Pages
1114-20
Language
English
Region
Germany
NLM ID
0006777
Subset
IM
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