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Table of Contents
Vol. 42, No. 5-6, 1982
Issue release date: 1982
Section title: Paper
Biol Neonate 1982;42:239–248
(DOI:10.1159/000241605)

Diabetes in Pregnancy: Growth of the Fetal Pancreatic B Cells in the Rat

Eriksson U. · Swenne I.
Department of Medical Cell Biology, University of Uppsala, Sweden

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: September 17, 2009
Issue release date: 1982

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 0

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: http://www.karger.com/NEO

Abstract

The development of the pancreatic B cells in the offspring of normal (N), subdiabetic (SD), manifest diabetic (MD) and insulin-treated diabetic (MDI) rats was studied with the aid of immunocytochemical staining for insulin. Morphometric evaluation of the B-cell volume density and weight was made by point sampling. The offspring were studied on gestational days 20 and 22 and in the newborn state. In the N offspring the weight of the B-cell parenchyma doubled during the last 2 days of gestation. This rapid increase may be ascribed not only to high mitotic activity but also to differentiation of putative percursor cells to B cells. The mild glucose intolerance of the SD mothers had no major effects on the fetal B-cell development. In the MD group both the volume density and the weight of the B cells were considerably lower than in the N and SD groups at all ages studied. Despite prolonged gestation, the weight of the fetal B cells in the MD newborns was not greater than that in the 20-day-old fetuses of the N group. Insulin treatment of the MD mothers restored the fetal B-cell development towards normal. This study indicates that manifest maternal diabetes in the rat retards the development of the fetal B cells. This is in obvious contrast to the corresponding situation in human diabetic pregnancy, in which hyperinsulinism represents a striking feature of diabetic fetopathy. It is suggested that a milder form of maternal glucose intolerance together with the relatively longer gestational period in man, compared with the rat, may create conditions that favour fetal B-cell hyperplasia.

© 1982 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: September 17, 2009
Issue release date: 1982

Number of Print Pages: 10
Number of Figures: 0
Number of Tables: 0

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: http://www.karger.com/NEO


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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