Summary
The influence of diabetic pregnancy on the fetal and newborn endocrine pancreas of
rats was investigated in vitro and in vivo. A mild diabetic state was induced experimentally
in the mother with 30 mg streptozotocin injected in the vein of the tail on the first
day of gestation. The maternal blood sugar was 326 ± 28 mg/dl at the end of the gestation.
The in vitro experiment was performed on fetuses of 21.5 days. The endocrine pancreases
were cultured during four or seven days and incubated the last 24 hours with tritiated
thymidine. The healthy state of the islet cells after the two respective periods of
culture was confirmed by an electron microscope study. After incubation with tritiated
thymidine, a significantly higher percentage of labelled nuclei was observed in the
islets of the diabetic group when compared with the controls. This was apparent after
four days (diabetics: 54% - controls: 50%) and is obvious after seven days (diabetics:
28.8% - controls: 18%).
For the in vivo experiment, two day old rats born at term from normal or diabetic
mothers were injected (s.c.) with tritiated thymidine and killed two hours later.
The proliferative capacity of the islet cells of pups born from diabetic mothers compared
to the controls was higher when the percentage of labelled nuclei was calculated (respectively
5.4% versus 3.8%). An islet hypertrophy was also found in the diabetic group.
In conclusion, our results combining in vitro techniques with in vivo observations
demonstrate the higher proliferative rate of the fetal endocrine pancreas induced
by a mildly diabetic feto-maternal environment. They suggest that B-cells are earmarked
during fetal life and have acquired features which they will display even when original
stimuli have disappeared.
Key-Words:
Diabetic Pregnancy
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Fetus
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Neonate
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Islet of Langerhans
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Cell Proliferation
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Thymidine Incorporation
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In Vivo
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In Vitro
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Rat
