The fetal endocrine pancreas.
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Biomedical subjects
Publications and source records attributed to L Aerts.
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Intrvenous injection of 30 mg of streptozotocin per kg body weight induces a mild diabetes in pregnant rats (first generation); the non-fasting blood glucose is increased and the percentage of endocrine tissue and also the percentage of granulated beta cells do not increase. The fetuses of these mildly diabetic pregnant rats have an increased percentage of pancreatic endocrine tissue and there is beta-cell degranulation. The modifications in the endocrine pancreas during intrauterine life causes persistent changes in later adult life (second generation), which are not perceptible in basal conditions, but become apparent in situations stressing the beta-cell activity, such as an intravenous glucose load or pregnancy. During pregnancy in the second generation rats an increased non-fasting blood glucose and no adaptation of the beta cells is seen. This inadequate adaptation to pregnancy causes changes in the fetal endocrine pancreas of the fetuses of the third generation. From these experiments it may be concluded that gestational diabetes is an acquired condition.
During human pregnancy an enlargement of the islets of Langerhans and hyperplasia of the beta cells is present. These morphological changes indicate that the endocrine pancreas is able to adapt to the metabolic changes of pregnancy.
The biochemical effects of progesterone and/or oestradiol treatments on castrated female rats have been compared to those of control olive-oil injections. 1. The steroid treatments used produced physiological concentrations of the two hormones in peripheral plasma, comparable to those obtained during pregnancy. 2. Glycemia remains within a normal range for all the treatments. 3. Circulating immunoreactive insulin (IRI) increases in the steroid-treated rats and the values reach those of the pregnant animals. 4. It was concluded that the biochemical modifications that occur during the steroid treatment (especially with the combined treatment) are quite comparable to what happens during pregnancy and explain, at least in part, the altered carbohydrate and lipid metabolism, and the hyperactivity in the B cell, resulting in an increased insulin secretion.
In a small series of pregnancies complicated by severe fetal growth retardation we found reduction of fetal endocrine pancreatic tissues and of the insulin producing beta cells.
The endocrine pancreas of foetuses and newborn rats of experimental diabetic mothers showed morphological and ultrastructural changes. Islet hypertrophy and beta cell hyperplasia were constantly present, but the beta cells of foetuses of severely diabetic mothers were degranulated. The ultrastructural changes indicated hyperfunction in the beta cells of foetuses of experimental diabetic mothers. The morphological changes mentioned were similar to those seen in human diabetic pregnancy.
The ultramicroscopic appearence of the B-cell of the pregnant rat suggests hyperinsulinism of the individual beta cell. In pregnant rats the B-cell contains an increased volume and an increased number of light granules as well as enlarged mitochondria.