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Biomedical subjects

F A Van Assche

Publications and source records attributed to F A Van Assche.

9 recordsLinked to original sources
PubMed1992

Islet transplantation in diabetic pregnant rats normalizes glucose homeostasis in their offspring.

Diabetes of the mother during pregnancy induces alterations in the fetus, resulting in impaired glucose homeostasis in the offspring. In youngsters of severely diabetic mothers, during glucose infusion, hyperinsulinemia is associated with hyperresponsiveness of the beta-cells and insulin resistance. In order to normalize maternal metabolism, isolated islets from neonatal rats were transplanted into the vena porta of severely hyperglycemic (Streptozotocin) rats at day 15 of gestation. Strict glycemic control of the mothers was achieved throughout further gestation and lactation. In the adult offspring of these transplanted rats insulin levels during glucose infusion were significantly lower than in the offspring of sham-transplanted diabetic mothers and were not different from controls. The work confirms that the diabetic state of the mother during late gestation (the period of development of the endocrine pancreas and of the insulin-receptor system) is the inducing factor for the abnormal glucose homeostasis in the offspring, and normalisation of the hyperglycemia eliminates these long-term consequences.

Analysis of Variance↗
PubMed1979

Morphological changes in the endocrine pancreas in pregnant rats with experimental diabetes.

This present study has demonstrated that during normal pregnancy in the rat the number of beta-cells is increased (hyperplasia) and the volume of the individual beta-cells is increased (hypertrophy). During experimental diabetes, however, the endocrine pancreas has an impaired capacity to compensate during pregnancy. In the experimental diabetic pregnant rat the beta-cells cannot replicate due to the unfavourable metabolic environment. This could reflect the complications caused by diabetes during human pregnancy.

Animals↗
PubMed1979

Is gestational diabetes an acquired condition?

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.

Animals↗
PubMed1978

Effects of progesterone and 17-beta-oestradiol treatments on the pancreatic B cell castrated female rats. Biochemical variations.

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.

Animals↗