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Islet transplantation in diabetic pregnant rats normalizes glucose homeostasis in their offspring
1Laboratory of Obstetrics & Gynaecology, U.Z. Gasthuisberg, Leuven, Belgium.
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.
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.