Placental glycogen accumulation and maternal-fetal metabolic responses in hyperglycaemic non-diabetic rats.
V Barash, Zvi Gimmon, Eleazar Shafrir
Abstract
V Barash, Zvi Gimmon, Eleazar Shafrir
Abstract
The effect of maternal hyperglycaemia on glycogen and triglyceride accumulation in the feto-placental unit of non-diabetic rats was studied. Hyperglycaemia was induced by continuous infusion of a 400 g/l glucose solution at the rate of 2-4 g/hr/kg, from day 18.5-20.5 of gestation. Hyperglycaemic mothers were hyperinsulinaemic; their fetuses were hyperglycaemic but their insulin levels were comparable with those of control pregnant rats (infused with a 50 g/l glucose solution at the same rate). Fetal pancreas insulin content in the hyperglycaemic fetuses was pronouncedly reduced. The hyperglycaemia produced an approximately 2-fold increase in placental glycogen content in association with increased activities of placental glycogen synthase and phosphorylase. Maternal serum triglycerides fell concomitant with the hyperglycaemia. Placental triglyceride content of hyperglycaemic rats did not change significantly, whereas up to a 2-fold increase in maternal and fetal liver triglyceride concentration was observed. There was no change in fetal and placental weight. Since we have shown previously an increase in both placental glycogen and triglycerides in diabetic rats with hyperglycaemia, concomitant with elevation of plasma triglycerides and free fatty acids, the present experiments demonstrate that these 2 factors causing placental glycogen and triglyceride accumulation can be dissociated. On the other hand, maternal and fetal liver triglycerides accumulate in the hyperglycaemic rats probably as a result of local de vovo lipogenesis.
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The effect of maternal hyperglycaemia on glycogen and triglyceride accumulation in the feto-placental unit of non-diabetic rats was studied. Hyperglycaemia was induced by continuous infusion of a 400 g/l glucose solution at the rate of 2-4 g/hr/kg, from day 18.5-20.5 of gestation. Hyperglycaemic mothers were hyperinsulinaemic; their fetuses were hyperglycaemic but their insulin levels were comparable with those of control pregnant rats (infused with a 50 g/l glucose solution at the same rate). Fetal pancreas insulin content in the hyperglycaemic fetuses was pronouncedly reduced. The hyperglycaemia produced an approximately 2-fold increase in placental glycogen content in association with increased activities of placental glycogen synthase and phosphorylase. Maternal serum triglycerides fell concomitant with the hyperglycaemia. Placental triglyceride content of hyperglycaemic rats did not change significantly, whereas up to a 2-fold increase in maternal and fetal liver triglyceride concentration was observed. There was no change in fetal and placental weight. Since we have shown previously an increase in both placental glycogen and triglycerides in diabetic rats with hyperglycaemia, concomitant with elevation of plasma triglycerides and free fatty acids, the present experiments demonstrate that these 2 factors causing placental glycogen and triglyceride accumulation can be dissociated. On the other hand, maternal and fetal liver triglycerides accumulate in the hyperglycaemic rats probably as a result of local de vovo lipogenesis.
Key concepts: Internal medicine, Endocrinology, Glycogen, Triglyceride, Fetus, Insulin, Lipogenesis, Biology