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Biomedical subjects

S Wijkstra

Publications and source records attributed to S Wijkstra.

7 recordsLinked to original sources
PubMed1999

Interaction of late pregnancy and lactation in rats.

The effect of pregnancy on lactation was studied during the third week of lactational pregnancy in postpartum pregnant rats with a delay in implantation of only 1 day (1d-LP rats). In an experimental design in which the suckling litter was prevented from consuming solid food, lactational performance was estimated by weighing the ten-pup suckling litters on days 16-21 of lactation or by measuring maternal weight loss after a nursing spell on day 21. In 1d-LP rats, food consumption as well as lactational performance was lower than it was in nonpregnant lactating rats (L rats) and pregnant-lactating rats with a normal long delay of implantation of at least 6 days (LP rats). The time spent by the pups sucking at the nipples was not different among the three groups, but the number of milk ejections was diminished in 1d-LP dams. Restriction of daily food supply during days 16 to 21 of lactation diminished lactational performance more strongly in 1d-LP rats than it did in L rats; 1d-LP rats conserved protein stores and mobilized fewer minerals than did L rats. The weight and composition of the litter in vitro were not affected by the food restriction. In pregnant-lactating rats (LP and 1d-LP rats), the number of early resorptions was increased in comparison with pregnant rats, showing that lactation can affect the earlier stages of pregnancy. It was concluded that late pregnancy does not affect nursing behaviour, but suppresses lactation by restricting maternal food intake and mobilization of maternal stores. Measurements in serum indicate a causative role for oestradiol, but not for leptin.

Animals↗
PubMed1995

Pancreatic beta-cell function and islet-cell proliferation: effect of hyperinsulinaemia.

Pancreatic beta-cell function was studied in adult female rats, in which endogenous insulin demand was fully met by SC infusion of human insulin (4.8 IU/24 h) for 6 days, resulting in hyperinsulinaemia and severe hypoglycaemia. The amount of pancreatic endocrine tissue declined by 40%, (pro)insulin mRNA, as determined by in situ hybridisation by 95%, and the amount of stored insulin by 90%. Islet-cell proliferation as determined by 24 h of BrdU infusion declined by 60%. Basal glucose levels normalized within 2 days after the insulin treatment was ended, whereas about 1 week was needed to restore the amount of pancreatic insulin, glucose-induced insulin release, and glucose tolerance to normal values. The amount of endocrine tissue recovered within 48 h and mRNA abundance within 96 h after discontinuation of the insulin infusion, whereas at that time islet-cell proliferation still showed a sixfold increase, before returning to control levels after 1 week. These results show that after a period of suppression of beta-cell function, recovery of insulin synthetic capacity does not immediately result in normalization of insulin stores and insulin release. Under these conditions, episodes of hyperglycaemia may occur, which may act as a stimulus for islet-cell proliferation.

Animals↗
PubMed1995

Effect of insulin on endocrine pancreas function during late pregnancy in the rat.

To partly or completely satisfy the increasing demand for insulin, pregnant rats were infused SC with human insulin (2.4 or 4.8 IU/day) from day 14 to day 20 of gestation. Cyclic control rats underwent the same procedure of 6 days of insulin-treatment. During the treatment all groups of rats were hypoglycaemic, but foetal survival was not affected. The low dose treatment prevented the characteristic rise of the insulin response to a glucose challenge during pregnancy, both in vivo and in vitro, while the high dose treatment suppressed the insulin response, as well as the pancreatic insulin content. The insulin responses and insulin contents of pregnant rats were higher than those of the corresponding cyclic control rats. These results support the hypothesis that during gestation the increased insulin demand, due to the actions of placental hormones, is the cause of the increased insulin secretion. However, it cannot be excluded that direct effects of placental hormones on the islets of Langerhans are also involved.

Animals↗
PubMed1992

Metabolism of pregnant-lactating rats is adapted to pregnancy rather than to lactation.

In pregnant-lactating rats implantation was induced on day 4 of lactation so that, as an exception, lactation coincided with the period of high fetal growth. The already present suckling litters of these animals lagged behind in growth, but the "second" litters were at birth normal in size and weight. Such pregnant-lactating rats were tested in vivo with intravenous glucose loads and compared with cyclic and lactating rats. Glucose tolerance was unaffected by the reproductive state. Pregnant-lactating rats showed, just as during their first pregnancy, low basal glucose levels. Their basal insulin levels and insulin responses, however, were decreased in comparison with the first pregnancy and resembled those of lactating rats. This may be due to an increased insulin turnover, because in vitro insulin responsiveness and insulin content of both "pregnant-lactating" and "pregnant" islets were increased in comparison with "cyclic" and "lactating" islets. It was concluded that the metabolism of pregnant-lactating rats is adapted to the pregnant rather than to the lactational state.

Adaptation, Physiological↗
PubMed1991

Endotoxin treatment of pregnant rats affects sexual behavior of the male offspring.

The offspring of endotoxin-infused pregnant rats (0.2 micrograms endotoxin, 53.3 min, day 18 of pregnancy) did not exhibit different behavior in the Hebb-Williams-type maze test, but the males showed aberrations in the sexual behavior test. Because endotoxin did not cross the placental barrier, it was concluded that the effect reflects abnormal brain development, caused by endotoxin-induced placental malfunction, notably impaired oxygen transport.

Animals↗