This study was designed to evaluate the relationship between fetal macrosomia and postnatal growth as well as the glucose homeostasis in young female rats. We produced fetal macrosomia by fetal insulin injection at 20 Vi days of gestation. The control subjects were injected with saline. The weights were recorded weekly from birth up to 12 wk. Only the female rats were studied. At 4, 6, 10, and 12 wk of age, oral glucose tolerance tests were performed. Also, at wk 6, 10, and 12, peri-renalovarian- salpingeal fat weights, the RNA, DNA, and protein contents of the abdominal muscle were determined. Onehundred seventeen control and 78 macrosomic rats were studied. The macrosomic rats showed a higher body weight (10-12%) than the control rats from birth up to 8 wk, but at 10 and 12 wk their weights were similar. The fat weights reflected the body weights, i.e. a higher fat weight in the macrosomic rats during the period of accelerated growth (from birth up to 8 wk), and a similar fat weight when the body weight of the two groups were similar at 10 and 12 wk. At 4 and 6 wk of age, the plasma glucose level measured in response to the oral glucose loading were similar in both groups. However, at 10 and 12 wk of age, the macrosomic rats had significantly higher fasting plasma glucose levels and exhibited consistently higher plasma glucose levels for the 3.5-h period of postglucose administration compared to the control rats. The plasma insulin levels rose significantly following glucose challenge. However, the values were similar in both groups at 10 and 12 wk. We conclude that the primary hyperinsulinemiainduced fetal macrosomia is associated with an increased fat deposition resulting in an increased weight gain during young adulthood. The increased fat deposition may manifest peripheral insulin resistance exhibiting the glucose intolerance at a later age. The mechanism involved in this development remains to be investigated.
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