To determine whether the insulin resistance, exaggerated fasting hypoglycemia, and hypoalaninemia of late human and rat gestation may reflect altered skeletal muscle metabolism, hindlimbs of nonpregnant (NPG) and 3-wk-pregnant (PG) rats were noncyclically perfused in situ. In 12- and 24-h-fasted NPG rats, 50–500 μU/ml of insulin significantly augmented glucose uptake 3-9-fold. In PG rats uptake was suppressed 40–50% at comparable hormone concentrations. Release of alanine and phenylalanine was suppressed 20–35% by 250 μU/ml or more of insulin in NPG rats. However, comparable insulin concentrations failed to suppress their release in PG rats. No differences between groups existed with respect to oxygen uptake, glycerol, lactate, or pyruvate release. Suppression of insulin sensitivity in 12-day-pregnant rats was not observed.

Since plasma estradiol (E) and progesterone (P) are increased in pregnancy, E-benzoate (5 μg/day) and/or P (5 mg/day) were injected s.c. into female rats for 21 days. In 12-h-fasted animals, E treatment potentiated whereas P treatment mildly antagonized insulin-induced glucose uptake relative to control values. Separate effects of E and P were offset when administered in combination. Individual or combined regimens did not alter oxygen uptake, or release of alanine, phenylalanine, lactate, or pyruvate.

In late gestation, insulin action on skeletal muscle is resisted with respect to glucose uptake, alanine release, and proteolysis. Fasting hypoalaninemia is not due to impaired alanine release from muscle, but may reflect increased fetal extraction. Fasting hypoglycemia may represent, in part, maternal gluconeogenic precursor deficiency due to fetal alanine removal. E and/or P treatment do not duplicate the observed metabolic Changes.

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