Fetal hyperinsulinemia causes fetal arterial hypoxia because fetal O2 use increases, whereas the supply of O2 to the fetus does not. To find which of the fetal tissues accounts for such an increase in fetal O2 use, we examined the effect of plasma hyperinsulinemia on O2, glucose, and lactate use by the hindquarters of 13 fetal sheep. Spinal anesthesia was used for the ewes, and local anesthesia was used for the fetuses during placement of catheters. The ewes then recovered for 5 days. After 18 h of insulin infusion, blood samples were drawn, and microspheres were injected to measure blood flow to the tissues of the hindquarters. Three to five infusions of various insulin concentrations in each fetus were followed by blood sampling and blood-flow measurements. Fetal hyperinsulinemia (≤437 pM) increased blood flow to and O2 use by the hindquarters of the fetal sheep but did not affect the glucose-O2 quotients of these tissues. Consequently, glucose use increased proportionately to the increased O2 use. Lactate production was not affected by insulin. We conclude that increased O2 use by all the nonvisceral fetal tissues accounted for the increased O2 use of the entire fetus reported during fetal hyperinsulinemia and, consequently, for the fetal arterial hypoxemia associated with fetal hyperinsulinemia. If the hyperinsulinemic human fetus (such as the infant of the diabetic mother) also increases O2 use in nonvisceral tissue, such an increase might contribute to the susceptibility of the infants to late intrauterine fetal death, polycythemia, and hyperbilirubinemia, all of which may be consequences of intrauterine arterial hypoxemia.

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