Serum IRI (immunoreactive insulin) in twenty-day fetuses from mothers fed ad libitum exceeded maternal levels. Increasing maternal IRI produced by injection of exogenous insulin or by intravenous glucose loading did not produce significant changes in fetal IRI. The twenty-day pregnant rat in the basal state distributed relatively more C-14 from radio glucose into lipid and glycogen and relatively less into protein than a nonpregnant control under similar conditions. Incorporation of C-14 from radioglucose was augmented by exogenous insulin at fifteen minutes into lipid in maternal liver and adipose tissue, protein into liver and glycogen in muscle. Neither the incorporation of C-14 into lipid, glycogen, or protein from radioglucose nor the incorporation of H3 (from H32O) into fatty acids was influenced by exogenous insulin in the fetus. This was true even when the insulin was injected directly into the fetus. On the other hand, fetal incorporation of radioglucose into glycogen was augmented significantly by an acute glucose load. The data suggest that although fetal serum contains significant concentrations of insulin derived from fetal (β-cells, the exact metabolic role of this insulin in the fetus is unclear.

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