There is no change in either basal carbohydrate oxidation or nonoxidizable carbohydrate metabolism but there is a significant 50-80% increase in fat oxidation during pregnancy both in the basal state and also during an euglycemic hyperinsulinemic clamp (11). These data underline the importance of the switch from carbohydrate to fat metabolism in pregnancy that is potentially regulated by placenta-produced leptin. During fasting, pregnancy is a state of accelerated starvation with increased maternal reliance on lipids rather than on carbohydrate for energy demands (62). These maternal responses to pregnancy have the result of sparing carbohydrates and amino acids for the fetus. Decreased PPARg expression, and hence signaling through its target genes, has been suggested to be the mechanism by which fat catabolism is enabled (63).
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