Objectives: This study investigated the effects of high ketone levels on fetal carcass metabolism. Specifically, we aimed to determine whether beta-hydroxybutyrate was taken up by fetal muscle and whether lactate production by the fetal hind limb contributed to the raised circulating lactate levels seen in high ketone states.
Study design: Hind limb metabolism was studied in 10 chronically catheterized fetal sheep. Substrate/oxygen quotients were measured before and after 2 hour infusions of beta-hydroxybutyrate and compared with the Wilcoxon signed-rank test.
Results: beta-Hydroxybutyrate was taken up by hind limb tissues in large amounts (butyrate/oxygen quotient = 1.02 +/- 0.40). Lactate was produced by the hind limb (lactate/oxygen quotient = -0.96 +/- 0.52) in amounts almost equivalent to glucose uptake (glucose/oxygen quotient = 1.32 +/- 0.29). Hind limb oxygen consumption increased 35% and fetal arterial oxygen content fell 16%.
Conclusion: beta-Hydroxybutyrate may be consumed by the fetal carcass in amounts sufficient to entirely substitute for glucose. Glucose may then be released as lactate for metabolism elsewhere. Ketones may be important fetal substrates during maternal starvation.