Fetal hepatic and neural substrate utilization as affected by induced nutritional ketosis in swine

Systemic ketosis was induced in first-parity gilts by the isocaloric substitution of glucose with 1,3-butylene glycol to supply 20% of the total dietary energy beginning on d 23 (23 BG) or d 60 (60 BG) of gestation. Ketosis reduced (P less than .05) maternal plasma glucose, urea N and insulin concentrations. Fetal carcass dry matter and carcass glycogen contents were reduced (P less than .05) by maternal ketogenic calorie substitution, whereas fetal hepatic glycogen and lipid contents were not influenced by maternal treatment. Neural acetate oxidation was reduced (P less than .05) in the 23 BG and 60 BG fetuses, with a concurrent increase (P less than .05) in beta-hydroxybutyrate (BOHB) oxidation. Neural lipogenesis measured from acetate and BOHB substrates was nominal in the d 105 pig fetus. Fetal hepatic acetate and BOHB utilization for lipogenesis were increased (P less than .05) by maternal ketosis. Reproductive performance characteristics (litter size, number stillborn and birth weight) were not improved by maternal ketosis. The substantial improvement in lactation weight gain by litters from 23 BG and 60 BG dams (20%, P less than .05) may suggest a carryover effect of gestation dietary treatment on lactation performance.