Effect of colostrum intake on hepatic gluconeogenesis and fatty acid oxidation in the neonatal pig.

A total of 24 newborn pigs were used to determine 1) the relationship between the quantity of colostrum consumed and the capacity for gluconeogenesis and fatty acid oxidation and 2) whether fatty acid oxidation limits gluconeogenesis in isolated hepatocytes. Neonatal pigs were obtained prior to nursing and allotted to one of three treatment groups; fed (ad libitum), limit-fed (25% of fed group), or fasted. Hepatocytes were isolated when pigs were 24 h old. Colostrum intake altered the metabolic status of neonates such that the capacity for glucose synthesis and oxidation of octanoate increased with intake. Glucose synthesis with lactate as the substrate was greater (P less than .01) for fed pigs (10.79 mumol glucose.h-1.mg DNA-1) than for either limit-fed (6.56) or fasted counterparts (4.78), which were similar (P greater than .10). Colostrum intake failed to stimulate synthesis from alanine. The oxidation rate for octanoate was similar for fed and limit-fed pigs (.62 and .61 nmol CO2.h-1.mg DNA-1, respectively) but greater (P less than .05) than that observed for fasted counterparts (.36). Oxidation of octanoate (2 mM) was approximately 30-fold greater than for oleate (1 mM); oxidation of the latter was not affected by either colostrum intake or the addition of carnitine (1 mM). The increase in octanoate oxidation, however, did not elicit an increase in glucose synthesis by fasting pigs with either lactate or alanine as precursors. Thus, we conclude that gluconeogenesis is a function of colostrum intake and that reducing equivalents and(or) ATP may not be primary factors limiting glucose synthesis in pigs fasted from birth.