Plasma folate binding capacity of the reproducing pig

Abstract

Altered folate utilization can be a secondary manifestation of iron (Fe) deficiency during reproduction. The purpose of the present investigation was to determine whether species differences with regard to high affinity plasma folate binders (HAFBP) makes the pig an inappropriate animal model for studying the interaction of Fe and folate in the human. Specifically, we assessed the impact of gestation, lactation, Fe, and folate status on the concentration and percent saturation of HAFBP in the pig. Reproducing pigs (sows) ( n = 18) were fed diets containing 1360 nmol/kg (0.6 mg/kg) folate and either 0.45 mmol/kg (25mg/kg; −) or 2.24 mmol/kg (125 mg/kg; +) Fe throughout gestation and lactation. Total folate binding capacity (TFBC) of plasma remained constant throughout gestation and lactation. Still, the mean TFBC of Fe+ sows was approximately four times that of mean plasma folate concentration. Unsaturated folate binding capacities (UFBC) of plasma were inversely correlated with plasma and red blood cell (RBC) folate values ( r = −0.57 and −0.62). Both TFBC and percent saturation of HAFBP were positively correlated with indices of folate nutriture. Mean folate values of serum samples treated to remove unbound folate (23.4 nmol/ L ± 2.8) did not differ from those of untreated samples (24.1 ± 2.0). Conversely, in the human the TFBC of plasma is 30 times less than plasma folate content and is not correlated with indices of folate nutriture and increases with gestation. Mean UFBC of Fe− sows was 28% greater than Fe+ sows, reflecting the lower plasma folate values among Fe− sows ( P = 0.0002). Only at day 56 of gestation was TFBC of Fe− sows less than Fe+ sows (26%, P < 0.05). Overall, pig TFBC did not appear to be altered by Fe nutrition, rather it changed in response to folate nutriture. In sum, differences between the pig and the human exist with regard to HAFBP, possibly limiting the usefulness of the pig for studying folate metabolism of humans. These differences, in addition to the fact that plasma folate values among Fe− sows, like those of Fe-deficient humans, are lower than their Fe+ counterparts, suggest that impaired cellular delivery of folate is not responsible for folate depletion secondary to Fe deficiency.