PLASMA FOLATE BINDING-CAPACITY OF THE REPRODUCING PIG

Altered folate utilization can be a secondary manifestation of iron (F e) deficiency during reproduction. The purpose of the present investig ation 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 hum an. 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 containin g 1360 nmol/kg (0.6 mg/kg) folate and either 0.45 mmol/kg (25 mg/kg; - ) or 2.24 mmol/kg (125 mg/kg; +) Fe throughout gestation and lactation . Total folate binding capacity (TFBC) of plasma remained constant thr oughout gestation and lactation. Still, the mean TFBC of Fe+ sows was approximately four times that of mean plasma folate concentration. Uns aturated folate binding capacities (UFBC) of plasma were inversely cor related 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 ser um 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 inc reases with gestation. Mean UFBC of Fe- sows was 28% greater than Fesows, 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 Fesows (26%, P < 0.05). Overall, pig TFBC did not appear to be altered b y Fe nutrition, rather it changed in response to folate nutriture. In sum, differences between the pig and the human exist with regard to HA FBP, possibly limiting the usefulness of the pig for studying folate m etabolism of humans. These differences, in addition to the fact that p lasma 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.