Basis for the diversity and extent in loss of digestible nutrients created by dietary phytin: Emphasis on fowl and swine

Abstract

Phytin is the Ca²⁺-Mg²⁺-K⁺ salt of phytic acid that is created and deposited in the aleurone layer and/or germ of grains and legumes. Its high presence in feedstuffs for fowl and swine diets results in it being a universal and significant impediment to optimum performance. Phytin impairs gastrointestinal recovery of a wide array of nutrients, the effect varying with the nutrient concerned. On exposure to low pH during gastric digestion, phytin dissociates into phytic acid and solubilized Ca²⁺. Even at low gastric pH, phytic acid is negatively charged which forms the basis of its anti-nutritive behavior. Pepsinogen has extensive basic amino acids on its activation peptide that are presented as cations at low pH which are targeted by pepsin for activation. Partially crystalized Ca²⁺ near the enzyme’s active site further stabilizes its newly formed structure. Thus, phytic acid appears to interfere with gastric digestion by several mechanisms; interfering with pepsinogen activation by binding to the polypeptide’s basic amino acids; Coordinating free Ca²⁺, destabilizing pepsin; binding some dietary proteins directly, further compromising gastric proteolysis. Upon digesta attaining neutrality in the duodenum, Ca²⁺ and other cations re-bind with accessible anions, phytic acid being a significant contender. Phytate not only binds free cations but can also strip them from enzymes (e.g. Ca^2+, Zn²⁺) which reduces their structural resistance to autolysis and ability as co-factors (e.g. Zn²⁺) to increase enzyme activity. Goblet cells initially employ Ca²⁺ as an electronic shield between mucin layers enabling granule formation and cell storage. After mucin granule release, Ca²⁺ is progressively displaced by Na⁺ to free the viscous mucins enabling its translocation. Mucin entangles with the glycocalyx of adjacent enterocytes thereby constructing the unstirred water layer (USWL). Excessive removal of Ca²⁺ from mucin by phytic acid increases its fluidity facilitating its loss from the USWL with its associated Na⁺. This partly explains increased mucin and Na⁺ losses noted with high phytate diets. This review suggests that phytic acid binding of Ca²⁺ and less so Zn²⁺ is the basis for the diversity in nutrient losses encountered and that such losses are in proportion to dietary phytate content.