Mechanisms involved in superdosing phytase

Mechanisms involved in superdosing phytase

The use of superdosing levels of microbial phytase in the diets of poultry or pigs results in improved animal performance via several possible mechanisms.

*Aaron J. Cowieson is with the Poultry Research Foundation at the University of Sydney in Australia. Mike Bedford is with AB Vista in the U.K. Tara York and Craig L. Wyatt are with AB Vista in the U.S.

THE term "superdosing phytase" has recently been defined and exploitation strategies discussed (Feedstuffs, Jan. 28).

However, the mechanisms involved require further understanding in order to maximize the magnitude and consistency of the animal response.

This article provides a brief overview of the most likely mechanisms involved and will identify knowledge gaps.

 

Background

Phytate is a unique dietary component in that, although it is a nutritional impediment, its components are biologically and economically valuable. Thus, the net benefit achieved via the removal of dietary phytate is a function of: (1) the reduction in phytate concentration, (2) the increase in phosphate concentration and (3) the increase in myo-inositol concentration.

This is, of course, simplistic, and the true net effect of the hydrolysis of phytate will depend on many other factors such as diet nutrient density and balance, bird age, feed form and so on. It is very difficult to decide from the observed response in animal trials what proportion of the response is delivered via each of the three contributing elements. However, it is firmly believed that these three components play a significant role in the positive response observed with the use of a phytase and, more specifically, to the performance enhancement observed when superdosing a phytase.

This article will briefly summarize these contributing mechanisms and suggest strategies by which animal performance may be maximized by superdosing phytase.

 

Phytate destruction

If phosphate release and the resulting inositol liberation are conceptually removed as potential contributing mechanisms, then the effect of phytate per se may become apparent.

Unfortunately, this is virtually impossible to achieve experimentally because even where phytate has been added to a diet, this will simultaneously alter both the available phosphorus (aP) and inositol status.

Nonetheless, the effect of dietary phytate concentration on the weight gain of broilers has been approximated previously, and the composite view is that 1% phytate (around 0.28% phytate-phosphorus) will depress broiler weight gain by around 5-7% (Cabahug et al., 1999; Liu et al., 2008a and b; Liu et al., 2009).

This view excludes reports where a phytate-free diet was used as a control, which may not offer a fair representation.

This depression in weight gain due to the anti-nutritive properties of phytate has been well established for both pigs and poultry (Selle et al., 2012). It follows logically that, at high concentrations, the anti-nutritive effects will be more pronounced than at low concentrations, so the negative effect on animal performance will be greater. What's important, in these few reports, the negative effect of phytate on weight gain is not associated with a change in feed intake. Thus, the removal of dietary phytate may be one route to improving the feed conversion ratio (FCR) of poultry and pigs.

For example, Liu et al. (2008a) found that in young Cobb 500 broilers, increasing phytate-phosphorus from 0.22% to 0.44% in diets with equivalent aP concentrations resulted in an increase (P < 0.05) in FCR from 1.49 to 1.57 with no change (P > 0.05) in feed intake.

In the same experiment, the addition of 500 FTU/kg of microbial phytase resulted in an increase (P < 0.05) in feed intake, showing that the removal of phytate per se may not influence intake, but the liberation of phosphorus may.

So, in a standard broiler or pig diet with around 1% phytate, removing this phytate via the use of superdoses of phytase may deliver around a 5% improvement in weight gain with no change in feed intake. These effects are most likely mediated via reduced maintenance requirements through lower endogenous loss of amino acids, minerals and energy (Cowieson et al., 2009).

The increases often see in feed intake when phytases are added to phosphorus-deficient diets is, therefore, unlikely to be related to phytate destruction per se but, rather, can be explained via the corresponding release of phosphate.

 

Phosphate release

The release of phosphorus from phytate by the action of phytase is well accepted, so it will not be discussed exhaustively here. Suffice it to note that phosphorus is a potent mediator of feed intake in most animals, including commercial poultry and swine.

While compensatory increases in feed intake may be observed for moderate deficiency of some nutrients such as amino acids or energy, diets formulated to be deficient in aP result in a substantial reduction in feed intake by the animal, further exacerbating the dietary insufficiency (Selle and Ravindran, 2007).

Thus, the addition of phytase to a diet with insufficient aP often results in increased feed intake and weight gain, with no obvious change in FCR (Selle et al., 2012).

Although phosphate release may not be the principal mechanism by which the superdoses of phytase elicit their benefit (Feedstuffs, Jan. 28), it is possible that the liberation of additional aP improves weight gain by further stimulating feed intake.

Trials have shown a relatively consistent response to the use of high doses of phytase in phosphorus-deficient diets, resulting in performance and bone ash improvements beyond the respective phosphorus-adequate positive control diets (Selle and Ravindran, 2007).

Furthermore, it is theoretically possible that phosphorus requirements are increased by super-dosing phytase in that animal growth is accelerated, and released inositol must be systemically re-phosphorylated for various secondary metabolic purposes.

 

Inositol liberation

The dose response curve for phytase (Feedstuffs, Jan. 28) shows only the release of aP from phytate and does not consider the accumulation of lower esters of inositol phosphate (IP) or the eventual release of free myo-inositol.

Few phytases de-phosphorylate phytate in a "linear" manner, i.e., systematically reducing each intact phytate (IP6) molecule to inositol and six free phosphates before moving on to the next IP6. Rather, most phytases reduce IP6 to IP4 until a critically low concentration of IP6 is reached and then degrade IP4 to IP3, IP2, IP1 and, eventually, free phosphate and myo-inositol (Wyss et al., 1999).

It is possible that the beneficial effects of super-dosing phytase are only observed when this secondary kinetic sequence is initiated by a low threshold of IP6 and IP5, which causes phytase to reprioritize to the lower esters, generating inositol in cooperation with the mucosal and/or systemic phosphatases.

This series of events is depicted in the Figure, which is based on kinetic data for degradation of sodium phytate by an Escherichia coli-derived phytase (Wyss et al., 1999). The reactive phases of phytate destruction occur in the following sequence: Phase 1 is the rapid destruction of IP6 and IP5 by phytase, yielding a moderate amount of aP as well as the majority of the "extra-phosphoric" effects such as calcium, sodium and certain amino acids. Phase 2 yields little or no calcium, sodium or amino acids but a modest amount of aP, predominantly from degradation of IP4 and IP3. Phases 3 and 4 are where inositol would begin to be generated through the concerted effort of exogenous phytase and the mucosal and/or systemic phosphatases.

Given sufficient time or a high dosage rate, most phytases will move through all four phases. However, in vivo time is limiting, and the environmental conditions in the gastrointestinal tract are not optimal for phytate solubility or phytase activity. Thus, in the animal's gastrointestinal tract, the only way to cycle phytate through all four phases is to superdose with phytase.

It is possible that 500 or even 1,000 FTU/kg of feed may only allow progression through phases 1 and 2, knocking out IP6 and IP5 (to release amino acids, calcium, phosphorus and sodium) and forming IP4. More than 1,500 FTU/kg may be required to progress the reaction to a more complete point, where inositol can be generated.

There will also be a difference among phytase sources in their ability to work effectively at these low substrate concentrations, and thus, even higher activity levels would be required for some phytases compared to others. This explains why, even though 1,500 FTU/kg will only yield a modest 0.02% aP beyond 1,000 FTU/kg, the benefits in animal performance may be substantial if 1,500 FTU/kg is required to degrade IP6 and IP5 completely and quickly enough to refocus the attention of phytase on the lower esters with sufficient urgency to generate free inositol.

Indeed, substantial growth-promoting effects of supplemental myo-inositol in broilers have been previously reported (Zyla et al., 2004) at inclusion concentrations similar to those that may be generated by complete degradation of dietary phytate. Cowieson et al. (2013) recently observed that the addition of 0.15% myo-inositol to a corn/wheat-based broiler diet resulted in an improvement in FCR of around five points, achieved through maintenance of bodyweight with reduced feed intake.

Mechanisms involved in superdosing phytase

Conclusions

The use of superdosing levels of microbial phytase in the diets of poultry or pigs results in increased feed intake (and commensurate weight gain) probably via an aP mechanism, whereas FCR may be improved via inositol liberation and phytate destruction (Table).

Within the U.S., the use of higher levels of an enhanced fourth-generation phytase is widespread, and performance enhancements are being observed in the field. Although the mechanisms are still not entirely clear, it is believed that these three components work together and contribute to the overall positive effects reported both in the literature and at the end user level.

 

Summary of the possible effects of phosphate release, inositol release and phytate destruction as contributors in response to superdosing phytase on the performance of broilers

 

Feed intake

Weight gain

FCR

Phytate removal

No effect

3-7% improvement

3-7% improvement

Phosphate release*

5-10% increase

5-10% increase

Limited effect

Inositol release**

Minor increase

3-4% increase

2-3% improvement

*Phosphorus-deficient diets.

**Effect of inositol on performance may be age related (weak in the neonate chick).

 

References

Cabahug, S., V. Ravindran, P.H. Selle and W.L. Bryden. 1999. Response of broiler chickens to microbial phytase supplementation as influenced by dietary phytic acid and non-phytate phosphorus contents. 1. Effects on bird performance and toe ash. Br. Poult. Sci. 40:660-669.

Cowieson, A.J., M.R. Bedford, P.H. Selle and V. Ravindran. 2009. Phytate and microbial phytase: Implications for endogenous nitrogen losses and nutrient availability. Worlds Poult. Sci. J. 65:401-418.

Cowieson, A.J., A. Ptak, P. Mackowiak, M. Sassek, E. Pruszynska-Oszmalek, K. Zyla, S. Swiatkiewicz and D. Jozefiak. 2013. The effect of phytase and myo-inositol on performance and blood biochemistry of broiler chickens fed wheat/corn-based diets. Poult. Sci. (under review).

Cowieson, A.J., P. Wilcock and M.R. Bedford. 2011. Super-dosing effects of phytase in poultry and other monogastrics. Worlds Poult. Sci. J. 67:225-236.

Liu, N., Y.J. Ru, A.J. Cowieson, F.D. Li and X.C. Cheng. 2008a. Effects of phytate and phytase on the performance and immune function of broilers fed nutritionally marginal diets. Poult. Sci. 87:1105-1111.

Liu, N., Y.J. Ru, F.D. Li and A.J. Cowieson. 2008b. Effect of diet containing phytate and phytase on the activity and messenger ribonucleic acid expression of carbohydrase and transporter in chickens. J. Anim. Sci. 86:3432-3439.

Liu, N., Y.J. Ru, F.D. Li, J.P. Wang and X.Q. Lei. 2009. Effect of phytate and phytase on proteolytic digestion and growth regulation in broilers. Arch. Anim. Nutr. 63:292-303.

Selle, P.H., and V. Ravindran. 2007. Microbial phytase in poultry nutrition. Anim. Feed Sci. Tech. 135:1-41.

Selle, P.H., A.J. Cowieson, N.P. Cowieson and V. Ravindran. 2012. Protein-phytate interactions in pig and poultry nutrition: A reappraisal. Nutr. Res. Rev. 25:1-17.

Wyss, M., R. Brugger, A. Kronenberger, R. Remy, R. Fimbel, G. Oesterhelt, M. Lehmann and A.P.G.M. Van Loon. 1999. Biochemical characterization of fungal phytases (myo-inositol hexakisphosphate phosphohydrolases): Catalytic properties. Appl. Env. Microbiol. 65:367-373.

Zyla, K., M. Mika, B. Stodolak, A. Wikiera, J. Koreleski and S. Swiatkiewicz. 2004. Towards complete dephosphorylation and total conversion of phytate in poultry feeds. Poult. Sci. 83:1175-1186. 

Volume:85 Issue:26

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