The benefits of improved chicken performance and litter quality coming from adding xylanase to poultry diets containing viscous grains, such as a wheat and rye, is widely known.
Adding xylanase to non-viscous poultry diets does not always, however, lead to consistent improvements, and its use in corn-based diets remains low.
Research clarifying the mechanisms by which xylanases improve nutrient digestibility in non-viscous diets suggests that this variability may be due to either poor targeting of the xylanase, or possible under- or over-dosing, and this has implications for its use in viscous diets.
While the majority of the improved performance due to optimized xylanase use in wheat-based diets may be due to a reduction in digesta viscosity, in some low viscosity wheat-based diets – depending on factors such as variety, growing season and extent of feed processing – viscosity may be much less important. The remaining response comes from improved nutrient digestibility, which is achieved via the same mechanisms responsible for improved performance in corn-based diets.
Achieving a consistent and reliable response to xylanase use across all diets requires a far greater focus on the actual dose and type of active xylanase reaching the site of action - the stomach and small intestine - than previously thought.
The key to successful xylanase application to poultry diets is to understand how differing xylanase characteristics and dose affect those mechanisms now believed to be responsible for these performance improvements.
It had been thought that, in addition to breaking down the long-chain soluble arabinoxylans (often called xylans), which are responsible for increased digesta viscosity, xylanases acted directly to degrade feed ingredient plant cell walls, so improving access to the starch and protein stored within. However, two recent findings have suggested that there may be additional mechanisms.
The first study evaluated the effect of xylanase addition on amino acid digestibility. It found that the amount of amino acid remaining undigested was consistently reduced by around 15 percent for all amino acids, not just those found within the cereal grains.
Separate microscopic examination of the degradation seen in plant cell walls with xylanase addition found that the effect was present as early as the jejunum, so possibly too early in the digestive tract for the effect to be entirely the result of direct xylanase action.
Together, these results suggest that xylanases are indirectly improving the digestibility of the whole diet, not only of the xylan-rich cereals, and that much of the improvement happens early within the gastrointestinal tract.
More recent research has begun to uncover the most likely mechanism by which this is being achieved, and offers insight into how xylanase use can be optimized.
We now know that addition of a well-targeted xylanase increases secretion of a number of entero-hormones, responsible for controlling the digestive process, and of the hormone peptide YY (PYY) in particular (see Figure 1). A rise in PYY levels acts to delay stomach emptying, with PYY secretion linked to the fermentation of undigested feed material, primarily in the cecum.
What appears to be happening is that certain specific prebiotic end-products of xylan breakdown by the xylanase (arabinoxylo-oligosaccharides, AXOS) are being fermented in such a way as to promote PYY synthesis. Where the right AXOS are produced, the rise in PYY levels results in feed being retained in the gizzard and stomach for longer, leading to a finer ‘grind’, potentially greater gizzard development and increased protein digestion within the stomach. Since much of the starch in corn-based diets is encapsulated in protein, starch digestibility and ileal digestible energy are also increased.
Correct PYY signaling therefore appears to be key in determining xylanase response, particularly where digesta viscosity is less important, such as in corn-based diets. The prebiotic AXOS may also provide some additional benefits.
Those gut microflora adapted to ferment the prebiotic AXOS tend to be beneficial, and proliferate at the expense of potentially pathogenic populations. The resulting mix of volatile fatty acids (VFA) produced by the fermentation – which act to signal PYY secretion – is also dominated by propionate, which may help suppress potential outbreaks of salmonella, for example.
In addition, improved digestion in the upper gastrointestinal tract reduces the supply of undigested starch and protein in the ileum, which can promote colonization by undesirable bacteria that compete for nutrients. The overall result may be a shift in both fermentation type, and location, to a more positive cecal fermentation producing VFAs that are also a potential source of additional energy for the bird.
However, producing the right prebiotic AXOS is critical, and this relies not only on using the correct xylanase, but also on accurate dosing.
Different xylanases vary in their ability to produce AXOS, with some acting to cleave the xylose backbone that constitutes the xylan molecule mid-chain (endo-acting), whilst others release simple xylose or arabinose sugars from the ends (exo-acting). There are even differences amongst endo-acting xylanases (see Figure 2), depending on the ability to cleave the xylose backbone adjacent to an arabinose side-chain, or break it down beyond a certain size.
Achieving the correct AXOS profile depends on a precise, controlled and targeted pattern of xylan hydrolysis that can only be achieved through application of the optimum dose of a correctly targeted xylanase (see Figure 3). Overdosing with xylanase will likely over-process the beneficial AXOS to smaller, less effective AXOS, whereas under-dosing will fail to deliver sufficient activity to produce the desired effect.
Just as critically, the use of additional enzyme activities alongside the xylanase, such as xylosidase or arabinosidase, risks breaking down the AXOS that trigger the PYY response. Further, high levels of free xylose from excess xylan degradation or the action of exo-acting xylanases can actually be detrimental to performance.
Ultimately, bird performance and consistency of response remain the benchmarks by which xylanase efficacy should be measured, and it would appear that the right dose of the right xylanase to trigger PYY signaling is critical. As such, it is highly likely that end-users have, to date, been using some products sub-optimally, and subsequently failing to maximize returns.
This new understanding of the mechanisms involved will not only improve the effectiveness of xylanase application, but it also puts renewed emphasis on the need for accurate, easy-to-use assays that can confirm in-feed enzyme activity levels post-feed processing.
Together with improved information about xylanase type and action from product suppliers, the net effect will be a significant improvement in xylanase efficacy across all poultry diets.