The various nutrients etc. are then presented to the gut membrane where they cross into body by a number of mechanisms. Primary is the transcellular route – this means across the cell, either by active or passive transport – but secondary is the paracellular route. The paracellular route is the permeation of components between the cells of the gut wall and is governed by a complex of actin and myosin (the same biochemicals as a contracting muscle) regulated by a number of factors. This entire complex is known as a Tight Junction and has the capacity to expand and contract, allowing different sized nutrients to pass across the gut barrier into the lymph system. And, critically, many of the regulatory mechanisms are derived from the microbiome. As an example, lactate – derived from glucose fermentation, loosens the tight junction, whilst butyrate tightens it. In an optimal scenario, the small intestine can absorb larger molecules as more lactate is fermented there, although mediated by lactate utilizing bacteria. The hindgut, where fibre fermentation is greatest, generates less lactate and more butyrate, so absorption is limited to smaller molecules (such as the slow release VFA’s themselves). Changing the diet to starch-rich means more starch – glucose – to enter the hindgut which releases more lactate; there being less lactate utilising bacteria, the increased lactate loosens the tight junctions allowing the absorption of larger molecules. As these are generally endotoxins from other fermentation pathways (amines, pathogenic antigens), their absorption can cause problems. Keeping the tight junctions at optimal function is down to a well-balanced microbiome. Also, butyrate is essential in energising the cells of the gut themselves, where acetate and propionate are the major components of slow release energy and energise every cell in the body.
This leads to the final characteristic of the microbiome; it is influenced by the diet, both indirectly and directly.
Indirectly, as various nutrients have a direct impact on the gut barrier. Pectins – the soluble fibre faction, particularly rich in beet products – can be incorporated into the mucus layer, especially the gastric barrier, and stimulate mucus production of the small intestine; other components such as plant bioactives can support antioxidative control of the barrier integrity, and so help maintain its function and permeability.
Directly, dietary profiles will affect the population dynamics of the microbiome and so the quantities and proportions of fermentation end products, both useful (slow release energy), less so (nitrite a vasoconstrictor) or toxic (amines, for example). Feeding beyond a horse’s ability to digest nutrients sufficiently (diets too high in protein, starch etc. will result in microbiome disruption), causes undigested nutrients being fermented in the hindgut, changing the environment and disrupting the normal balance. By feeding within the parameters of what the horse is capable of digesting in the upper gut, the subsequent environment of the hindgut is not compromised. In the case of the horse, this is best achieved by ensuring that protein, oil and sugar/starch are kept at modest levels (oil has a specific role in the absorption of nutrients, but too much can lead to endogenous problems) and that fibre is the main energy source. Certainly, high energy diets can be achieved by choosing the right fibre sources, and the fibre profile is also a tool in maintaining an optimal microbiome.
In animals and plants, the microbiota has evolved alongside the host species. The modern horse has, through selective breeding, changed remarkably over the past few thousand years; however, its gut has not and is still suited to the microbiome of the nomadic species of the Asian steppes. Modern feeding practices need to recognise the central role of the microbiome and match it to the different lifestyles that the horse can achieve.