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Reaching genetic potential with medium chain fatty acids (MCFAs)

Reaching genetic potential with medium chain fatty acids (MCFAs)

Due to a worldwide decrease in usage of antibacterial growth promoters (AGP) and even a ban on AGP use in the EU, gut health in poultry is becoming an issue of utmost importance. With a  ontinuous broiler breeding focus on better growth rate and feed conversion, pressure on gut health becomes immense. Several non-antibiotic, plant-derived antimicrobial substances have been proposed as promising alternatives for AGP use, but lots of them lack scientific proof. The use of free (i.e. not coated, micro-encapsulated or esterified as mono-, di-, or triglycerides) medium-chain fatty acids (MCFA) as a poultry functional feed ingredient (FFI) is an effective way to overcome the stressors faced by the current poultry industry since they exert lots of beneficial effects along the gastro-intestinal tract (GIT) of poultry animals, both on pathogen level as well as on host level. MCFA are saturated fatty acids consisting of aliphatic tails of 6-12 carbon atoms and a polar head.

Balancing the microbiota
MCFA have a hydrophilic-lipophilic balance (HLB) that is quite similar to the HLB of the cell membrane of bacterial pathogens. Therefore, when both come in close contact in the low pH environment of the stomach, un-dissociated MCFA molecules are capable of penetrating the
phospholipid bilayer, thereby destabilising the cell membrane. Destabilisation happens through the formation of pores, resulting in cell content leakage on the one hand and MCFA entrance on the other hand. Inside the bacterial cell, MCFA encounter a near-neutral environment resulting in accumulation of dissociated MCFA molecules and protons in the bacterial cytoplasm.
Intracellular acidification will eventually lead to killing of the bacterium, while dissociated MCFA molecules will intercalate with the bacterial DNA, thereby inhibiting DNA duplication
and thus bacterial growth. Free MCFA therefore provide an early pathogen barrier already in the
stomach of the animal, compared to MCFA esters which are only active in the intestinal tract after their release into free MCFA molecules by gut lipases. Due to structural differences of the cell membrane, a different intracellular pH regulation system and the presence of a nucleus (protecting the DNA) ineukaryotic cells compared to bacterial cells, the former are unresponsive
against the mechanisms of MCFA, so that the use of MCFA as an FFI in poultry (and other animals) can be regarded as safe. In contrast to MCFA, short- (SCFA) and long-(LCFA) chain fatty
acids have a higher, respectively lower HLB compared to that of the bacterial cell membrane and therefore show less affinity for the phospholipid bilayer, making them less active against bacterial pathogens. This is confirmed by multiple, independent in vitro trials where MCFA were shown to have significantly lower minimal inhibitory concentrations compared to SCFA for numerous bacteria, including salmonella. Even at non-bactericidal concentrations, MCFA can have a dramatic
effect on pathogen persistence in poultry. By reducing the virulence of bacterial pathogens, the outcome of disease may be altered and intestinal and systemic colonisation may be reduced. The combination of these antibacterial actions will eventually result in: l Growth inhibition and killing of bacterial pathogens in the stomach. l Reduced virulence of surviving pathogens in the intestine. A largely unaffected beneficial microbial ecosystem (for example, acid-tolerant lactobacilli).

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Zootechnical performance
In comparison with LCFA, MCFA provide the body cells with a quicker and more efficient source of energy. In the gut, this energy is used by the crypts to create new intestinal epithelial cells (IEC), which migrate towards the top of the villi resulting in an increased villus height. Next to directly increasing the number of live IEC, MCFA indirectly reduce pathogen-induced IEC cell death by lowering the infection pressure in the intestinal lumen (due to an antibacterial effect more upstream in the GIT). Less renewal of epithelial villi cells is therefore necessary, meaning a sparing of energy for growth of the animal.

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Decreased infection pressure also results in a lower crypt depth, which together with increased villus height results in a lower migration and decreased loss of enterocytes along the villi, eventually resulting in more fully mature enterocytes. Therefore, the increase in villus/crypt ratio that is accomplished by MCFA (Table 1) favours the digestive and absorptive capacities
of the small intestine...

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