The research team compared two groups of late-laying ducks: those still producing eggs, designated the egg-laying phase, and those that had stopped, designated the ceased-laying phase. Because birds route virtually all yolk lipid synthesis through the liver, the organ is exquisitely sensitive to shifts in reproductive status. In mammals, the adipose tissue and liver share the burden of lipid handling, but in laying birds the liver takes on an extraordinary load, synthesizing and exporting vast quantities of very low density lipoprotein and vitellogenin to supply the developing ovarian follicles. When the ovary regresses and that demand evaporates, the question becomes what happens to the liver’s lipid-processing machinery, and whether it recalibrates gracefully or slips into dysfunction.

The first answer came from simple anatomy and biochemistry. The liver index, a measure of liver weight relative to body weight, was significantly higher in the ceased-laying ducks than in their still-laying counterparts. Histopathological examination of liver tissue revealed greater infiltration of inflammatory cells and a marked accumulation of lipid droplets in the ceased layers. These structural changes were accompanied by shifts in serum chemistry: levels of aspartate aminotransferase, an enzyme that leaks into the bloodstream when liver cells are damaged, were elevated in the ceased-laying birds, as were total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Together, these findings paint a picture of a liver under strain, storing fat it can no longer efficiently export and showing biochemical signatures consistent with hepatic injury.

To understand the molecular underpinnings of these changes, the researchers turned to transcriptomics, the systematic measurement of gene activity across the liver. The analysis identified a substantial set of differentially expressed genes between the two groups, and when those genes were mapped onto known biological pathways, several functional themes emerged. The affected pathways included the adipocytokine signaling pathway, which links fat tissue-derived hormones to hepatic metabolism; the PPAR signaling pathway, a master regulator of fatty acid oxidation and lipid transport; the insulin signaling pathway, which governs nutrient storage and glucose-lipid partitioning; and steroid hormone biosynthesis, the biochemical route by which cholesterol is converted into reproductive hormones.

The involvement of these particular pathways makes biological sense in the context of ovarian regression. The PPAR family of nuclear receptors sits at the crossroads of lipid uptake, synthesis, and breakdown, and its dysregulation is a hallmark of hepatic steatosis in many species. Adipocytokines such as adiponectin and leptin modulate insulin sensitivity and fatty acid metabolism in the liver, and their signaling networks are known to shift when energy balance changes. The appearance of steroid hormone biosynthesis among the enriched pathways underscores the intimate two-way conversation between the liver and the ovary: the liver supplies the cholesterol substrate for hormone synthesis, and the ovary’s hormonal output feeds back on hepatic gene expression. When the ovary regresses, that feedback loop is severed, and the liver’s transcriptional program appears to drift accordingly.

Gene expression, however, tells only half the story. To capture the actual chemical end points of the altered metabolic program, the team performed lipidomic profiling, cataloguing the lipid species present in the livers of both groups. The differential lipids fell into four major categories: glycerophospholipids, the phosphorus-containing molecules that form cellular membranes; glycerolipids, which include triglycerides and other storage fats; sphingolipids, a class of structural and signaling lipids; and fatty acyls, the free fatty acids and their derivatives. The redistribution of lipid species across these classes indicates that ceasing egg production does not simply cause a uniform buildup of fat, but rather a wholesale reorganization of the liver’s lipid inventory, affecting membrane composition and signaling molecules as well as storage triglycerides.

The most ambitious part of the study was the integration of the two data layers. By combining the transcriptomic and lipidomic datasets, the researchers identified coordinated changes linking specific gene-expression shifts to specific lipid alterations. Four metabolic axes stood out: the adipocytokine signaling pathway, arachidonic acid metabolism, glycerophospholipid metabolism, and glycerolipid metabolism. Arachidonic acid is an omega-6 polyunsaturated fatty acid that serves as the precursor for eicosanoids, potent inflammatory mediators, so its altered metabolism dovetails with the histological observation of inflammatory cell infiltration in the ceased-laying livers. The concurrent disruption of glycerophospholipid and glycerolipid metabolism suggests that both the membrane lipid pool and the storage lipid pool are remodeled simultaneously, consistent with the visible accumulation of lipid droplets in the tissue.

What emerges from the integrated analysis is a coherent mechanistic narrative. As the ovary regresses, the hepatic demand for yolk precursor synthesis collapses, but the liver’s lipid import and synthesis machinery does not shut down in lockstep. Genes governing fatty acid handling, insulin responsiveness, and inflammatory signaling shift their activity, and the lipidome follows, with triglycerides and other lipids accumulating in droplets while phospholipid and fatty acid profiles diverge from the laying state. The elevated serum cholesterol fractions and liver enzymes in the ceased-laying ducks suggest that this hepatic disarray has systemic consequences, extending beyond the organ itself into circulating lipid transport and markers of cell damage.

The practical implications reach into poultry science and agriculture. Ducks are an economically important egg-laying species, and the late-laying period, when production declines and birds approach the end of their productive cycle, represents a management challenge. If hepatic metabolic disorder accompanies ovarian regression, it may affect bird health, welfare, and the economics of extended laying cycles. The differentially expressed genes and lipid metabolites identified in this study provide a molecular toolkit that breeders and nutritionists could potentially use to monitor hepatic status in aging flocks, or to design dietary interventions that ease the liver’s transition out of its egg-production mode. The study was supported by the National Natural Science Foundation of China, the China Agriculture Research System, and the Yangzhou Municipal Science and Technology Plan Project.

Beyond its agricultural relevance, the work speaks to a broader biological question: how the liver adapts, or fails to adapt, when a tissue’s primary metabolic export demand disappears. In laying birds, the liver-ovary axis is an extreme example of a reproductive-metabolic coupling that also exists, in modified form, in mammals during pregnancy and lactation. Understanding how the avian liver copes with the withdrawal of that demand, and which genes and lipids mark the transition, may illuminate general principles of hepatic plasticity and vulnerability. The authors caution that their findings identify correlations between the altered gene and lipid profiles and the modified hepatic lipid status concurrent with ovarian regression; establishing causation and testing interventions will be the work of future studies. For now, the study stands as a detailed molecular snapshot of a metabolic crossroads, capturing the moment when a duck’s liver, built for the extraordinary demands of egg production, confronts their sudden end.

Subject of Research: Hepatic lipid metabolism changes associated with ovarian regression in late-laying ducks

Article Title: Transcriptomic and lipidomic analysis reveal hepatic metabolic disorders associated with ovarian regression in late-laying ducks

Article References: Zhou, N., Weng, K., Liu, J., Lu, L., Xu, W., Zeng, T., Chen, L., Tian, Y., Zhang, Y., & Gu, T. (2026). Transcriptomic and lipidomic analysis reveal hepatic metabolic disorders associated with ovarian regression in late-laying ducks. BMC Genomics. https://doi.org/10.1186/s12864-026-13441-z

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13441-z

Keywords: ducks, liver, ovarian regression, lipid metabolism, transcriptomics, lipidomics, PPAR signaling, adipocytokine signaling, glycerophospholipids, arachidonic acid, poultry science, hepatic steatosis

The research team, led by Hande Işıl Akbağ, worked with 114 one-day-old squabs drawn from three pigeon breeds: the Homing pigeon, prized for its long-distance flying ability, and two native Turkish breeds, the Takla and the Dolapçı, both famous for their acrobatic tumbling and spinning flight. For the first three days after hatching, all squabs were fed crop milk by their parents, ensuring that every chick received the same natural start. The birds were then randomly assigned to one of three feeding groups. A control group remained with their parents and continued to be fed naturally until 28 days of age. A second group was hand-fed a commercial artificial crop milk, diluted with water at a one-to-one ratio as the manufacturer recommends. The third group received the same artificial crop milk, but supplemented with kefir at 2 percent of daily feed intake, a level chosen so that the kefir’s own nutritional contribution would be negligible and its probiotic and bioactive effects could be assessed independently.

The logic behind the kefir trial was compelling. Kefir is a fermented milk beverage produced by kefir grains, complex symbiotic communities of lactobacilli, streptococci, and yeasts. During fermentation, these microbes generate not only lactic acid but also bioactive compounds such as kefiran, a heteropolysaccharide with documented antioxidant and antimicrobial properties. Previous work in broiler chickens had shown that kefir supplementation can improve growth performance, feed intake, and feed conversion. More importantly, natural pigeon crop milk itself harbors a rich microbiota, including Lactobacillus, Enterococcus, and Bifidobacterium species, which are thought to seed the squab’s developing gut and immune system. The researchers hypothesized that kefir, with its similar combination of beneficial microbes and bioactive molecules, might partially mimic what artificial crop milk lacks and bring hand-reared squabs closer to the performance of parent-fed birds.

Before any performance data could be interpreted, the team needed to understand what the squabs were missing. They collected crop milk samples from the parents three days after hatching and analyzed the chemical and microbiological composition. The results showed that breed made no difference to the macronutrient profile of the milk: crude protein, ether extract, ash, and water-soluble carbohydrates were statistically indistinguishable across the Takla, Dolapçı, and Homing lines. On a dry matter basis, the crop milk contained roughly 42.75 percent crude protein and an ether extract level consistent with earlier reports. The microbiological picture was more nuanced. Total aerobic bacteria and yeast counts were similar across breeds, but lactic acid bacteria levels differed significantly, with Homing pigeons producing milk with the highest counts at 3.96 log10 colony-forming units per gram, compared with 3.50 for Dolapçı and 3.24 for Takla birds. This variation in lactic acid bacteria, the authors suggest, may translate into differences in lactic acid production and possibly in the microbial environment that each breed’s chicks experience.

The growth results were unambiguous and, for anyone hoping for a kefir miracle, disappointing. By the end of the 28-day trial, parent-fed control squabs reached an overall body weight of 236.05 grams, dramatically outperforming both hand-fed groups. Squabs receiving kefir-supplemented artificial crop milk averaged 152.18 grams, while those on plain artificial crop milk reached only 146.02 grams. Feed conversion ratios told the same story: the control group converted feed into body mass with an overall efficiency of 2.61, whereas the kefir and artificial milk groups required 8.37 and 8.92 grams of feed per gram of gain, respectively. The gap was especially stark in the first ten days, when control squabs achieved a feed conversion ratio of 0.95 against 2.95 for the kefir group and 3.14 for the artificial milk group. Breed mattered as well, with Homing pigeons achieving the highest overall body weights, followed by Dolapçı and Takla birds, but no breed escaped the penalty of artificial rearing.

There was, however, one glimmer of breed-specific promise. Among Homing pigeons, squabs fed the kefir-supplemented diet showed higher feed intake and greater body weight than those fed plain artificial crop milk, suggesting that the response to kefir may depend on the genetic background of the bird. In the Takla and Dolapçı breeds, by contrast, the two hand-fed groups performed similarly. The authors caution against overinterpreting this pattern, but it hints that future attempts to optimize artificial rearing might need to account for breed-specific physiology rather than applying a one-size-fits-all formula. Notably, the artificial milk actually delivered more crude protein per feeding than natural crop milk when diluted as recommended, yet the hand-fed birds still grew poorly, underscoring that protein quantity alone cannot explain the superiority of parental feeding.

Mortality data added another layer of concern. No deaths occurred in the parent-fed control group, but 23.8 percent of squabs in the artificial milk group and 19.5 percent in the kefir group died between days 3 and 28. Although the statistical difference between the two hand-fed groups was not significant, and the kefir group fared marginally better, the overall mortality in both hand-reared groups was high compared with figures of around 2 to 4 percent reported in some earlier studies using different artificial feeding protocols. The authors note that the timing of separation from parents matters greatly: previous research found mortality rates of 26.7 percent when squabs were separated at hatching, but only about 3 percent when separation occurred at 7 days of age. Because parents produce pure crop milk only until roughly the third day after hatching, after which its composition gradually shifts, the three-day separation point used in this study may represent a particularly vulnerable window.

The serum biochemistry results provided a window into the metabolic state of the birds. At 28 days of age, blood samples revealed that total protein and albumin were the only serum parameters significantly affected by feeding treatment, with the control group showing the highest concentrations of both. Elevated total protein and albumin are generally interpreted as markers of greater anabolic activity, consistent with the superior weight gain observed in parent-fed birds. Breed, meanwhile, influenced nearly every measured parameter except aspartate aminotransferase. Homing pigeons had the lowest serum glucose, which the authors link to their long-distance flight capacity and larger body size, while the smaller Takla and Dolapçı breeds showed higher glucose levels, in line with the general avian pattern that smaller species maintain higher blood sugar. Cholesterol concentrations were higher in the larger Dolapçı and Homing breeds, plausibly reflecting their greater energy requirements.

What does this all mean for the future of intensive pigeon production? The study’s conclusion is clear: kefir, at least at the 2 percent inclusion level tested, did not rescue the growth performance or survival of hand-reared squabs. The problem appears to lie deeper than the absence of probiotics. Natural crop milk contains a complex array of bioactive proteins, growth factors, and immunomodulatory compounds that industrial formulations have yet to replicate, and the frequency and manner of parental feeding may also play a role that hand-feeding protocols cannot easily mimic. The authors also flag a methodological caveat: feed intake in the control group was estimated by weighing squabs before and after feeding, and because parent birds may feed their chicks more frequently than the twice-daily schedule imposed on the hand-fed groups, actual intake in the control group may have been underestimated. Even accounting for this, the magnitude of the growth gap is difficult to dismiss.

The research opens several avenues for follow-up. The authors suggest that compensatory growth processes in squabs after weaning from artificial diets, and the effects of artificial crop milk formulations with different nutrient compositions on later growth and reproductive traits, remain largely unexplored. The breed-dependent response to kefir, particularly the improved performance of Homing squabs, deserves targeted investigation with larger sample sizes and possibly higher inclusion rates. For now, the message for pigeon breeders is that there is still no substitute for the real thing. The crop milk produced by parent pigeons, a substance so distinctive that scientists have compared its function to mammalian lactation, remains an irreplaceable foundation for healthy squab development, and closing the artificial rearing gap will require far more than a splash of fermented milk.

Subject of Research: Effects of kefir supplementation on growth performance and serum biochemistry of artificially reared pigeon squabs

Article Title: Can kefir supplementation influence the growth performance and serum biochemistry of artificially reared squabs of three pigeon breeds?

Article References: Akbağ, H. I., Şensoy, A., Erdem, H., Yiğit, S., Tölü, C., & Savaş, T. (2026). Can kefir supplementation influence the growth performance and serum biochemistry of artificially reared squabs of three pigeon breeds?. Archives Animal Breeding, 69(3), 529-539. https://doi.org/10.5194/aab-69-529-2026

Image Credits: AI Generated

DOI: 10.5194/aab-69-529-2026

Keywords: pigeon, squab, crop milk, kefir, probiotics, artificial rearing, growth performance, serum biochemistry, animal nutrition, poultry science, microbiota, feed conversion ratio

The experiment began with fifty one-day-old yellow-feather broilers, housed in standard cages under a controlled 16-hour light and 8-hour dark cycle and fed a commercial diet. At 28 days of age, the birds were sorted into body-weight-matched pairs and randomly assigned to two groups. One group received daily subcutaneous injections of corticosterone—the principal stress hormone in birds—at a dose of 4 milligrams per kilogram of body weight for seven consecutive days. The control group received injections of a 15% ethanol solution at the same volume. This corticosterone regimen is a well-established way to simulate chronic stress in poultry, allowing researchers to isolate the hormonal component of stress without confounding factors such as heat, crowding, or transport.

The physiological consequences were swift and clear. After 35 days, corticosterone-treated broilers had significantly lower final body weights and reduced average daily gain compared with controls. Paradoxically, they ate more: average daily feed intake rose significantly, and the feed-to-weight ratio worsened, meaning the stressed birds converted feed into body mass far less efficiently. The authors suggest this pattern reflects a metabolic shift under chronic stress, with energy diverted toward fat deposition through increased proteolysis and gluconeogenesis—essentially, the birds were burning muscle to fuel a stress response while consuming more feed overall.

Behavioral testing, conducted on days 35 and 36 using video-recorded encounters between unfamiliar birds from the same treatment group, revealed a striking escalation in aggression. Corticosterone-exposed chickens pecked their opponents significantly more often, and the total number of aggressive acts rose sharply. The effect spanned the social hierarchy: both dominant birds—identified by how frequently their opponents avoided them—and subdominant birds showed elevated aggression, though dominant individuals displayed the strongest increases, including more twisting attacks. This aligns with earlier observations that dominant animals may have aggression reinforced through mesolimbic reward circuitry, and with prior reports that prenatal corticosterone exposure and social stress both heighten injurious pecking in hens.

Crucially, the team also measured serotonin, the neurotransmitter long associated with behavioral inhibition. Chronic corticosterone significantly reduced serotonin concentrations in the hypothalamus—a key brain region for stress regulation—while paradoxically increasing serotonin levels in the plasma. Dopamine levels in the plasma, hippocampus, and hypothalamus remained unchanged. Because more than 90% of the body’s serotonin is produced by enterochromaffin cells in the gut, and because peripheral serotonin cannot cross the blood-brain barrier, this split pattern points to a gut-centered mechanism: stress may boost peripheral serotonin synthesis while starving the brain of the tryptophan precursor it needs to maintain central serotonergic tone. Low central serotonin activity is consistently associated with heightened aggression and impulsivity across species, from fish and rodents to humans.

Sequencing of the cecal microbiota added a microbial dimension to the story. Overall diversity metrics told a subtle tale: seven alpha-diversity indices showed no significant differences between stressed and control birds, and principal coordinate analysis based on Bray-Curtis distances found their community structures broadly similar. Firmicutes and Actinobacteria dominated both groups, with Faecalibacterium, Bifidobacterium, and Lactobacillus as the most abundant genera. But linear discriminant analysis effect size screening identified 29 differentially abundant taxa. Stressed birds carried more Shigella, Holdemania, and Clostridium, and fewer Desulfovibrio, Cellulosimicrobium, Enterococcus, Coriobacteriaceae, and Bacteroidales.S24_7. The message is that chronic stress reshapes the gut ecosystem in targeted ways rather than broadly collapsing it.

The metabolomics analysis, performed on plasma using ultra-high-performance liquid chromatography coupled to an Orbitrap mass spectrometer, identified 281 metabolites, of which 53 differed significantly between groups—23 upregulated and 30 downregulated under stress. Pathway enrichment pointed to tryptophan metabolism, pantothenate and CoA biosynthesis, and beta-alanine metabolism as the most affected networks. Tryptophan and its derivatives were upregulated in the plasma of stressed birds, even as hypothalamic serotonin fell. The researchers propose that immune activation under chronic stress may divert tryptophan away from serotonin production and into the kynurenine pathway, whose rate-limiting enzymes, IDO and TDO, are highly responsive to inflammatory cytokines. Kynurenine pathway metabolites such as quinolinic acid are themselves neuroactive and have been implicated in behavioral disorders.

Spearman correlation analyses then wove the threads together. Aggressive behavior correlated positively with the genus Clostridium and negatively with Actinomycetales and Coriobacteriaceae—relationships the authors note had not been described before. Clostridium, in turn, correlated positively with indole, L-tryptophan, and butyryl-L-carnitine, while Actinomycetales and Coriobacteriaceae tracked with beneficial compounds such as niacinamide and salicylic acid. Of 31 metabolites linked to the three key microbial taxa, 18 were also associated with aggression, including indole, L-tryptophan, biochanin A, niacinamide, leucodopachrome, and pyroglutamic acid. The mechanism may run through the vagus nerve: Clostridium species are known to metabolize tryptophan into neuroactive indoles and tryptamines that stimulate vagal afferents, and microbial metabolites such as kynurenine and indole derivatives are ligands for the aryl hydrocarbon receptor, a regulator of intestinal immune tone that can further bias tryptophan toward the kynurenine route.

The findings carry immediate practical weight for an industry where aggression translates directly into economic loss—non-beak-trimmed hens, for instance, show roughly a tenfold increase in mortality from aggressive pecking. The authors outline nutrition-based interventions supported by prior work: ensuring adequate dietary tryptophan, with commercial target tryptophan-to-lysine ratios around 16 to 19 percent, can support serotonergic tone and reduce abnormal pecking; probiotics such as Lactobacillus rhamnosus and Bacillus subtilis have been shown to mitigate stress-linked injurious behavior; and sodium butyrate, a microbial postbiotic, counters corticosterone-induced oxidative stress. The team is careful to stress that correlation is not causation, and that the observed taxa-metabolite-behavior links should be validated under different housing systems, stocking densities, lighting programs, and diets. Future experiments using fecal microbiota transplantation from donors with divergent stress phenotypes, gnotobiotic colonization, and targeted tryptophan manipulation could establish whether these gut communities truly transfer aggressive tendencies—a question made more plausible by mammalian studies in which microbiota transfer has conveyed anxiety- and depression-like behaviors between animals.

Subject of Research: Gut microbiota and plasma metabolite mechanisms underlying stress-induced aggressive behavior in broiler chickens

Article Title: Integrative analysis of gut microbiota and plasma metabolites reveals mechanisms underlying aggressive behavior in chronically stressed broiler chickens

Article References: Wu, X., Zhang, J., Ren, H., Cheng, X., Gao, J., & Ma, W. (2026). Integrative analysis of gut microbiota and plasma metabolites reveals mechanisms underlying aggressive behavior in chronically stressed broiler chickens. Stress Biology, 6(1), Article 30. https://doi.org/10.1007/s44154-026-00297-2

Image Credits: AI Generated

DOI: 10.1007/s44154-026-00297-2

Keywords: gut microbiota, broiler chickens, chronic stress, aggressive behavior, tryptophan metabolism, serotonin, corticosterone, metabolomics, microbiota-gut-brain axis, Clostridium, animal welfare, poultry science

The research arrives at a critical moment for global poultry farming. Antibiotics were once routinely added to feed as growth promoters, enhancing gut health and nutrient utilization across commercial flocks. But mounting evidence that this practice fuels antimicrobial resistance, and specifically the risk of horizontal gene transfer from livestock bacteria to the human microbiome, has triggered sweeping regulatory crackdowns. The European Union led the way with its 2006 ban on antibiotic growth promoters under Regulation (EC) No. 1831/2006, and producers worldwide have been scrambling to find effective substitutes ever since.

Probiotics have emerged as the leading candidate among these alternatives. These live, non-pathogenic microorganisms confer measurable health benefits to the host by improving mucosal integrity, modulating the intestinal microflora, enhancing nutrient uptake, and strengthening immune responses. Previous work has shown that probiotic supplementation can improve the architecture of intestinal villi, the finger-like projections that dramatically increase the absorptive surface of the gut, translating directly into better feed efficiency. Yet results with single-strain products, particularly the widely used B. subtilis and S. cerevisiae, have been notoriously inconsistent, likely because outcomes depend heavily on dosage, strain specificity, administration route, and rearing conditions.

The Saudi research team reasoned that a multi-strain formulation might overcome this variability through synergistic interactions between different microbial species. Their product contains B. subtilis and both Lactobacillus harbinensis and Lactobacillus parabunchneri at one billion colony-forming units per milliliter each, S. cerevisiae and Candida ethanolic at one hundred thousand CFU per milliliter, and two photosynthetic Rhodopseudomonas species at ten million CFU per milliliter. The diversity spans bacteria, yeasts, and even phototrophic organisms, an unusually broad consortium that the authors hypothesized could reshape gut ecology, antioxidant status, and nutrient utilization simultaneously.

To test this hypothesis rigorously, the researchers ran a controlled feeding trial with 288 one-day-old male Ross 308 broiler chicks, individually weighed and randomly assigned to six treatment groups, each with eight replicate cages of six birds. From days 1 to 14, treatments were delivered through drinking water; from days 15 to 28, they were mixed into feed. The groups comprised an unsupplemented negative control, three RNFS doses at 0.1%, 0.2%, and 0.4%, a single-strain B. subtilis product (CloSTAT), and a yeast product (SafMannan). All birds were housed under climate-controlled conditions, vaccinated against major poultry pathogens, and fed diets formulated to Aviagen’s Ross 308 specifications.

The results pointed clearly toward a mid-range dose. Birds receiving 0.2% RNFS reached an average body weight of 1557.5 grams at day 28, significantly heavier than the control (1449.7 g), the B. subtilis group (1444.7 g), and the S. cerevisiae group (1513.0 g), with a reported p-value of 0.04. During the grower phase from days 14 to 28, this dose lifted daily weight gain to 80.7 grams per bird, outpacing the control by 11.77%, the B. subtilis group by 9.80%, and the S. cerevisiae group by 4.67%. Notably, these gains came without significant changes in feed intake or feed conversion ratio, suggesting the probiotic improved how efficiently nutrients were utilized rather than simply stimulating appetite.

Chemical analysis of the formulation hints at why it might work. Gas chromatography–mass spectrometry identified 45 volatile and semi-volatile compounds in RNFS, including phenol (9.17% of the extract) and 2,4-di-tert-butylphenol (6.86%), both recognized for antioxidant and antimicrobial properties. Fatty acid esters such as methyl stearate and methyl linoleate, along with organic acids like lactic acid, rounded out a phytochemically diverse profile. The authors propose that these bioactive compounds act synergistically with the live microbes, reinforcing gut integrity, modulating microbial balance, and supporting metabolic efficiency. Concentrations of phenolic and naphthalene-derived compounds were low and within ranges considered safe for poultry diets under prior European Food Safety Authority evaluations.

Carcass characteristics told a subtler story. At day 28, slaughter weight, hot and cold carcass weights, carcass yield, and the weights of most internal organs, including breast, liver, heart, kidney, pancreas, and lymphoid tissues such as the thymus, bursa of Fabricius, and spleen, did not differ significantly among treatments. The one clear exception was the gizzard, the muscular grinding organ of the avian digestive tract, which was heaviest in birds given 0.2% RNFS or 0.1% S. cerevisiae and lightest in the unsupplemented control group, a difference the researchers linked statistically (p = 0.023). A larger gizzard typically indicates more vigorous digestive function, which could partially explain the growth advantages observed in those groups.

The divergence between growth performance and carcass traits, the authors argue, reflects genuinely different physiology. Growth metrics respond quickly to improvements in digestibility and gut health, whereas carcass composition is governed by genetic potential, slaughter age, and metabolic partitioning of nutrients, factors that a 28-day trial window may simply be too short to reveal. Earlier studies from the same group had already shown that RNFS improves breast meat texture, juiciness, and tenderness, and that a 1 mL per kilogram dose mitigates heat-stress damage to meat quality and growth efficiency. The new trial extends that record by demonstrating that a combined water-and-feed administration strategy can deliver measurable growth benefits during the crucial starter-to-grower transition.

Limitations remain. Organ-level comparisons relied on eight birds per group, a sample size that may have missed subtle differences, and the study did not include microbiome profiling or antioxidant biomarkers that would pin down the mechanisms at work. The authors call for molecular-level follow-up studies and validation across varied production conditions. Still, the evidence assembled so far positions RNFS as a practical, antibiotic-free candidate for broiler production, particularly in hot climates where heat stress compounds the challenge of maintaining flock performance. For an industry under pressure to eliminate growth-promoting antibiotics while feeding a growing global population, a probiotic blend that outperforms its single-strain rivals may be exactly the kind of solution the field has been waiting for.

Subject of Research: Effects of a multi-strain probiotic blend on growth performance and carcass traits in broiler chickens

Article Title: Effect of RISCO–NUTRIFOUR Probiotic on Growth and Carcass Traits in Broilers During Starter and Grower Phases

Article References: Al‐abdullatif, A. A., Al‐Garadi, M. A., Qaid, M. M., Matar, A. M., Al‐Badwi, M., Alobre, M. M., Suliman, G. M., & Hussein, E. O. (2026). Effect of RISCO–NUTRIFOUR Probiotic on Growth and Carcass Traits in Broilers During Starter and Grower Phases. Food Science & Nutrition, 14(9), Article e71335. https://doi.org/10.1002/fsn3.71335

Image Credits: AI Generated

DOI: 10.1002/fsn3.71335

Keywords: probiotics, broilers, poultry, Bacillus subtilis, Saccharomyces cerevisiae, antibiotic alternatives, gut health, growth performance, carcass traits, feed conversion, animal nutrition, Poultry Science