Gut health in dogs and cats: physiological functions and evolving market trends

In pet food development, “gut health” is no longer a simple matter of “adding oligosaccharides or lactic acid bacteria.”

The gut is not only the site of nutrient digestion and absorption—it is increasingly viewed as a functional organ that can influence the whole body through fermentation (microbial metabolism), the mucosal barrier, and gut-associated immunity, potentially affecting systemic inflammatory tone, metabolism, and even behavior.

In addition, because dogs and cats differ in digestive physiology and nutrient utilization, the optimal approach to “gut health support” is not the same for both species. In this article, aimed at R&D leaders at pet food companies, we organize the following points with clear rationale and supporting evidence.

• What happens in the small intestine vs. the large intestine (division of roles)
• Practical design targets for defining a “healthy gut state”
• Mechanisms by which gut health can influence the whole body
• Evidence-based effects shown in studies (dogs and cats)
• Practical formulation and process considerations for product design
• Validation design: what to measure to say “it worked”
• Current demand trends in Western markets and what’s next (research × market)

Digestive tract basics in dogs and cats: roles of the small and large intestine

Small intestine: the main battlefield for digestion and absorption

Most digestion and absorption of key nutrients occurs in the small intestine. With pancreatic enzymes, bile acids, and brush-border enzymes, nutrients are broken down into absorbable forms, taken up by intestinal epithelial cells, and delivered to the liver primarily via the portal vein.

• Protein:
  After initial breakdown in the stomach, proteins are further digested in the small intestine by pancreatic proteases into peptides and amino acids. Final absorption occurs mainly through small-intestinal epithelial cells and nutrients move to the liver via the portal circulation.
  　
• Fat:
  Fats are emulsified by bile acids and then hydrolyzed by lipase into fatty acids and monoglycerides. Long-chain fatty acids are absorbed and then transported as chylomicrons, largely via the lymphatic system into the bloodstream.
  　
• Carbohydrates (starch, etc.):
  Pancreatic amylase breaks starch into oligosaccharides, which are then converted to monosaccharides by brush-border enzymes and absorbed. Some fractions—such as resistant starch—escape digestion and reach the large intestine.
  　
• Vitamins and minerals:
  Many are absorbed in the small intestine. When digestion/absorption is impaired (e.g., mucosal damage or exocrine pancreatic insufficiency), weight loss and chronic diarrhea can result.

Large intestine: water/electrolyte absorption and fermentation

The large intestine’s primary roles are maintaining water and electrolyte balance through reabsorption, storing and excreting feces, and providing a “fermentation tank” for intestinal microbes. While it absorbs fewer nutrients than the small intestine, it is often the more important site from a dietary-design perspective.

Fermentation in the colon affects stool consistency, odor, and gas—and can also influence immune responses and systemic inflammatory tone.

• Reabsorption of water and electrolytes (e.g., sodium):
  The colon reabsorbs water and electrolytes, helping stool achieve appropriate firmness. If colonic function is compromised, water is not adequately absorbed and “large-bowel diarrhea” can occur (often characterized by mucus, straining, and frequent small-volume stools).
  　
• Fermentation:
  Dietary fibers, non-digestible oligosaccharides (e.g., FOS), and resistant starch are fermented by microbes to produce short-chain fatty acids (SCFAs: acetate, propionate, butyrate). SCFAs serve as key energy sources for colonic epithelial cells. For example, in dogs, acetate/propionate/butyrate are often produced in approximate molar ratios around 60:20:10, and butyrate is particularly important as an energy source for colonocytes.
  　
• Putrefaction (protein fermentation):
  When large amounts of undigested protein reach the colon, microbial protein fermentation increases, producing putrefactive metabolites such as ammonia, phenols, and indoles. These contribute to fecal odor and may burden the colonic mucosa and potentially promote inflammation.

Key differences between dogs and cats

Dogs and cats are both monogastric, but their nutritional physiology differs significantly.

• Cats (Felis catus):
  Cats are obligate carnivores. They rely heavily on protein and fat metabolism for energy. Their ability to utilize carbohydrates is limited, and their physiological adaptation to high-carbohydrate diets is considered lower.
  　
• Dogs (Canis lupus familiaris):
  Dogs are more omnivorous and have greater carbohydrate digestion and absorption capacity than cats. For instance, dogs generally have higher pancreatic amylase activity and can adapt (to some extent) to higher-starch diets.

Anatomically, both dogs and cats have a relatively small cecum and a non-sacculated colon, so their hindgut fermentation capacity is limited compared with herbivores. Reports suggest cats have an even smaller/shorter cecum than dogs (dogs may have a relatively longer, more spiral cecum, while cats often have a short, comma-shaped cecum).

Therefore, they are not suited to designs that “generate energy via extensive hindgut fermentation,” like ruminants or horses. For gut-health in dogs and cats, the goal is typically “high-quality fermentation even at low volumes (SCFA production)” plus stabilization of stool quality, barrier function, and immune balance.
　

What happens if undigested substrates reach the colon?

What occurs depends largely on the type of substrate that flows into the large intestine.

A) Substrates that tend to promote “beneficial fermentation”

Highly fermentable fibers, non-digestible oligosaccharides (e.g., FOS), and resistant starch can increase SCFA production, lower intestinal pH, and potentially support the mucosal barrier and local immunity. However, excessive amounts can also cause soft stool and gas—dosage and speed of fermentation must be managed.

For example, studies in dogs report that adding fructooligosaccharides can lower colonic pH and increase SCFAs and beneficial bacteria such as Bifidobacterium and Lactobacillus.

B) Substrates that tend to strengthen “putrefaction”

When large amounts of undigested protein reach the colon, putrefactive metabolites increase (ammonia, phenols, indoles), worsening fecal odor and potentially increasing mucosal burden. Research also indicates that high-protein diets can increase protein fermentation markers and putrefactive metabolites in dogs.

For instance, Xu et al. (2017) reported that in healthy, non-obese dogs, a high-protein diet (HP) significantly increased fecal ammonia, branched-chain fatty acids, phenols, and indoles compared with a low-protein diet (LP). Meanwhile, beneficial SCFAs such as acetate and butyrate did not significantly differ, suggesting that under high-protein conditions, “fermentation quality” can deteriorate more easily.

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In addition, dogs with chronic enteropathy (e.g., IBD-like conditions) have been reported to show reduced fecal SCFAs and reduced microbial diversity, suggesting that disruption of fermentation quality may be linked to disease. Isaiah et al. (2019) found that dogs with chronic enteropathy had significantly lower key SCFAs (e.g., acetate, propionate) than healthy dogs, along with reduced diversity and evidence of dysbiosis.
　

Four practical indicators to define a “healthy gut state”

In simple terms, good gut health means the intestinal environment and function remain stable across digestion/absorption, defense, and metabolic roles—supporting whole-body health. From a development standpoint, the following four indicators are a useful framework.

1) Microbiome (gut microbial community)

A “good microbiome” is not only about “higher diversity.” Important properties include:

• Stability (resistance): less likely to be disrupted by diet changes or stress
• Recovery (resilience): ability to return after disruption
• Functional redundancy: multiple microbes able to perform similar functions

In dogs and cats, microbiome composition is strongly influenced by diet (protein/fiber/fat levels; raw vs cooked; etc.). Daily formulation choices shape microbial composition and metabolic capacity.

Some reports suggest dogs may have relatively strong resilience (stability and recovery) even under dietary shifts.
　

2) Controlled fermentation (SCFAs)

SCFAs are microbial metabolites, and butyrate is particularly important as fuel for colonic epithelium. However, fermentation that is too rapid can cause gas and osmotic diarrhea/soft stool.

In development, the key is not simply “increase SCFAs,” but rather control:

• Control fermentation speed by adjusting solubility, particle size, viscosity, and inclusion level
• Reduce bias/peaks by blending multiple substrates instead of “dumping” one fast-fermenting ingredient

If you include large amounts of highly fermentable soluble fiber, fermentation can accelerate in the colon and lead to gas and soft stool. Combining with less fermentable insoluble fiber (e.g., cellulose) can slow fermentation and improve stool formation.

Empirically, blending fibers with different fermentation rates (fast → medium → slow) tends to stabilize stool.

Studies in dogs also report that appropriate levels of FOS can increase SCFAs (including butyrate), increase Lactobacillus/Bifidobacterium, and reduce pH. But excessive fiber can reduce digestibility and increase stool volume. The “why” of fiber inclusion must be explicit (stool forming, fermentation support, calorie control, etc.).

3) Mucosal barrier (mucus layer)

The mucosal barrier is a coordinated “breakwater” formed by the mucus layer, epithelial cells, tight junctions, and immune cells. Especially in the colon, mucus helps prevent pathogen invasion, while immune cells beneath the epithelium help maintain microbial homeostasis.

Rather than claiming “this ingredient strengthens the barrier,” a more fundamental strategy is to avoid conditions that damage the barrier (over-fermentation, putrefaction, irritants).

For example, butyrate supports epithelial energy needs and contributes to tight-junction maintenance. Beneficial microbial metabolites such as acetate and butyrate have been reported to support epithelial barrier integrity. Conversely, excessive translocation of endotoxins (e.g., LPS) may contribute to systemic inflammation, making barrier impairment something to avoid.

From a development perspective: prevent excessive fermentation/putrefaction that irritates the mucosa, while using controlled fermentable substrates or postbiotic approaches that can “nourish” the epithelium gently.

4) Gut immunity

The gut contains extensive GALT (gut-associated lymphoid tissue), one of the body’s largest immune systems. Healthy function requires balance between immune tolerance (not overreacting) and appropriate defense.

A commonly measured marker is IgA, a secretory antibody that blocks pathogen binding at mucosal surfaces and is often used as a marker of mucosal immune status.

Some studies report changes in immune markers with probiotics. For example, Benyacoub et al. (2003) reported that supplementation with Enterococcus faecium SF68 increased fecal and serum IgA in puppies. The same study also reported enhanced vaccine antibody responses (IgG/IgA) and increased B-cell proportions—an example of probiotic-mediated immune modulation.
　

Why gut health can influence the whole body

The gut is a hub that interacts with multiple organs and functions. As a result, improving gut environment may influence skin, brain, kidneys, and more—often discussed as “X–gut axes.” Below is an overview of four major axes, with mechanisms and evidence concepts.

Gut–immune axis

Microbial metabolites (SCFAs, etc.) and barrier status can affect local immunity and systemic inflammatory signaling. Butyrate supports epithelial health and may contribute to controlled immune responses. Acetate and butyrate can inhibit pathogen growth via pH reduction and are suggested to influence immune regulation (e.g., regulatory T-cell induction, anti-inflammatory signaling).

There are also veterinary reviews summarizing probiotic applications and evidence across use cases, including diarrhea management, allergy support, and stress modulation.

Gut–skin axis

In canine atopic dermatitis (cAD), links to the gut microbiome have been discussed. Some trials report improved clinical scores and microbiome changes after probiotic supplementation.

A Korean study (2025) reported that in 23 atopic dogs receiving probiotics for 16 weeks, symptom scores (CADESI-4 and pruritus index) improved significantly and microbial diversity increased. Dogs with greater diversity improvement also tended to have better skin outcomes.

Earlier single-strain studies (e.g., Lactobacillus rhamnosus GG; Marsella et al., 2012) reported limited effects, but multi-strain probiotics and synbiotics have shown more promising results in later work.
　

Gut–brain axis

In dogs, some research suggests probiotics may influence behavior. One example is Bifidobacterium longum BL999 (a specific strain used by Nestlé Purina), reported to improve anxiety-related behaviors. Purina markets this concept as the supplement “Calming Care.”

Proposed mechanisms include microbe-derived neuroactive compounds (e.g., GABA), tryptophan-related metabolites (serotonin pathways), vagus nerve signaling, and modulation of stress responses such as cortisol. Inflammation and increased intestinal permeability may also affect brain function, as suggested in human/animal models.

However, behavioral outcomes are harder to measure and more variable. From a product perspective, it’s often safer to frame benefits as “digestive stability supports comfortable daily life,” rather than making strong “calming” claims.

Gut–kidney/urinary axis

Interest is growing in the relationship between chronic kidney disease (CKD) and gut dysbiosis in dogs and cats (the “gut–kidney axis”). Reviews suggest that dysbiosis may worsen kidney disease via microbe-derived uremic toxins and systemic inflammation, and that interventions targeting gut metabolism may help support CKD management.

Microbial uremic toxins (e.g., indoxyl sulfate, p-cresol sulfate) have been reported to increase in CKD and may correlate with disease progression. There is also discussion of oxalate metabolism: in dogs, the presence of Oxalobacter formigenes (an oxalate-degrading gut bacterium) has been associated with reduced calcium oxalate stone risk in some studies.
　

Effects that gut-health approaches may support

Gut involvement is plausible across many conditions, but disease causes are multifactorial. Here we separate what research suggests from what is realistically targetable in product development and safe communication.

Whole-body health: immune balance, inflammation, allergy

Dogs: Some probiotic studies show changes in IgA, vaccine antibody responses, and inflammatory markers.

Cats: While fewer studies exist, some work suggests probiotics may help maintain microbial stability under stressors (e.g., antibiotics). A study (Torres-Henderson et al., 2017) reported that SF68 helped reduce microbiome disruption and also suggested fewer chronic feline herpesvirus symptoms over time.

For development and communication, safer language is “supports intestinal barrier function and a healthy immune balance,” rather than “boosts immunity.”

GI signs: diarrhea, constipation, gas, stool quality

The most direct and consumer-visible outcome is stool quality. Many digestive-support products focus on this.

Evidence examples include synbiotic/probiotic use in chronic diarrhea management and antibiotic-associated diarrhea, with improvements in stool scoring and owner-reported outcomes in some studies.

From a development standpoint, stool is also easy to quantify via standardized scoring systems (e.g., Purina 7-point fecal score; normal often around 2–3).

Behavior/mental state: stress, anxiety, sleep

This is a growing research area, but measurement and reproducibility are challenging. From a product standpoint, it’s generally safer to keep messaging modest and indirect.

Skin/coat: dermatitis, coat gloss, barrier maintenance

Evidence is accumulating in dogs, especially for atopic dermatitis and probiotic interventions, though results vary by strain and study design. In cats, evidence is thinner; practical entry points often focus on stool comfort and hairball-related issues, with skin/coat positioned as a secondary benefit.

Kidney/urinary: potential supportive benefits

Some early studies suggest gut-targeted interventions may affect uremic markers, but the field is still developing. Messaging should remain conservative and supportive.

From concept to product: practical formulation and process considerations

Digestibility-first design

A common failure mode is: “We added gut-health ingredients (fiber/probiotics), but stools got softer.” In many cases, the root cause is increased undigested flow into the colon—triggering fermentation/putrefaction instability.

Recommended order of operations

1. Improve raw-material digestibility:
   Choose high-quality protein sources; avoid over-reliance on high-ash meals. Consider hydrolysis or enzyme processing when appropriate. In cats (high-protein requirement), protein digestibility strongly drives stool quality.
2. Optimize processing conditions:
   In extrusion, adjust temperature/shear/moisture to achieve appropriate starch gelatinization and controlled protein denaturation. Excessive heat is not automatically better; over-denaturation can reduce enzymatic digestibility. Manage drying to avoid scorching, and balance post-extrusion fat coating for palatability/energy without triggering fat-related loose stool.
3. Starch gelatinization and particle size:
   Raw starch is less digestible and can behave like resistant starch, increasing colonic fermentation. Aim for adequate gelatinization (often cited as ideally high, e.g., >90%), while tuning grind size for enzymatic accessibility. Avoid excessive micronization if blood-glucose response is a concern.
4. Cat-specific caution:
   Cats have limited hindgut fermentation capacity; design should assume “finish digestion in the small intestine.” Excessive fiber strategies that may work in dogs can more easily cause soft stool in cats.

First, ensure “what should be digested/absorbed in the small intestine is completed there.” Then intentionally deliver targeted substrates (fiber/oligosaccharides) to tune colonic fermentation.

Fiber is not “add or don’t add”—it must be designed

Fiber includes insoluble and soluble types, and fermentation speed (fast vs slow) is also critical.

Insoluble-leaning fibers:

Support stool formation and bulking; can help firm loose stool. Overuse may increase stool volume without providing fermentation benefits.

Examples: cellulose, peanut hulls, some resistant dextrins (varies by type).

Soluble/fermentable fibers:

Support SCFA production and can help with stool odor reduction (e.g., via pH reduction and ammonia capture mechanisms). Overuse can cause gas and soft stool.

Examples: inulin, FOS, pectin fractions in beet pulp.

Blending strategy:

Use blends to create a “fermentation gradient”: fast (e.g., FOS) + medium (e.g., beet pulp) + slow (e.g., cellulose). This approach often stabilizes stool by avoiding fermentation spikes while supporting SCFA production.

Define the purpose clearly (firm stool, promote fermentation, weight management, etc.) and manage trade-offs (digestibility, palatability, energy density).

Choosing between “biotics”: how to use them in pet food

Prebiotics (substrates for microbes):

Oligosaccharides and fibers that feed beneficial microbes. Generally stable and easy to use in dry foods. Some can work at low inclusion levels.

Probiotics (live microbes):

Strain-specific and potentially strong, but stability is challenging in extrusion and during shelf life. Special technologies (e.g., post-process coating) may be required. Spore-formers (e.g., Bacillus) are more heat-resistant, but evidence can be thinner than for some lactic acid bacteria.

Synbiotics (probiotic + prebiotic):

Combining live microbes with substrates to support them. Offers good product-design flexibility and can align with clinical “when GI is unstable” messaging.

Postbiotics (inactivated microbes and/or microbial metabolites):

Growing interest due to processing and storage stability; easier to incorporate into dry foods. In pet food, postbiotic-focused papers and IP analyses are increasing, and some studies suggest benefits related to barrier and immune balance. This category is becoming more prominent partly because “live probiotics” are hard to guarantee through manufacturing and distribution.

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What matters is not “which one,” but “how it is used” given your product form (dry, wet, freeze-dried), process constraints, and the claim level you want to support.

Barrier/immune-support ingredients: use with careful positioning

Barrier/immune messaging is higher-risk if overstated. The practical approach is:

• First, design a gut environment that is hard to irritate (avoid over-fermentation/putrefaction; reduce undigested flow).
• Then add supportive ingredients for mucosal immune maintenance as “reinforcement,” not the main story.

Examples include yeast beta-glucans, nucleotides, fermented extracts, and functional peptides. Some canine studies suggest immune-marker changes and vaccine response effects, but mechanisms are not always simple or consistent. For product communication, conservative phrasing such as “supports barrier function and healthy immune balance” is typically safer than strong claims.

Avoid the “everything plus the kitchen sink” problem

Gut-health formulas always involve trade-offs:

• Higher fermentable substrate → potentially more SCFAs but higher gas/soft stool risk
• Higher total fiber → easier stool formation/weight management but lower palatability and energy density
• Higher protein → supports feline needs and lean mass but increases putrefaction risk if digestibility cannot keep up

The development team should be able to explain how the formulation resolves these trade-offs, supported by rationale and data.

How to validate gut-health effects: what to measure

Priority KPIs: stool score, frequency, gas, odor

The strongest—and most practical—KPI for gut-health products is stool.

Implementation examples

• Fecal score: Use a standardized scale such as Purina’s 7-point system; ideal often around 2–3. Record daily and compare averages.
• Defecation frequency: Track per day; too high suggests intolerance or excessive fiber; too low suggests constipation risk.
• Gas: Use pre-defined qualitative categories (high/normal/low) scored by caretakers or veterinarians.
• Odor: Sensory evaluation or owner questionnaires under standardized conditions.

If you can show “stool moved into the ideal range within 2 weeks,” that is both scientifically manageable and highly persuasive in the market.

SCFAs, pH, and putrefactive metabolites

Chemical markers in feces or intestinal contents can strengthen mechanistic credibility.

• SCFAs (acetate/propionate/butyrate): Often measured by GC-MS; interpret using balance and context, not “higher is always better.”
• Branched-chain fatty acids (BCFAs): Often reflect protein fermentation; increases can indicate excess undigested protein reaching the colon.
• pH: Lower pH can indicate fermentation; extremes can indicate risk (very low may align with diarrhea risk; very high can suggest putrefactive dominance).
• Ammonia, indoles, phenols: Putrefactive markers; reductions support a “less putrefactive” shift.

Barrier, immunity (IgA), and inflammation

These add credibility but are more research-intensive.

• IgA: Serum or fecal IgA via ELISA (interpret carefully; context matters)
• Inflammation markers: Fecal calprotectin, serum CRP, cytokines (IL-6, TNF-α, etc.)
• Intestinal permeability: Marker tests (e.g., lactulose/mannitol ratio), typically more advanced

Microbiome analysis: important caveats

• 16S profiling shows composition but not direct function; metagenomics is richer but costly.
• Feces reflects luminal microbiota, not mucosa-adherent communities.
• The field is shifting from “which bacteria” to “what functions/metabolites.” Pair microbiome data with SCFAs and metabolite data to build a stronger story.

Western market trends and what’s next (research × market)

Why demand is growing

In the US and Europe, “digestion,” “gut,” and “microbiome” have become established value themes within broader premiumization and wellness trends. Preventive mindsets are also spreading: maintaining daily digestive comfort through food is increasingly valued.

What sells well: typical successful positioning

Gut health is often strongest when connected to broader needs:

• Digestive comfort: stool quality, gas, and odor
• Skin/coat: “gut–skin” narrative for sensitive-skin products
• Mental/behavioral support: cautiously positioned, often indirectly
• Senior health: gut as part of multi-support concepts (immune, muscle, kidney)

Likely research trends

• Expansion of gut–brain studies (stress, anxiety, cognition)
• Growth in gut–kidney research (uremic toxins, inflammation, metabolism)
• Continued shift from “bacteria names” to “metabolites/functions”
• Exploration of next-generation probiotics (with safety and manufacturing hurdles—postbiotics may expand first)

Likely market trends

• Personalization: microbiome tests linked to custom diets/subscriptions
• Clean label: preference for familiar ingredient names (pumpkin, sweet potato) over complex additive terminology
• Less “live probiotic” emphasis: more postbiotic or fermented-ingredient positioning due to stability/expectation gaps
• Sustainability synergy: many prebiotic fibers are plant-derived and can align with eco-focused messaging

Overall, gut-health is moving from “a fad” to a long-term category, supported by expanding science and increasing consumer literacy. For R&D leaders, the advantage comes from translating up-to-date research into coherent, manufacturable product designs with measurable outcomes.

参考文献

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