Gut Taste Receptors – Getting Fat With Them

To Summarize:

The Taste Receptors

The receptors of interest and which have a large part to play in gut metabolism are mainly of two types – T1R or TAS1R receptors, and the T2R or TAS2R receptors. Both naming conventions are used. They are both members of the same class of receptors, the GPCR receptors. The TAS nomenclature is used in genetic databases and protein classification such as UniProt and NCBI.

The T1R Receptors

T1R sweet/umami sensors are a group of taste receptors that detect sweet and umami (savoury) flavors. They belong to the T1R (taste receptor type 1) family, which are G protein-coupled receptors (GPCRs) found primarily on the tongue but also in other tissues such as the gut.

Main T1R Receptors and Their Roles

1. T1R1 + T1R3 (heterodimer)

   • Function: Detects umami taste (savoury), primarily from amino acids like glutamate (e.g., MSG).

   • Ligands: L-glutamate, L-aspartate, and 5′-ribonucleotides (like IMP or GMP enhance response).

2. T1R2 + T1R3 (heterodimer)

   • Function: Detects sweet taste.

   • Ligands: Natural sugars (e.g., glucose, sucrose), artificial sweeteners (e.g., aspartame, sucralose), and some D-amino acids.

Key Features:

• These receptors are heterodimers, meaning they need to pair with another T1R subunit to function.

• They activate downstream signaling pathways (via G proteins like gustducin) leading to taste perception.

• T1R3 is shared by both sweet and umami receptors.

Expression Beyond the Tongue:

• T1R receptors are also found in the gut, pancreas, and brain, where they may help regulate nutrient sensing, insulin secretion, and appetite.

The T2R Receptors

T2R receptors (short for Type 2 Taste Receptors) are a family of G protein–coupled receptors (GPCRs) primarily responsible for detecting bitter compounds. They were originally discovered on the tongue, but are now known to exist in various tissues throughout the body, where they serve non-taste functions such as hormone secretion, immune defense (mainly control of airway innate immunity), breathing function especially asthma and regulation of gut motility (Avau & Depootere, 2016).

 Overview of T2R Receptors

 Functions by Tissue

 Examples of Specific Human T2Rs

 Clinical and Research Significance

• Dietary response: T2Rs in the gut modulate satiety and metabolism.

• Respiratory defense: T2Rs in nasal and airway epithelium help fight infection.

• Drug development: T2R agonists are being explored for obesity, diabetes, respiratory infections, and even cancer.

• Genetics: Variations in T2R genes (e.g., T2R38) affect taste preferences and disease susceptibility (e.g., chronic sinusitis, asthma).

Summary

T2R receptors are bitter-sensing GPCRs that function far beyond taste, helping regulate appetite, immunity, digestion, and more. They are part of the body’s defense and regulatory system, sensing potentially harmful or bioactive compounds throughout the body.

The GPRs (Fat Sensors)

The GPRs (G protein-coupled receptors) involved in fat sensing are a set of receptors that detect fatty acids—primarily free fatty acids (FFAs) such as the short-chain fatty acids (SCFAs)—and play key roles in both taste perception and metabolic regulation.

Here are the major fat sensors in the GPR family:

GPR40 (FFAR1 – Free Fatty Acid Receptor 1)

• Ligands: Medium- and long-chain fatty acids (e.g., palmitic acid, oleic acid)

• Function:

  • Stimulates insulin secretion in pancreatic β-cells (glucose-dependent).

  • Found in the pancreas, gut, and taste buds.

GPR41 (FFAR3)

• Ligands: Short-chain fatty acids (SCFAs) like acetate, propionate, butyrate

• Function:

  • Involved in energy homeostasis and gut hormone regulation (e.g., PYY, GLP-1).

  • Expressed in gut enteroendocrine cells and nervous tissue.

GPR43 (FFAR2)

• Ligands: Same SCFAs as GPR41

• Function:

  • Influences inflammation, appetite regulation, and immune responses.

  • Found in the intestine, immune cells, and adipose tissue.

GPR120 (FFAR4)

• Ligands: Long-chain unsaturated fatty acids (especially omega-3s)

• Function:

  • Plays a role in fat taste perception, anti-inflammatory signaling, and insulin sensitization.

  • Expressed in taste buds, gut, macrophages, and adipose tissue.

GPR119

• Ligands: Lipid-derived molecules (e.g., oleoylethanolamide, some lysophospholipids)

• Function:

  • Stimulates GLP-1 and GIP secretion.

  • Regulates glucose metabolism and satiety.

  • Found in the gut and pancreatic islets.

Summary Table

These GPRs are part of how the body senses dietary fats and translates them into metabolic responses, including hormone secretion, appetite regulation, and energy storage.

Gut taste receptors don’t work in isolation. They interact with, complement, and sometimes counteract other biochemical pathways that regulate appetite, energy balance, and food reward. A number of hormones have already been referenced but it is useful to summarize how they interact with each other. 

1. Integration with Hormonal Pathways

Complementary Actions

Gut taste receptors activate and work alongside key appetite-regulating hormones:

These hormones signal to the hypothalamus and brainstem to coordinate hunger and fullness.

2. Interaction with the Central Nervous System (CNS)

Complementary: Gut-Brain Axis

• Gut taste receptors send afferent signals via the vagus nerve to the brainstem (particularly the nucleus tractus solitarius, NTS).

• These signals are integrated in the hypothalamus, especially:

  • Arcuate nucleus (ARC): balances hunger-promoting neurons (NPY/AgRP) and satiety-promoting neurons (POMC/CART).

So, gut receptor activity directly shapes how the brain interprets hunger and satiety signals.

3. Cross-talk with Nutrient and Energy Sensors

Gut taste receptor activity intersects with cellular energy sensors, like:

AMPK (AMP-activated protein kinase)

• A cellular energy sensor that promotes food intake when activated in the hypothalamus.

• GLP-1 and CCK, released via gut receptors, inhibit AMPK to reduce appetite.

• High-fat diets or fasting increase AMPK activity, overriding satiety signals.

mTOR (mechanistic target of rapamycin)

• Activated by amino acids (especially leucine).

• Promotes anabolic processes and reduces appetite when nutrients are sufficient.

• Gut taste receptor–driven nutrient sensing enhances mTOR signaling in the brain and periphery.

4. Interaction with Reward Pathways (Dopamine/Endocannabinoids)

Complementary and Sometimes Counteractive

• Nutrient sensing in the gut boosts dopamine release in the striatum, reinforcing food preference.

• If the expected caloric payoff doesn’t arrive (e.g. artificial sweeteners), the gut-to-brain reward feedback may weaken, potentially increasing cravings.

Endocannabinoid System (ECS)

• Stimulates appetite and enhances the palatability of food.

• Can counteract gut-derived satiety signals by overriding them—especially during energy restriction or stress.

5. Immune and Inflammatory Pathways

Counteractive Potential

• Chronic inflammation (e.g., due to obesity or gut dysbiosis) may impair gut taste receptor expression or signaling.

• This leads to blunted hormone release, reduced satiation, and disrupted appetite regulation.

• Conversely, some gut receptors (like T2Rs, bitter taste receptors) may also serve immune roles, triggering antimicrobial responses.

Final Thoughts

Gut taste receptors are like nutrient scouts, sensing the biochemical landscape of your meals and reporting back to the brain’s command center. Their signals are interpreted in concert with hormones, energy sensors, and reward circuits, forming a complex network that helps you decide when, how much, and what to eat.

On the Tongue: Classical Taste Organization

Before diving into the gut, here’s a quick refresher on oral taste receptors:

Tongue taste cells are grouped into taste buds, and each taste bud contains cells that specialize in one or more taste qualities.

In the Gut: Distributed but Selective Organization

Unlike the tongue, the gut doesn’t have taste buds, but enteroendocrine cells (EECs) act as “taste cells” scattered throughout the lining of the stomach, small intestine, and colon.

Organization by Taste Type in the Gut:

Functional Specialization by Region

These receptors are found on subtypes of enteroendocrine cells, like:

• L-cells (secrete GLP-1 and PYY)

• I-cells (secrete CCK)

• K-cells (secrete GIP)

Each of these has a unique receptor expression profile.

 Co-expression and Redundancy

Gut taste receptors often co-express multiple taste types to ensure redundancy and nutrient-specific responses:

• Some EECs express both sweet and umami receptors, enabling them to respond to mixed meals.

• Bitter receptors (T2Rs) are especially diverse, with 20–30 subtypes that detect a wide array of compounds.

• Fat-sensing receptors like GPR120 may also co-occur with CD36, amplifying detection of long-chain fatty acids.

 Regulation and Plasticity

Taste receptor expression in the gut is not fixed:

• Diet-induced changes (e.g., high-fat or high-sugar diets) can upregulate or downregulate receptor expression.

• Inflammation, stress, or microbial metabolites can also influence receptor distribution and sensitivity.

• Fasting may increase the expression of sweet or fat receptors to enhance sensitivity to nutrients once feeding resumes.

Summary Table

The simultaneous activation of sweet and bitter receptors can trigger a complex and sometimes conflicting physiological response. Let’s break it down across different levels of the gut-brain axis:

 1. Cellular Level: Competing Signals

Sweet receptors (T1R2 + T1R3) and bitter receptors (T2Rs) are both G-protein-coupled receptors (GPCRs), but they often elicit opposing effects:

So when activated together, the gut faces a kind of nutrient safety paradox:

• Sweet receptor says: “This is safe and calorically rewarding.”

• Bitter receptor says: “This might be harmful. Be cautious.”

2. Neural Integration: Balancing Reward and Defense

Brain reward vs. aversion systems

• Sweet activation → dopamine in the striatum (reward and motivation).

• Bitter activation → may trigger aversive responses via the nucleus tractus solitarius (NTS) and amygdala.

When both are stimulated:

• The brain tries to weigh pleasure vs. potential danger.

• If the bitter signal is strong, it may override the sweet signal, dampening appetite or triggering aversion.

This dynamic underlies why for example:-

• Some bitter medicines remain unpalatable even when sweetened.

• Bitterness can blunt sweetness perception, both orally and in the gut.

3. Hormonal Output: Synergy, Suppression, or Mixed Messages

Examples of gut hormone interplay:

If both receptor types are activated:

• Some hormones (GLP-1, PYY) may be additively or synergistically released.

• Others (e.g., appetite signals like ghrelin) are uniformly suppressed, reinforcing satiety.

4. Behavioral Outcome: Context-Dependent

What happens depends on:

A. Relative Signal Strength:

• If sweetness dominates: food may still be palatable and reinforcing.

• If bitterness dominates: food may be rejected or less satisfying, even if caloric.

B. Source and Context:

• Dark chocolate is both sweet and bitter, yet enjoyable due to cultural conditioning and balance.

• In contrast, sweetened medications (like bitter antibiotics) often remain unpleasant—bitterness can override sweetness unless fully masked.

C. Metabolic State:

• During fasting or energy deficit, sweet signaling may be amplified, making the brain more tolerant of bitter signals.

5. Functional Interpretation in the Gut

From an evolutionary view:

Simultaneous sweet + bitter signaling is a safety mechanism that says: “There may be energy here, but it could be risky—proceed with caution.”

In practice:

• It may slow gastric emptying, giving the body time to evaluate the ingested material.

• It could modulate insulin sensitivity, especially if sweetness is artificial and not matched by calories.

• It might also trigger immune responses (some bitter receptors are expressed on immune cells in the gut lining).

Want to explore how this plays out in real-life food systems? For example:

• Why grapefruit or tonic water can suppress appetite?

• Or how artificial sweeteners + bitter aftertaste affect satiety?

Bitter taste receptors (T2Rs) in the gut are not organized in the same spatial pattern as they are on the tongue.

On the tongue:

• T2Rs are mainly located on the circumvallate, foliate, and fungiform papillae.

• Each taste receptor cell typically expresses multiple T2R subtypes, giving broad sensitivity to many bitter compounds.

• The tongue is organized for sensory discrimination (i.e., “this tastes bitter”), triggering immediate aversive responses.

In the gut:

• T2Rs are expressed throughout the gastrointestinal tract, but with different patterns and purposes:

• Unlike on the tongue, gut T2Rs are not organized to “map” tastes, but rather to monitor internal chemical environment and regulate physiological responses.

 Key Differences

Additional Insights:

• Gut T2Rs are also found on non-taste cells like tuft cells and immune cells, especially in the small intestine and colon.

• These cells can influence:

  • Mucosal immunity

  • Microbiota interactions

  • Inflammatory signaling in response to bacterial metabolites

 Summary

Bitter taste receptors in the gut are not arranged like they are on the tongue. Instead of mapping flavour, they act as sentinels spread across various parts of the GI tract, detecting potentially harmful compounds and adjusting digestion, motility, immune responses, and satiety accordingly.

Yes — some taste receptors are significantly more abundant in the gut than in the tongue, and their distribution reflects their functional roles.

Tongue vs. Gut: A Division of Labour

 Notable Gut-Enriched Taste Receptors:

1. Bitter (T2Rs)

• The gut expresses more types and more cells with T2Rs than the tongue.

• Found in:

  • Enteroendocrine cells

  • Tuft cells

  • Immune cells

• Roles include:

  • Triggering GLP-1, PYY, CCK release

  • Slowing gastric emptying

  • Activating immune surveillance in the small intestine and colon

2. Fat receptors (e.g., GPR120)

• These aren’t classical taste receptors on the tongue but are prominent in the gut.

• Involved in:

  • Sensing long-chain fatty acids

  • Promoting CCK and GLP-1 release

  • Regulating inflammation and gut motility

3. Sweet (T1R2/T1R3)

• While abundant in the tongue for sensing sugars, they’re also densely expressed in the small intestine.

• Important for:

  • Detecting glucose in the GI lumen

  • Upregulating glucose transporters like SGLT1

  • Modulating insulin and incretin hormone secretion

Why the Gut Needs More Receptors

• The tongue evaluates food before swallowing: it’s about flavour and pleasure.

• The gut needs to:

  • Monitor nutrients and toxins at a chemical level

  • Regulate hormone release (like GLP-1, CCK, PYY)

  • Coordinate digestion, absorption, immunity, and appetite

So, the gut acts more like a chemical sensor array than a flavour detector.

Summary

Yes — receptors for bitter, sweet, umami, and especially fatty acids are often more abundant in the gut than in the tongue. This reflects their roles in nutrient sensing, metabolic regulation, and immune defense rather than conscious taste perception.

Not exactly — gut sensitivity to bitter compounds is functionally different and less discriminating than tongue sensitivity, but in some ways it is more sensitive at lower thresholds, especially when it comes to physiological response rather than conscious perception.

 Tongue Sensitivity to Bitterness:

• The tongue contains multiple T2R receptors across taste bud cells.

• Each cell may express multiple T2Rs, enabling the tongue to:

  • Discriminate between bitter compounds

  • Trigger a rapid aversive reaction

• Sensitivity can be very high — we can detect nanomolar concentrations of quinine or PTC (e.g., PROP tasters vs non-tasters).

• This is about flavour detection and behavioral avoidance.

Gut Sensitivity to Bitterness:

• The gut also expresses many T2Rs, often more broadly and in higher quantity than on the tongue.

• Gut T2Rs are expressed on enteroendocrine, tuft, and immune cells — not taste buds.

• Instead of conscious perception, they influence:

  • Hormone release (GLP-1, CCK, PYY, serotonin)

  • Gastric emptying

  • Satiety and motility

  • Immune responses

• Sensitivity is less about discriminating fine differences, and more about detecting the presence of potentially harmful compounds.

• Some gut cells can react to very low concentrations (micromolar to nanomolar), triggering hormonal or protective responses without conscious awareness.

 A Comparison

Evolutionary Perspective:

• On the tongue, bitterness signals “don’t eat this.”

• In the gut, it says “something slipped through — deal with it.”

That means gut T2Rs may be more sensitive in some respects — especially in their functional potency — but they’re not tuned to fine distinctions like taste buds are.

 Summary:

Gut sensitivity to bitter compounds is more focused on physiological action than conscious perception. While it might not “taste” bitterness the way the tongue does, the gut is very sensitive to bitter substances, and even small amounts can trigger hormonal, immune, and digestive responses — often faster than we’d consciously notice anything.

1. Use of T2R Agonists vs. Antioxidants Separately

Researchers compare:

• Known T2R agonists that lack antioxidant activity (e.g., denatonium, quinine)

• Versus compounds like polyphenols, which may both activate T2Rs and act as antioxidants.

What helps:

• If both compounds activate a pathway, it’s likely T2R-driven.

• If only the polyphenol produces an effect, it’s more likely due to antioxidant activity or another mechanism.

2. Receptor Knockout or Knockdown Models

Using T2R gene knockout mice, or siRNA to silence T2R genes in vitro, helps determine:

• If the effect disappears when the receptor is removed → it’s T2R-specific.

• If the effect persists → likely due to non-T2R properties, like antioxidant activity or interaction with other pathways (e.g., Nrf2).

3. Selective Receptor Antagonists or Inhibitors

• T2R antagonists (like probenecid for T2R38) can be used to block T2R activation.

• If antioxidant or metabolic effects persist despite the blockade, they’re likely independent of T2Rs.

 4. Cellular Context Matters

• T2Rs are expressed on specific cell types: enteroendocrine cells, tuft cells, etc.

• Antioxidant effects occur in almost all cells, typically in the cytosol or mitochondria.

 Example:

• Polyphenols (like epigallocatechin gallate, EGCG) may:

  • Activate T2Rs on enteroendocrine cells → trigger GLP-1 release.

  • Scavenge ROS in epithelial cells or mitochondria → reduce inflammation.

You can test which is occurring by looking at:

• Hormone secretion changes → T2R likely involved.

• Oxidative stress markers → antioxidant role.

5. Pathway and Biomarker Profiling

Different mechanisms activate different intracellular signaling cascades:

6. Temporal Resolution

• T2R effects tend to be rapid (seconds to minutes) — especially hormonal or neuronal signaling.

• Antioxidant effects may take longer (minutes to hours) to impact gene expression, ROS levels, or cell survival.

Summary:

To distinguish T2R-mediated effects from non-receptor properties like the antioxidant actions of polyphenols, scientists use receptor-specific tools (knockouts, antagonists), compare to non-antioxidant T2R agonists, assess signaling pathways, and observe the time course of effects.

Probiotics, which are live microorganisms that confer health benefits when consumed in adequate amounts, can have a significant influence on gut taste receptors (T1Rs [sweet/umami] and T2Rs [bitter]) through various mechanisms. This area of research is still being explored extensively. Probiotic microorganisms most certainly  modulate the expression of nutrient-responsive receptors and transporters.  This leads to changes in digestion and to altered food consumption.

1. Microbial Metabolism of Tastants

• Probiotics can metabolize certain dietary compounds, such as polyphenols, fibres, or sugars, into bioactive metabolites that may interact with gut taste receptors.

  • For example, probiotics in the gut can break down complex carbohydrates into short-chain fatty acids (SCFAs), like butyrate or acetate, which can influence T1R activation (involved in sweet and umami taste).

  • Similarly, gut bacteria can ferment polyphenols into bioactive compounds, which may activate bitter receptors (T2Rs).

2. Influence on Gut Microbiota Composition

• Probiotics modulate the composition of gut microbiota, which in turn can affect the levels of bitter and sweet compounds available for T1R/T2R activation.

  • For example, some bacterial strains might increase the production of bitter compounds (like phenolic acids), thereby enhancing T2R activation in the gut.

  • On the other hand, probiotics might help increase the availability of oligosaccharides, which can enhance T1R (sweet) receptor activity and influence glucose homeostasis.

3. Modulation of Gut Barrier Function

• Probiotics help maintain gut barrier integrity, which ensures that bioactive compounds have better access to the intestinal epithelial cells where T1R and T2R receptors are located.

  • A healthy gut barrier allows tastants to reach these receptors more effectively, enhancing their role in regulating satiety, gut motility, and immune response.

4. Influencing Gut Hormone Release

• Probiotics can stimulate the release of hormones such as GLP-1 (glucagon-like peptide-1), PYY (peptide YY), and CCK (cholecystokinin), all of which can be influenced by T1R and T2R activation.

  • Sweet taste receptors (T1R) in the gut, when activated by compounds like glucose or SCFAs, can stimulate GLP-1 secretion, which promotes satiety and helps regulate insulin.

  • Bitter taste receptors (T2R), when activated by certain metabolites or compounds, can trigger the release of CCK and PYY, which also contribute to feelings of fullness and reduce appetite.

5. Inhibition of Inflammation

• Some probiotic strains have anti-inflammatory effects that modulate gut immune function. This could influence T2R-mediated responses, as T2Rs are involved in regulating immune responses.

  • Inflammatory cytokines can alter the expression of taste receptors in the gut, so probiotics might help restore normal T2R activity, leading to more efficient regulation of intestinal motility and immune surveillance.

6. Changes in Microbial-Derived Compounds

• Bacterial metabolites (e.g., indole, tryptamine, and SCFAs) can directly influence T2Rs in the gut.

  • Certain probiotics may enhance the production of these metabolites, which can activate T2Rs, triggering gut responses such as changes in motility, secretion of digestive enzymes, or modulation of appetite-regulating hormones.

Research indicates that probiotic microorganisms are essential for suppressing glucose uptake because their absence leads to increased sucrose intake. In a mouse model Swartz et al., (2012) examined preference for either sucrose or saccharin in mice (GF, C57BL/6J) which are free of germs compared to a control of ‘normal’ (conventional) mice. They examined mRNA and protein expression of the T1R3 receptor, and the amount of α-gustducin and Na glucose luminal transporter-1 (SGLT-1) activity from the intestinal epithelium of the proximal small intestine. They also measured gene expression of the T1R2, T1R3 and α-gustducin in the lingual epithelium.

The preference for sucrose was the same in both types of mouse but the germ-free mice consumed more of the sucrose solution than the conventional mice. There was no noticeable difference in preference or level of intake for saccharin. The germ-free mice expressed more sweet taste receptor (T1R3) and SGLT-1 mRNA and protein than the conventional mice. The lingual taste receptor mRNA levels were the same for both types of mouse. On that basis they reasoned that missing probiotic MOs in the gut produced an increased consumption of nutritionally important solutions such as sucrose which is digested to glucose and fructose.

Summary of Mechanisms:

Practical Example: Probiotics and Bitter Compounds

• Certain Lactobacillus and Bifidobacterium strains have been shown to increase the bioavailability of polyphenols or bitter compounds, enhancing T2R-mediated signaling in the gut. This could lead to improved immune regulation and possibly appetite control through gut-brain axis pathways.

Summary:

Probiotics influence gut taste receptors through microbial metabolism, changes in gut microbiota composition, gut barrier function, and the modulation of hormone release. These effects can enhance or reduce T1R/T2R activation, contributing to appetite regulation, satiety, immune response, and overall gut health.

Would you like to dive deeper into specific probiotic strains and their effects on taste receptor activation, or how probiotics can influence satiety signaling?

Prebiotics like fiber (fibre) have a significant impact on gut taste receptors (T1Rs and T2Rs) through several mechanisms. These mechanisms mostly revolve around the fermentation of fiber by gut microbiota and the subsequent production of bioactive compounds that can interact with taste receptors in the gut. 

1. Fermentation of Fiber by Gut Microbiota

• Prebiotic fibers, such as inulin, fructooligosaccharides (FOS), and resistant starch, are not digested in the small intestine. Instead, they travel to the colon, where they are fermented by gut microbiota. During fermentation, short-chain fatty acids (SCFAs) like acetate, butyrate, and propionate are produced.

  • SCFAs can activate T1R receptors (sweet receptors) in the gut, promoting the release of hormones like GLP-1 and PYY, which already mentioned are involved in satiety and appetite regulation.

  • Butyrate, in particular, has been shown to enhance the activation of sweet taste receptors (T1R2/T1R3) and may play a role in promoting feelings of fullness and improving insulin sensitivity.

2. Influence on Bitter Compounds (T2R Activation)

• Fiber fermentation can also affect the production of bitter compounds (e.g., phenolic acids) by the gut microbiota. These compounds can activate T2R (bitter) receptors in the gut.

  • Activation of T2Rs can lead to the release of gut hormones like CCK (cholecystokinin), which promotes satiety and digestive enzyme secretion.

  • In some cases, fiber fermentation leads to the production of compounds that alter the bitterness of food, either by enhancing the availability of bitter compounds or by masking bitterness.

3. Fiber’s Effect on Gut Microbiota Composition

• Prebiotics can modulate the composition of the gut microbiota, promoting the growth of beneficial bacteria like Bifidobacteria and Lactobacilli. These bacteria are involved in fiber fermentation and can also affect the balance of compounds that activate taste receptors.

  • Changes in microbiota composition can lead to different fermentation end-products, including SCFAs and bioactive polyphenols, which can have varying effects on T1R and T2R activation.

4. Impact on the Gut-Liver Axis

• Prebiotics like fiber can modulate the gut-liver axis by influencing bile acid production. Bile acids have been shown to interact with bitter receptors (T2Rs) in the gut.

  • The interaction of bile acids with T2Rs can enhance gut motility, influence bile secretion, and affect digestion. This is especially relevant after fiber fermentation, which may alter bile acid concentrations and their interaction with taste receptors.

5. Alteration of Taste Perception

• Over time, dietary fiber may influence taste perception by modifying the bioavailability of tastants and altering the expression of taste receptors in the gut. For example:

  • Enhanced SCFA production may make sweet-tasting foods more satisfying because the gut’s response to sweetness is heightened.

  • Bitter compounds may become more noticeable or less noticeable depending on how the fiber impacts their bioavailability and T2R activation.

6. Fiber’s Effect on Gut Hormones and Appetite Regulation

• Fiber influences T1R and T2R receptor activity through its impact on gut hormones:

  • SCFAs, produced during fiber fermentation, can activate sweet receptors (T1Rs) and promote the release of GLP-1, a hormone that plays a key role in reducing appetite and enhancing insulin sensitivity.

  • Bitter compounds, released through fermentation, can activate T2Rs, triggering the release of CCK and PYY, hormones involved in satiety and digestion.

Summary of Key Mechanisms:

Practical Example:

• Inulin (a prebiotic fiber) promotes the growth of Lactobacilli, which enhances butyrate production. Butyrate can then activate T1R receptors, promoting satiety and improving insulin sensitivity. Additionally, fiber fermentation may produce phenolic compounds that activate T2R receptors, contributing to enhanced gut motility and satiety.

 Conclusion:

Prebiotics like fiber influence gut taste receptors through their fermentation by gut microbiota, leading to the production of SCFAs and bitter compounds that activate T1R (sweet) and T2R (bitter) receptors. This activation affects appetite regulation, satiety, and digestion, offering an exciting link between dietary fiber, gut microbiota, and taste perception.

Would you like to explore specific types of fiber or probiotic-fiber combinations and their impact on gut taste receptor signaling in more detail?

Yes, both T1R and T2R receptors are present in the colon, along with other parts of the gastrointestinal tract. These receptors are found in various regions of the gut, including the small intestine and colon, and they play an important role in the detection of tastants (e.g., sweet, umami, and bitter compounds) that influence digestion, satiety, and gut motility.

Here’s a breakdown of where these receptors are found and how they function in the colon:

1. T1R Receptors (Sweet and Umami) in the Colon

• T1R1/T1R3: These receptors are typically involved in detecting umami (savoury) tastes, and they can be found in various parts of the gut, including the colon.

• T1R2/T1R3: These receptors are involved in detecting sweet compounds and are also expressed in the colon. They are activated by sugars or sweet-tasting compounds.

  • In the colon, activation of T1Rs by sweet compounds (such as glucose or SCFAs, which are products of fiber fermentation) can influence gut motility and satiety by stimulating the release of glucagon-like peptide 1 (GLP-1) and other appetite-regulating hormones.

  • Sweet taste receptors are also involved in sensing SCFAs (like acetate and butyrate), which are produced from the fermentation of dietary fiber by the gut microbiota. This interaction helps regulate appetite, insulin secretion, and overall gut health.

2. T2R Receptors (Bitter) in the Colon

• T2Rs are primarily involved in detecting bitter compounds, and they are also found in the colon, especially in the epithelial cells of the intestinal lining.

  • T2Rs in the colon can be activated by bitter compounds such as polyphenols, alkaloids, and other bitter-tasting molecules from food or microbial fermentation.

  • Activation of T2Rs in the colon triggers a variety of responses:

    • Increased secretion of digestive enzymes

    • Alteration of gut motility

    • Modulation of appetite and satiety by influencing the release of cholecystokinin (CCK) and PYY (peptide YY).

    • Immune modulation, as T2Rs are involved in the detection of microbial signals and regulating inflammation in the gut.

3. Functional Implications in the Colon

• The presence of T1R and T2R receptors in the colon is important for gut homeostasis and digestive processes. These receptors help the colon:

  • Sense nutrients (like sugars, amino acids, and bitter compounds) that enter the gut, which then triggers appropriate physiological responses.

  • Regulate gut hormones that affect satiety (fullness) and intestinal motility.

  • Influence immune responses and potentially contribute to gut health by regulating the balance of the gut microbiota and inflammatory pathways.

Summary of T1R and T2R Presence in the Colon:

 Conclusion:

Both T1R and T2R receptors are present in the colon, where they play a significant role in sensing tastants (such as sweet, umami, and bitter compounds) that influence gut motility, satiety, and hormonal regulation. Their activation is important for digestive health and appetite regulation, linking gut microbiota activity and food intake.

Would you like more details on the functional roles of these receptors or specific compounds that activate them in the colon?