We have collected 5 of the most relevant and most frequently asked questions for you and will answer them here. Scroll down to read answers to:
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We actually receive this question quite a lot and it’s a very relevant one. ‘Who am I?’ is one of life’s big questions that will always be complex to answer. It’s the same for people and companies. Especially one as old as Perstorp, which has been around since ! Even back then acids were important as one of the first products by the company was acetic acid. Over the decades since then Perstorp has made a habit of reinventing itself successfully to blossom into the world-leading specialty chemicals company that it is today, boasting a total of around 1.500 employees all over the world enjoying a rich company culture.
Since you’re following this channel, one might assume that you have an interest in our animal nutrition team within Perstorp. Animal Nutrition is one of Perstorp’s main segments today and started its business in the s. Similar to the entire Perstorp Group, Perstorp Animal Nutrition has reinvented itself over time. It has grown from supplying organic acids for silage and grain preservation exclusively, to a solution and science driven team that prides itself in being the first to introduce innovative new molecules to the market and package them into holistic solutions that can support gut health, acidify feed or help optimize dEB – to name but a few. Perstorp produces key organic acids such as propionic acid, formic acid, butyric acid and valeric acid. Perstorp Animal Nutrition has researched those molecules and their results in animal nutrition and focused on finding the best ways to apply them. Today that often means combining several esterified organic acids with other compounds for broad functionality and synergetic effects for specific goals, such as growth or facing weaning challenges.
It is our mission to remove the concerns our customers may have about the gut health of their animals. Through the products we create, but also through the advice we can supply from the combined knowledge and decades of experience in our team.
The presence of butyric acid in the gastrointestinal tract was discovered a long time ago and some of its benefits became clear shortly after. Adding butyric acid products to animal nutrition is far from a new practice. However, two challenges had to be overcome in order to effectively deliver the potential advantages of butyric acid to farm animals.
Firstly, the odor of pure butyric acid had to be managed. Even humans can detect the unpleasant scent at as little as 10 parts per million. Secondly butyric acid does its best work in the gastrointestinal tract (GIT). Simply adding it to feed means that it will be rapidly absorbed in the upper gastrointestinal tract, often before reaching the intestinal areas where it could potentially support epithelial cells.
Up until around the most common solution tackling both these challenges was to coat with sodium butyrate. The idea is that the coating protects the butyric acid from evaporating (no smell) and it protects it in the stomach until the fat coating is broken down in the GIT for release where it makes a difference. These products have proven effective and are still available today. There is however always a compromise between efficacy of the coating versus the concentration of butyric acid in the product. More stable coatings often delay release until the large intestine, which may reduce the potential benefits for small intestine health. Products with a low percentage of coating are more likely to release the acid and spread that undesired smell. Products with a high percentage of coating don’t display that drawback, but instead require higher dosage in the feed as the concentration of butyric acid is much lower, taking the place of nutrients or other additives.
In Perstorp had researched the workings of a new butyric acid solution for animal feed and launched ProPhorce™ SR (tributyrins) to the market. This innovative solution is created through an esterification process combining butyric acid with glycerol. The new molecule that is formed contains 3 butyric acid molecules attached to the glycerol backbone. Tributyrins overcome the challenges presented by butyric acid effectively. The product has a high concentration of butyric acid, and is stable until released under the influence of lipase enzymes act on it in the gastrointestinal tract. A breakthrough in animal nutrition!
Fast forward a decade or so and the benefits of tributyrins have not remained unnoticed by the market. However, as with any established technology, quality variations have emerged between different tributyrin products. Today new challenges face the market as not all tributyrins are created equal. Producing consistent, high-quality tributyrins requires specialized knowledge and access to premium raw materials, along with controlled esterification processes.
ProPhorce™ SR products remain a benchmark in their field for product stability, consistency, quality and concentration levels. If you’re in the market for a dry product, the flowability of many dry tributyrin solutions is also something to evaluate your sources on. ProPhorce™ SR 130 leaves many competitor products in the dust (pun intended) in that regard. Lastly there is the real proof.
As ProPhorce™ SR is the original tributyrin solution, the extensive body of research and field trial data accumulated over years of use is unmatched. This provides users with substantial technical support and reference material when making their product selection. When you choose ProPhorce™ SR, you also choose for that unmatched technical background.
One of the questions we get most often nowadays is about the dosage of one of our most recent innovations: Gastrivix™ Avi and it’s dosing. Customers want to know if dosing at only 250 grams per ton is recommendable?
Gut health remains a key factor in broiler production. When intestinal function is supported, birds may utilize nutrients more effectively, which can contribute to consistent production cycles.
Perstorp was the first to produce and successfully trial the commercial use of esterified valeric acid in animal nutrition. Like butyric acid, valeric acid also occurs naturally in broilers’ gut microbiota, however typical production within the animal are limited. We have applied our well-established esterification technique, successfully used in our ProPhorce™ SR brand, and have adapted it to valeric acid. By combining valeric and butyric acid esters, we’ve developed Gastrivix™ Avi – a blend designed to support intestinal morphology, barrier function, and microbial balance. After five years of research into this synergistic approach, our trials suggest optimal inclusion levels under controlled conditions: 500 g/t in starter and early grower phases, reducing to 250 g/t during finisher phases. These levels were selected based on observed outcomes regarding nutrient utilization and intestinal health markers.
Since we all know optimal conditions are rarely perfect, farm-specific factors like chick quality, housing systems, and health challenges all influence results. We’d love to connect, understand your reality, and create a tailor-made dosing program just for you! All so you can experience the magic of growth you only get with Gastrivix™ Avi!
ProPhorce™ SR 130 sets itself apart from competition not just by the advanced technology behind it, but also by the superior quality of the raw materials and carrier used. Perstorp controls the entire production process, from the selection of top-tier ingredients to the final product. This integration ensures that the butyric acid, glycerol, and carrier are of the highest quality, leading to a product that excels in flowability, particle size distribution and thermostability.
The quality of the carrier used for the butyric acid in ProPhorce™ SR 130 plays a crucial role in maintaining the integrity of the product during mixing and feed production. This attention to detail results in a product that is not only effective but also easy to handle and incorporate into various feed formulations.
In a recent test conducted in the Asia-Pacific region, five samples from different batches of shrimp feed were analyzed for butyric acid content after pelleting. The results showcased an impressive average recovery rate of 92%, with all samples falling within a 90–95% recovery range. This consistency ensures that the product retains its efficacy from production to consumption, delivering reliable performance when it matters most.
If you'd like to learn more, we're happy to share additional insights. Don't hesitate to reach out – we'd love to connect and discuss how our product can support your business. Contact Tony >>
One of the latest additions to our portfolio is the combination of butyric and valeric acid glycerides, developed to align with current research into nutritional strategies for monogastric diets. Both of these short-chain fatty acids occur naturally in the intestinal tract. Given the growing scientific interest in this area, we are frequently asked about the latest findings related to this combination.
Butyric acid (BA) and valeric acid (VA) are naturally occurring short chain fatty acids produced by the gut microbiota and play essential roles in animal health. While naturally present, targeted supplementation depends on effective delivery systems. Our esterification technology facilitates the controlled release of BA and VA along the gastrointestinal tract. By binding these acids to glycerol (as mono-, di-, and tri-esters), we aim to:
Butyric acid (BA) has been studied in animal nutrition in relation to intestinal morphology and epithelial structure. It is known to act as an energy source for specific intestinal cells and has been reported in studies to support features such as villus height and epithelial integrity.
Valeric acid (VA), while less widely studied, has been investigated for its potential role in animal nutrition. Studies on VA glyceride esters have reported numerical improvements in performance indicators such as feed conversion ratio (FCR) and intestinal morphology, including villus-to-crypt ratios.
Recent trial data indicate that a combination of BA and VA glycerides may yield more consistent results than individual acids alone. Poeikhampha et al. () compared a BA-VA blend to tributyrin in broilers, observing improved average FCR (1.37 vs. 1.42 in controls) and body weight gain. The authors noted a potential positive effect with the 2 acids compared to butyrin’s alone.
Similarly, Gracia et al. () evaluated a butyric acid and valeric acid glycerides blend across six trials in Europe. The trials showed higher final body weights (+2.5%), improved FCR (1.58 vs. 1.60), and lower finisher-phase mortality in supplemented groups. The authors discussed these observations in the context of potential product effects on gut-related performance factors.
Perstorp’s pioneering work with valeric acid, combined with our deep understanding of the balance between valeric and butyric acids, highlights the crucial role this synergy plays in our solutions. Our work continues to explore how these components interact under commercial production conditions.
Butyric acid ( ; from Ancient Greek: βούτῡρον, meaning "butter"), also known under the systematic name butanoic acid, is a straight-chain alkyl carboxylic acid with the chemical formula CH3CH2CH2COOH. It is an oily, colorless liquid with an unpleasant odor. Isobutyric acid (2-methylpropanoic acid) is an isomer. Salts and esters of butyric acid are known as butyrates or butanoates. The acid does not occur widely in nature, but its esters are widespread. It is a common industrial chemical[7] and an important component in the mammalian gut.
Butyric acid was first observed in an impure form in by the French chemist Michel Eugène Chevreul. By , he had purified it sufficiently to characterize it. However, Chevreul did not publish his early research on butyric acid; instead, he deposited his findings in manuscript form with the secretary of the Academy of Sciences in Paris, France. Henri Braconnot, another French chemist, was also researching the composition of butter and was publishing his findings and this led to disputes about priority. As early as , Chevreul claimed that he had found the substance responsible for the smell of butter.[8] By , he published some of his findings regarding the properties of butyric acid and named it.[9] However, it was not until that he presented the properties of butyric acid in detail.[10] The name butyric acid comes from βούτῡρον, meaning "butter", the substance in which it was first found. The Latin name butyrum (or buturum) is similar.
Triglycerides of butyric acid make up 3–4% of butter. When butter goes rancid, butyric acid is liberated from the glyceride by hydrolysis.[11] It is one of the fatty acid subgroup called short-chain fatty acids. Butyric acid is a typical carboxylic acid that reacts with bases and affects many metals.[12] It is found in animal fat and plant oils, bovine milk, breast milk, butter, parmesan cheese, body odor, vomit and as a product of anaerobic fermentation (including in the colon).[13][14] It has a taste somewhat like butter and an unpleasant odor. Mammals with good scent detection abilities, such as dogs, can detect it at 10 parts per billion, whereas humans can detect it only in concentrations above 10 parts per million. In food manufacturing, it is used as a flavoring agent.[15]
In humans, butyric acid is one of two primary endogenous agonists of human hydroxycarboxylic acid receptor 2 ( HCA2), a Gi/o-coupled G protein-coupled receptor.[16][17]
Butyric acid is present as its octyl ester in parsnip (Pastinaca sativa)[18] and in the seed of the ginkgo tree.[19]
In industry, butyric acid is produced by hydroformylation from propene and syngas, forming butyraldehyde, which is oxidised to the final product.[7]
H2 + CO + CH3CH=CH2 → CH3CH2CH2CHOoxidation→butyric acidIt can be separated from aqueous solutions by saturation with salts such as calcium chloride. The calcium salt, Ca(C4H7O2)2 · H2O, is less soluble in hot water than in cold.
Butyrate is produced by several fermentation processes performed by obligate anaerobic bacteria.[20] This fermentation pathway was discovered by Louis Pasteur in . Examples of butyrate-producing species of bacteria:
The pathway starts with the glycolytic cleavage of glucose to two molecules of pyruvate, as happens in most organisms. Pyruvate is oxidized into acetyl coenzyme A catalyzed by pyruvate:ferredoxin oxidoreductase. Two molecules of carbon dioxide ( CO2) and two molecules of hydrogen ( H2) are formed as waste products. Subsequently, ATP is produced in the last step of the fermentation. Three molecules of ATP are produced for each glucose molecule, a relatively high yield. The balanced equation for this fermentation is
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C6H12O6 → C4H8O2 + 2CO2 + 2H2Other pathways to butyrate include succinate reduction and crotonate disproportionation.
Action Responsible enzyme Acetyl coenzyme A converts into acetoacetyl coenzyme A acetyl-CoA-acetyl transferase Acetoacetyl coenzyme A converts into β-hydroxybutyryl CoA β-hydroxybutyryl-CoA dehydrogenase β-hydroxybutyryl CoA converts into crotonyl CoA crotonase Crotonyl CoA converts into butyryl CoA (CH3CH2CH2C=O−CoA) butyryl CoA dehydrogenase A phosphate group replaces CoA to form butyryl phosphate phosphobutyrylase The phosphate group joins ADP to form ATP and butyrate butyrate kinaseSeveral species form acetone and n-butanol in an alternative pathway, which starts as butyrate fermentation. Some of these species are:
These bacteria begin with butyrate fermentation, as described above, but, when the pH drops below 5, they switch into butanol and acetone production to prevent further lowering of the pH. Two molecules of butanol are formed for each molecule of acetone.
The change in the pathway occurs after acetoacetyl CoA formation. This intermediate then takes two possible pathways:
For commercial purposes Clostridium species are used preferably for butyric acid or butanol production. The most common species used for probiotics is the Clostridium butyricum.[21]
Highly-fermentable fiber residues, such as those from resistant starch, oat bran, pectin, and guar are transformed by colonic bacteria into short-chain fatty acids (SCFA) including butyrate, producing more SCFA than less fermentable fibers such as celluloses.[14][22] One study found that resistant starch consistently produces more butyrate than other types of dietary fiber.[23] The production of SCFA from fibers in ruminant animals such as cattle is responsible for the butyrate content of milk and butter.[13][24]
Fructans are another source of prebiotic soluble dietary fibers which can be digested to produce butyrate.[25] They are often found in the soluble fibers of foods which are high in sulfur, such as the allium and cruciferous vegetables. Sources of fructans include wheat (although some wheat strains such as spelt contain lower amounts),[26] rye, barley, onion, garlic, Jerusalem and globe artichoke, asparagus, beetroot, chicory, dandelion leaves, leek, radicchio, the white part of spring onion, broccoli, brussels sprouts, cabbage, fennel, and prebiotics, such as fructooligosaccharides (FOS), oligofructose, and inulin.[27][28]
Butyric acid reacts as a typical carboxylic acid: it can form amide, ester, anhydride, and chloride derivatives.[29] The latter, butyryl chloride, is commonly used as the intermediate to obtain the others.
Butyric acid is used in the preparation of various butyrate esters. It is used to produce cellulose acetate butyrate (CAB), which is used in a wide variety of tools, paints, and coatings, and is more resistant to degradation than cellulose acetate.[30] CAB can degrade with exposure to heat and moisture, releasing butyric acid.[31]
Low-molecular-weight esters of butyric acid, such as methyl butyrate, have mostly pleasant aromas or tastes.[7] As a consequence, they are used as food and perfume additives. It is an approved food flavoring in the EU FLAVIS database (number 08.005).
Due to its powerful odor, it has also been used as a fishing bait additive.[32] Many of the commercially available flavors used in carp (Cyprinus carpio) baits use butyric acid as their ester base. It is not clear whether fish are attracted by the butyric acid itself or the substances added to it. Butyric acid was one of the few organic acids shown to be palatable for both tench and bitterling.[33]
The substance has been used as a stink bomb by the Sea Shepherd Conservation Society to disrupt Japanese whaling crews.[34] The Dutch branch of Extinction Rebellion has used it as a chemical agent in a clothing store; several people who became unwell were treated on site by an ambulance crew.[35]
Butyric acid (pKa 4.82) is fully ionized at physiological pH, so its anion is the material that is mainly relevant in biological systems. It is one of two primary endogenous agonists of human hydroxycarboxylic acid receptor 2 ( HCA2, also known as GPR109A), a Gi/o-coupled G protein-coupled receptor (GPCR),[16][17]
Like other short-chain fatty acids (SCFAs), butyrate is an agonist at the free fatty acid receptors FFAR2 and FFAR3, which function as nutrient sensors that facilitate the homeostatic control of energy balance; however, among the group of SCFAs, only butyrate is an agonist of HCA2.[38][39][40] It is also an HDAC inhibitor (specifically, HDAC1, HDAC2, HDAC3, and HDAC8),[36][37] a drug that inhibits the function of histone deacetylase enzymes, thereby favoring an acetylated state of histones in cells.[40] Histone acetylation loosens the structure of chromatin by reducing the electrostatic attraction between histones and DNA.[40] In general, it is thought that transcription factors will be unable to access regions where histones are tightly associated with DNA (i.e., non-acetylated, e.g., heterochromatin).[medical citation needed] Therefore, butyric acid is thought to enhance the transcriptional activity at promoters,[40] which are typically silenced or downregulated due to histone deacetylase activity.
Butyrate that is produced in the colon through microbial fermentation of dietary fiber is primarily absorbed and metabolized by colonocytes and the liver[note 1] for the generation of ATP during energy metabolism; however, some butyrate is absorbed in the distal colon, which is not connected to the portal vein, thereby allowing for the systemic distribution of butyrate to multiple organ systems through the circulatory system.[40][41] Butyrate that has reached systemic circulation can readily cross the blood–brain barrier via monocarboxylate transporters (i.e., certain members of the SLC16A group of transporters).[42][43] Other transporters that mediate the passage of butyrate across lipid membranes include SLC5A8 (SMCT1), SLC27A1 (FATP1), and SLC27A4 (FATP4).[36][43]
Butyric acid is metabolized by various human XM-ligases (ACSM1, ACSM2B, ASCM3, ACSM4, ACSM5, and ACSM6), also known as butyrate–CoA ligase.[44][45] The metabolite produced by this reaction is butyryl–CoA, and is produced as follows:[44]
Adenosine triphosphate + butyric acid + coenzyme A → adenosine monophosphate + pyrophosphate + butyryl-CoAAs a short-chain fatty acid, butyrate is metabolized by mitochondria as an energy (i.e., adenosine triphosphate or ATP) source through fatty acid metabolism.[40] In particular, it is an important energy source for cells lining the mammalian colon (colonocytes).[25] Without butyrates, colon cells undergo autophagy (i.e., self-digestion) and die.[46]
In humans, the butyrate precursor tributyrin, which is naturally present in butter, is metabolized by triacylglycerol lipase into dibutyrin and butyrate through the reaction:[47]
Tributyrin + H2O → dibutyrin + butyric acidButyrate has numerous effects on energy homeostasis and related diseases (diabetes and obesity), inflammation, and immune function (e.g., it has pronounced antimicrobial and anticarcinogenic effects) in humans. These effects occur through its metabolism by mitochondria to generate ATP during fatty acid metabolism or through one or more of its histone-modifying enzyme targets (i.e., the class I histone deacetylases) and G-protein coupled receptor targets (i.e., FFAR2, FFAR3, and HCA2).[38][48]
Butyrate is essential to host immune homeostasis.[38] Although the role and importance of butyrate in the gut is not fully understood, many researchers argue that a depletion of butyrate-producing bacteria in patients with several vasculitic conditions is essential to the pathogenesis of these disorders. A depletion of butyrate in the gut is typically caused by an absence or depletion of butyrate-producing-bacteria (BPB). This depletion in BPB leads to microbial dysbiosis. This is characterized by an overall low biodiversity and a depletion of key butyrate-producing members. Butyrate is an essential microbial metabolite with a vital role as a modulator of proper immune function in the host. It has been shown that children lacking in BPB are more susceptible to allergic disease[49] and type 1 diabetes.[50] Butyrate is also reduced in a diet low in dietary fiber, which can induce inflammation and have other adverse affects insofar as these short-chain fatty acids activate PPAR-γ.[51]
Butyrate exerts a key role for the maintenance of immune homeostasis both locally (in the gut) and systemically (via circulating butyrate). It has been shown to promote the differentiation of regulatory T cells. In particular, circulating butyrate prompts the generation of extrathymic regulatory T cells. The low-levels of butyrate in human subjects could favor reduced regulatory T cell-mediated control, thus promoting a powerful immuno-pathological T-cell response.[52] On the other hand, gut butyrate has been reported to inhibit local pro-inflammatory cytokines. The absence or depletion of these BPB in the gut could therefore be a possible aide in the overly-active inflammatory response. Butyrate in the gut also protects the integrity of the intestinal epithelial barrier. Decreased butyrate levels therefore lead to a damaged or dysfunctional intestinal epithelial barrier.[53] Butyrate reduction has also been associated with Clostridioides difficile proliferation. Conversely, a high-fiber diet results in higher butyric acid concentration and inhibition of C. difficile growth.[54]
In a research study conducted by Furusawa et al., microbe-derived butyrate was found to be essential in inducing the differentiation of colonic regulatory T cells in mice. This is of great importance and possibly relevant to the pathogenesis and vasculitis associated with many inflammatory diseases because regulatory T cells have a central role in the suppression of inflammatory and allergic responses.[55] In several research studies, it has been demonstrated that butyrate induced the differentiation of regulatory T cells in vitro and in vivo.[56] The anti-inflammatory capacity of butyrate has been extensively analyzed and supported by many studies. It has been found that microorganism-produced butyrate expedites the production of regulatory T cells, although the specific mechanism by which it does so is unclear.[57] More recently, it has been shown that butyrate plays an essential and direct role in modulating gene expression of cytotoxic T-cells.[58] Butyrate also has an anti-inflammatory effect on neutrophils, reducing their migration to wounds. This effect is mediated via the receptor HCA1.[59]
In the gut microbiomes found in the class Mammalia, omnivores and herbivores have butyrate-producing bacterial communities dominated by the butyryl-CoA:acetate CoA-transferase pathway, whereas carnivores have butyrate-producing bacterial communities dominated by the butyrate kinase pathway.[60]
The odor of butyric acid, which emanates from the sebaceous follicles of all mammals, works on ticks as a signal.
Butyrate's effects on the immune system are mediated through the inhibition of class I histone deacetylases and activation of its G-protein coupled receptor targets: HCA2 (GPR109A), FFAR2 (GPR43), and FFAR3 (GPR41).[39][61] Among the short-chain fatty acids, butyrate is the most potent promoter of intestinal regulatory T cells in vitro and the only one among the group that is an HCA2 ligand.[39] It has been shown to be a critical mediator of the colonic inflammatory response. It possesses both preventive and therapeutic potential to counteract inflammation-mediated ulcerative colitis and colorectal cancer.
Butyrate has established antimicrobial properties in humans that are mediated through the antimicrobial peptide LL-37, which it induces via HDAC inhibition on histone H3.[61][62][63] In vitro, butyrate increases gene expression of FOXP3 (the transcription regulator for Tregs) and promotes colonic regulatory T cells (Tregs) through the inhibition of class I histone deacetylases;[39][61] through these actions, it increases the expression of interleukin 10, an anti-inflammatory cytokine.[61][39] Butyrate also suppresses colonic inflammation by inhibiting the IFN-γ–STAT1 signaling pathways, which is mediated partially through histone deacetylase inhibition. While transient IFN-γ signaling is generally associated with normal host immune response, chronic IFN-γ signaling is often associated with chronic inflammation. It has been shown that butyrate inhibits activity of HDAC1 that is bound to the Fas gene promoter in T cells, resulting in hyperacetylation of the Fas promoter and up-regulation of Fas receptor on the T-cell surface.[64]
Similar to other HCA2 agonists studied, butyrate also produces marked anti-inflammatory effects in a variety of tissues, including the brain, gastrointestinal tract, skin, and vascular tissue.[65][66][67] Butyrate binding at FFAR3 induces neuropeptide Y release and promotes the functional homeostasis of colonic mucosa and the enteric immune system.[68]
Butyrate has been shown to be a critical mediator of the colonic inflammatory response. It is responsible for about 70% of energy from the colonocytes, being a critical SCFA in colon homeostasis.[69] Butyrate possesses both preventive and therapeutic potential to counteract inflammation-mediated ulcerative colitis (UC) and colorectal cancer.[70] It produces different effects in healthy and cancerous cells; this is known as the "butyrate paradox". In particular, butyrate inhibits colonic tumor cells and stimulates proliferation of healthy colonic epithelial cells.[71][72] The explanation why butyrate is an energy source for normal colonocytes and induces apoptosis in colon cancer cells, is the Warburg effect in cancer cells, which leads to butyrate not being properly metabolized. This phenomenon leads to the accumulation of butyrate in the nucleus, acting as a histone deacetylase (HDAC) inhibitor.[73] One mechanism underlying butyrate function in suppression of colonic inflammation is inhibition of the IFN-γ/STAT1 signalling pathways. It has been shown that butyrate inhibits activity of HDAC1 that is bound to the Fas gene promoter in T cells, resulting in hyperacetylation of the Fas promoter and upregulation of Fas receptor on the T cell surface. It is thus suggested that butyrate enhances apoptosis of T cells in the colonic tissue and thereby eliminates the source of inflammation (IFN-γ production).[74] Butyrate inhibits angiogenesis by inactivating Sp1 transcription factor activity and downregulating vascular endothelial growth factor gene expression.[75]
In summary, the production of volatile fatty acids such as butyrate from fermentable fibers may contribute to the role of dietary fiber in colon cancer. Short-chain fatty acids, which include butyric acid, are produced by beneficial colonic bacteria (probiotics) that feed on, or ferment prebiotics, which are plant products that contain dietary fiber. These short-chain fatty acids benefit the colonocytes by increasing energy production, and may protect against colon cancer by inhibiting cell proliferation.[22]
Conversely, some researchers have sought to eliminate butyrate and consider it a potential cancer driver.[76] Studies in mice indicate it drives transformation of MSH2-deficient colon epithelial cells.[77]
Owing to the importance of butyrate as an inflammatory regulator and immune system contributor, butyrate depletions could be a key factor influencing the pathogenesis of many vasculitic conditions. It is thus essential to maintain healthy levels of butyrate in the gut. Fecal microbiota transplants (to restore BPB and symbiosis in the gut) could be effective by replenishing butyrate levels. In this treatment, a healthy individual donates their stool to be transplanted into an individual with dysbiosis. A less-invasive treatment option is the administration of butyrate—as oral supplements or enemas—which has been shown to be very effective in terminating symptoms of inflammation with minimal-to-no side-effects. In a study where patients with ulcerative colitis were treated with butyrate enemas, inflammation decreased significantly, and bleeding ceased completely after butyrate provision.[78]
Butyric acid is an HDACTooltip histone deacetylase inhibitor that is selective for class I HDACs in humans.[36] HDACs are histone-modifying enzymes that can cause histone deacetylation and repression of gene expression. HDACs are important regulators of synaptic formation, synaptic plasticity, and long-term memory formation. Class I HDACs are known to be involved in mediating the development of an addiction.[79][80][81] Butyric acid and other HDAC inhibitors have been used in preclinical research to assess the transcriptional, neural, and behavioral effects of HDAC inhibition in animals addicted to drugs.[81][82][83]
The butyrate or butanoate ion, C3H7COO−, is the conjugate base of butyric acid. It is the form found in biological systems at physiological pH. A butyric (or butanoic) compound is a carboxylate salt or ester of butyric acid.
This article incorporates text from a publication now in the public domain: Chisholm, Hugh, ed. (). "Butyric Acid". Encyclopædia Britannica (11th ed.). Cambridge University Press.
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