Lit Review Friday · Why butyrate is still the sexy metabolite · Published 2026 · Reading time ~24 minutes

---

The Finding That Ran Cause and Effect Backwards

Butyrate has been the celebrity of microbiome science for a decade, and it earned the position honestly. It is the short chain fatty acid your gut bacteria produce when they ferment fiber, and it is the preferred fuel of the cells lining your colon. Not glucose delivered by your bloodstream, which is what almost every other cell in your body runs on. A fermentation byproduct, manufactured on site, by organisms that are not you.

Donohoe and colleagues established the dependency in 2011 in Cell Metabolism. Take the bacteria away and colonocytes fall into an energy deficit, turning to autophagy, consuming their own components to stay alive. Restore butyrate and the deficit resolves. It is one of the cleanest demonstrations in the field that a human tissue has outsourced part of its metabolism to a microbial community.

The paper anchoring this week's episode approaches that relationship from the opposite direction, and the reversal is what makes it interesting. Gabandé-Rodríguez and colleagues, publishing in Nature Communications in 2026, were not studying the microbiome. They were studying mitochondrial disease. What they found on the way through is that when the host's own energy machinery fails, the bacterial output fails with it.

What They Did

The team built a tamoxifen-inducible, whole-body knockout of TFAM, the mitochondrial transcription factor A, a nuclear-encoded protein required to maintain mitochondrial DNA. Switching it off in adult mice produces progressive mitochondrial decline across many tissues at once. The resulting animals develop lipodystrophy, sarcopenia, metabolic disruption, kidney failure, neurodegeneration and impaired movement, and they die early.

Critically, they did not rely on a single model. They repeated the key gut observations in mtDNA-mutator mice, animals carrying a proofreading-deficient version of mitochondrial DNA polymerase gamma, which accumulate mitochondrial mutations through an entirely different mechanism. Two independent routes to mitochondrial failure, one shared consequence.

Measurements included 16S rRNA sequencing of the gut community, targeted quantification of short chain fatty acids by UPLC-MS/MS, intestinal histology and barrier assessment, a fecal microbiota transplant arm using healthy donor animals, a dietary arm supplying tributyrin at 10 percent of the diet by weight, and immunoblots of histone acylation marks in intestinal tissue.

What They Found

The intestine was not spared by the systemic collapse. Barrier integrity was disrupted, crypts atrophied, proliferating cells in the crypts declined, and the senescence marker P21 rose in the ileum. Alongside the structural damage, microbial output dropped.

The mechanism the authors landed on is epigenetic rather than energetic, and it is the most interesting chemistry in the paper.

Butyrate is not just the signal. It is the ink.

DNA is wound around histone proteins, and small chemical groups are attached to those histones to control which genes can be read. The familiar modification is acetylation: attach an acetyl group to a lysine residue and the associated gene becomes more accessible. What this team measured alongside acetylation is a second modification, butyrylation, and it is exactly what the name suggests. The butyrate molecule itself is covalently attached to lysine residues on histone H3, at positions 9 and 27.

This is a meaningful distinction. Butyrate is not merely signaling to the enzymes that modify chromatin, in the way an HDAC inhibitor does. It is serving as the acyl donor. The bacterial fermentation product becomes a physical, covalent component of the epigenetic mark itself. Combined with the two roles already established, that gives one small molecule three distinct jobs: mitochondrial fuel, regulator of the enzymes that write chromatin marks, and the chemical raw material those marks are made from.

In the TFAM-deficient mice, all three marks measured in the ileum fell: H3K9 acetylation (P=0.0016), H3K9 butyrylation (P=0.0004) and H3K27 butyrylation (P=0.0067).

Tributyrin supplementation restored all three marks in the TFAM-deficient animals (H3K9ac P=0.0225, H3K9bu P=0.0353, H3K27bu P=0.035). Bulk RNA sequencing of the ileum then showed that treated animals clustered with healthy controls rather than with untreated knockouts.

And the genes that returned are the ones that matter for everything else in this article. Examining transcripts previously reported to depend on the H3K27 butyrylation mark, the authors found tributyrin upregulated genes governing cell-to-cell junction architecture (Tjp2, encoding tight junction protein 2, along with Cdh2 and Dsp), cytoskeletal organization (Nck2, Rhpn2, Dyrk1a, Krt78) and the oxidative stress response (Jun, Src). Separately, the broader transcriptome showed recovery of genes for mucosal structural integrity (Vill, Krt80, Loxl1, Matn2) and immune regulation (FoxP3, Ctla4).

That is the chain worth carrying out of this paper. Bacteria ferment fiber into butyrate. Butyrate is written directly onto chromatin as a covalent mark. The genes that mark governs include the ones that physically construct the seal between intestinal cells. Which is the mechanistic floor beneath the claim, made later in this article, that butyrate's contribution to the rest of the body runs through a barrier that holds.

And the authors are direct about why they think the molecule performed at least as well as the transplant. Tributyrin, in their words, provides a sustained source of butyrate directly, bypassing the need for bacterial colonization, whereas the transplant strategy depends on successful engraftment of a healthy microbiota into what they describe as a hostile intestinal environment.

The Loop That Keeps the Whole Thing Running

To understand why a defect in the host's mitochondria should change bacterial chemistry, you need the loop, which we built in detail in the hydrogen sulfide episode and will summarize rather than repeat here.

Colonocytes oxidize butyrate in their own mitochondria. That oxidation consumes oxygen, and the consumption is what keeps the interior of the colon nearly anaerobic. Anaerobic conditions are precisely what the butyrate-producing bacteria require, because oxygen is lethal to them. The bacteria then produce the butyrate that fuels the colonocytes that consume the oxygen. Kelly and colleagues (2015) showed that this oxidation stabilizes epithelial HIF, which in turn strengthens barrier function.

Byndloss and colleagues (2017) demonstrated what happens when the loop breaks. When colonocyte metabolism shifts away from fatty acid oxidation, oxygen leaks into the lumen and facultative anaerobes expand into the space. Litvak, Byndloss and Bäumler summarized the principle in Science in 2018 under a title that could serve as this article's thesis: colonocyte metabolism shapes the gut microbiota. More recently, Ribeiro Castro and colleagues (2025) showed that dietary inulin drives epithelial hypoxia and HIF-1 stabilization only when microbes are present to ferment it. No fermentation, no signal, no benefit to the lining.

Kroon and colleagues (2025) broke the same loop from the outside. A single sublethal systemic pulse of bacterial endotoxin in mice raised oxygen species in the caecum, and commensal fermentation halted within hours, with no change in which bacteria were present or how many. Acetate and butyrate fell, the resident community shifted its transcription toward damage repair, and oxygen-tolerant opportunists bloomed by orders of magnitude. Same organisms, same diet, different output, driven entirely by the chemical environment.

Gabandé-Rodríguez breaks it from the inside. Let the host's own power plants fail, and the habitat stops supporting the organisms that make the fuel those power plants would have used.

How Much Butyrate Does Your Gut Actually Make?

This is where the story stops being purely mechanistic and starts having consequences for what anyone should do.

Total colonic short chain fatty acid production is conventionally estimated at 400 to 600 millimoles per day, with butyrate representing roughly 15 to 20 percent of the pool. Butyric acid has a molar mass of 88.11 grams per mole. Run the arithmetic and you land somewhere between about five and ten grams of butyrate per day in a healthy adult.

Grams is a startling quantity for a signaling molecule. It is also a quantity no capsule delivers. And that mismatch is the beginning of a more interesting question than "how do I get more."

Why Doesn't Butyrate Reach Your Bloodstream?

Cummings and colleagues answered the first half of this in 1987, in a study that remains a reference point almost forty years later. They measured short chain fatty acids in the contents of every region of the large intestine, and in portal, hepatic and peripheral venous blood, in people who had died suddenly and were sampled within four hours.

Concentrations were high throughout the colon, running from 131 millimoles per kilogram in the caecum down to 80 in the descending colon, with pH tracking inversely from 5.6 to 6.6. In blood, total short chain fatty acids measured 375 micromoles per liter in the portal vein, 148 in the hepatic vein, and 79 in peripheral blood. The molar ratios shifted at each step, and the authors attributed the pattern to greater uptake of butyrate by the colonic epithelium and of propionate by the liver.

Bloemen and colleagues (2009) measured the same question directly and quantitatively, in living people. Twenty-two patients undergoing major upper abdominal surgery had blood sampled simultaneously from a radial artery, the portal vein and a hepatic vein, with blood flow measured by intraoperative Duplex ultrasonography.

So there are two extraction stages, not one. The colonocytes take most of it where it is made. The liver removes much of the remainder. Butyrate is the short chain fatty acid least likely to reach your general circulation, and the reason is not that something has gone wrong. The reason is that it is the most useful, and nobody upstream is willing to let any of it go.

Which reframes what butyrate actually is. It is not a compound that circulates and finds its targets. It is a continuous local manufacturing process, running all day, with the customer standing at the end of the production line. You are not trying to raise a blood level. You are trying to restart a process.

So Where Does the Anti-Inflammatory Reputation Come From?

If butyrate barely leaves the gut, and butyrate is famous for calming inflammation, something has to reconcile those two facts. Two things do, and they work differently.

The cousins travel

Acetate and propionate do reach general circulation, as Bloemen's numbers show. Trompette and colleagues demonstrated in Nature Medicine in 2014 what that traffic can do. Mice fed a diet high in fermentable fiber showed increased circulating short chain fatty acids and were protected against allergic inflammation in the lung, while a low-fiber diet lowered circulating levels and worsened the disease. The mechanism ran through the bone marrow: propionate altered hematopoiesis, generating macrophage and dendritic cell precursors that seeded the lung with cells having high phagocytic capacity but an impaired ability to drive type 2 helper T cell responses. The effect depended on GPR41.

That is fermentation in the colon reprogramming immune cell production in the bone marrow and changing inflammation in an organ nowhere near the gut. Note that the effector was propionate, which is exactly consistent with Bloemen. The molecule that gets out is the molecule that does the distant work.

The local immune work is better characterized still. Arpaia and colleagues (Nature, 2013) and Smith and colleagues (Science, 2013) independently showed that short chain fatty acids, butyrate prominently among them, drive the generation and homeostasis of regulatory T cells in the colon. Vinolo and colleagues (2011) showed short chain fatty acids direct neutrophil chemotaxis through GPR43.

Butyrate prevents a problem rather than delivering a benefit

The second route is indirect, and it may be the larger one. Butyrate feeds the cells that hold the barrier closed and, through HIF stabilization, actively strengthens that barrier (Kelly 2015; Beisner 2021). A barrier that holds keeps bacterial fragments where they belong instead of trickling into circulation and holding the immune system at a low simmer for decades.

On this account, butyrate's contribution to the rest of your body is largely that it stops something bad from happening. Lose fermentation and you lose three things simultaneously: the fuel for the epithelium, the integrity of the wall, and the circulating signals that reach distant tissue.

In people, the association is measurable. Ma and colleagues (2021, Genome Medicine) profiled the gut microbiomes of 307 generally healthy men by shotgun metagenomic and metatranscriptomic sequencing alongside long-term and recent fiber intake, using plasma C-reactive protein as the marker of chronic inflammation. Greater fiber intake was associated with significantly greater CRP reduction, most strongly for fruit-derived fiber such as pectin. The size of the effect depended on microbiome configuration, notably on Prevotella copri status. Same fiber, different ecosystems, different inflammatory outcomes.

The Same Molecule, Two Completely Different Jobs

Of everything in this literature, one finding does the most work for understanding why context matters more than compound, and it comes from Donohoe and colleagues again, this time in Molecular Cell in 2012.

In a normally respiring colonocyte, butyrate is oxidized in the mitochondria to acetyl-CoA. Acetyl-CoA is not only an energy currency: it is also the substrate that histone acetyltransferases use to acetylate histones. So even when butyrate is behaving as fuel, it is driving histone acetylation on the way through.

In a cell that has shifted toward glycolysis, the Warburg state characteristic of tumor cells, butyrate is not oxidized. It accumulates and inhibits histone deacetylases instead. Both routes increase histone acetylation. They upregulate different target genes.

And the functional consequence inverts. Butyrate stimulated the proliferation of normal colonocytes. It inhibited the proliferation of cancerous colonocytes undergoing the Warburg effect. When the authors prevented the Warburg effect from occurring in those cancerous cells, butyrate went back to stimulating them.

The same molecule. The same cell type. Two different mechanisms and opposite effects on growth, determined by nothing except the metabolic state of the cell receiving it. It is not that butyrate is inherently anti-proliferative or inherently pro-growth. It does what the receiving cell's metabolism dictates.

This also explains why the Gabandé-Rodríguez readout was histone acylation rather than energy status. When mitochondrial oxidation is compromised, butyrate's fate changes, and its epigenetic role becomes the visible one.

What Actually Raises Butyrate in People?

Three honest answers, in descending order of how much they change the system.

Feed the organisms that make it

Fermentable substrate is the only intervention that produces butyrate at the scale the colon produces it. Fiber, resistant starch, and prebiotic carbohydrates are what the butyrate producers actually consume. Birkeland and colleagues (2020) showed inulin-type fructans shifting fecal microbiota and short chain fatty acid profiles in a randomized controlled trial.

But it does not work equally for everyone, and the exception is instructive rather than discouraging. Long and colleagues (2025, Cell Metabolism) ran a randomized placebo-controlled trial of resistant starch plus an independent multicenter replication. In the first trial, 22 of 89 participants in the resistant starch arm were low responders, about 24.7 percent. The replication found 20 of 55, about 36.4 percent. Transplanting responder and non-responder microbiota into mice carried the effect with the microbiome, establishing that baseline gut community was causal. The mechanism they identified is competitive: Prevotella suppressed the starch-degrading bacteria, and supplementing a Bifidobacterium pseudocatenulatum strain restored the conversion. The converters were present. They were being outcompeted.

Deliver butyrate in a form that survives the trip

Plain oral butyrate is largely absorbed in the upper gastrointestinal tract before it reaches the colon, which is why delivery chemistry exists. Clarke and colleagues (2011) showed that butyrate esterified to starch is released in the human gastrointestinal tract. Tributyrin, a triglyceride ester of butyric acid, is the form used in the anchor paper.

It is worth being precise about the dose gap, because it is easy to misread. The mice in Gabandé-Rodríguez received tributyrin at 10 percent of their diet by weight, for life. Scaled to a person by conventional allometric methods, that lands in the tens of grams per day, which is not a supplement anyone takes. But the mice were attempting to replace an entire failed manufacturing system in an animal engineered to lack one. Human supplemental doses in the range of a gram to two grams are doing a different and smaller job: supporting the gut lining while the ecosystem recovers. That is a bridge, not a replacement, and the distinction is the useful one.

Repair the environment that permits the conversion

This is the least developed of the three and, on the evidence above, the most consequential. If inflammation floods the lumen with oxygen (Kroon 2025), if colonocyte metabolism shifts away from fatty acid oxidation (Byndloss 2017), or if the host's mitochondria fail (Gabandé-Rodríguez 2026), then substrate alone will not produce the output. You can eat the fiber and not get the metabolite.

Environment Over Precursor

This is the pattern the last several episodes keep arriving at from different directions, and it is worth stating plainly. The precursor is necessary and not sufficient. Choline can become acetylcholine or it can become TMAO. Fiber can become short chain fatty acids or, in an inflamed and oxidative gut, something less useful. Butyrate can be burned as fuel or accumulate as an epigenetic modifier. In every case, what decides is the state of the system doing the converting.

The food is the easy part. The hard part is the ecosystem.

This is where Thaena's work sits, and it is worth being explicit about what is and is not established. ThaenaBiotic contains butyrate at microgram concentrations. Against five to ten grams a day of endogenous production, that is not a delivery mechanism, and we have never believed it was. Whatever the preparation does, it does not do it by supplying butyrate.

The hypothesis we are pursuing is different. A full-spectrum postbiotic derived from screened healthy human donors carries something no single compound does: the emergent chemistry that only appears in a functional microbial community, more than 10,000 molecular signals, and the possibility of shifting the metabolic environment rather than substituting for one of its products. Our own preclinical work is consistent with that idea. In a Caenorhabditis elegans model of oxidative stress, run against a vitamin C comparator dosed molar-for-molar against the oxidant, ThaenaBiotic produced a substantially broader transcriptional response, and the aging-related and neuronal pathway enrichments in the human-ortholog gene set appeared for ThaenaBiotic and not for vitamin C.

That is a worm, and that work is not yet published. The literature is consistent with the broader thesis. It is not a hypothesis that any single trial has proven. ThaenaBiotic is one tool in your toolbox, and the toolbox matters more than any tool in it.

The Honest Limitations

The anchor paper is mice with engineered mitochondrial disease. Not aging humans. The TFAM knockout and the mtDNA-mutator model are genetic tools for producing mitochondrial failure quickly, and neither reproduces the gradual decline of normal human aging. The bridge from these animals to a person is an inference, and it should be labeled as one.

No human trial has tested butyrate or tributyrin for lifespan or healthspan. The lifespan numbers in this article are mouse numbers from disease models.

The systemic inflammation evidence is associational in humans. Ma and colleagues measured associations in an observational cohort. Trompette's causal mechanism is mouse work. Bloemen's measurements are human and direct but describe physiology, not outcomes.

The daily production figure is an estimate. See the caveat above. Five to ten grams is a defensible range built on assumptions about total production and butyrate's share of the pool.

Direction of causation in human aging is unresolved. Older people have different mitochondria and different microbiomes. Which drives which, in people, is not settled.

---

Frequently Asked Questions

Should I take a butyrate supplement?

That is a question for you and your clinician, and the useful framing is what job you expect it to do. A supplement cannot reproduce the several grams a day a healthy colon manufactures and consumes on site. Delivery forms such as tributyrin are designed to reach the colon rather than being absorbed early, and can support the gut lining, but they work alongside a fermenting ecosystem rather than replacing one.

Why does butyrate barely show up in blood tests?

Because it is consumed twice before it could get there. Colon cells use it as their preferred fuel at the site of production, and the liver removes much of what escapes, as Bloemen and colleagues (2009) measured directly in people during surgery. Low circulating butyrate is the normal state, not a deficiency signal.

Does fiber lower inflammation?

In observational human data, higher fiber intake is associated with lower markers of chronic inflammation, and Ma and colleagues (2021) found that association in 307 adults using C-reactive protein. The strength of the association varied with which microbes were present, which suggests the conversion step matters as much as the intake.

Why does fiber work for some people and not others?

Because the organisms doing the fermenting differ between people. In two human trials of resistant starch, Long and colleagues (2025) found roughly a quarter to a third of participants responded poorly, and transplanting their microbiomes into mice carried the poor response along with it. Competition between resident organisms, not absence of the right ones, explained much of the difference.

Is a little leaky gut a good thing?

The evidence does not support that idea, at least not as a route for beneficial molecules to enter. Short chain fatty acids cross the gut lining through dedicated transporters rather than through gaps between cells. And the transient permeability that follows hard exercise reflects the gut temporarily losing blood flow, which van Wijck and colleagues (2011) documented alongside markers of cell damage.

What is the difference between a probiotic, a prebiotic and a postbiotic?

A probiotic supplies live organisms, a prebiotic supplies the substrate those organisms ferment, and a postbiotic supplies the molecules a microbial community produces, without live bacteria. The anchor paper offers an unusually direct comparison of the first and third approaches: the authors note that delivering the molecule bypasses the need for bacterial colonization, while a transplant depends on organisms successfully establishing in an inhospitable gut.

---

The Bottom Line

There is no molecule here that substitutes for an ecosystem doing its job. There are several things that support one while it recovers. Those are different claims, and the difference is where most of the confusion in this category lives.

---

References

1. Gabandé-Rodríguez E, Gómez de las Heras MM, Ramírez-Ruiz de Erenchun P, et al. Butyrate extends health and lifespan in mice with mitochondrial deficiency. Nature Communications. 2026;17:3909. https://doi.org/10.1038/s41467-026-70547-4 · FREE FULL TEXT
2. Donohoe DR, Garge N, Zhang X, et al. The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon. Cell Metabolism. 2011;13(5):517-526. https://doi.org/10.1016/j.cmet.2011.02.018 · FREE FULL TEXT
3. Donohoe DR, Collins LB, Wali A, Bigler R, Sun W, Bultman SJ. The Warburg effect dictates the mechanism of butyrate-mediated histone acetylation and cell proliferation. Molecular Cell. 2012;48(4):612-626. https://doi.org/10.1016/j.molcel.2012.08.033 · FREE FULL TEXT
4. Cummings JH, Pomare EW, Branch WJ, Naylor CM, Macfarlane GT. Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut. 1987;28(10):1221-1227. https://doi.org/10.1136/gut.28.10.1221 · FREE FULL TEXT
5. Bloemen JG, Venema K, van de Poll MC, Olde Damink SW, Buurman WA, Dejong CH. Short chain fatty acids exchange across the gut and liver in humans measured at surgery. Clinical Nutrition. 2009;28(6):657-661. https://doi.org/10.1016/j.clnu.2009.05.011
6. Trompette A, Gollwitzer ES, Yadava K, et al. Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis. Nature Medicine. 2014;20(2):159-166. https://doi.org/10.1038/nm.3444
7. Ma W, Nguyen LH, Song M, et al. Dietary fiber intake, the gut microbiome, and chronic systemic inflammation in a cohort of adult men. Genome Medicine. 2021;13:102. https://doi.org/10.1186/s13073-021-00921-y · FREE FULL TEXT
8. Long X, Wang H, Lu Y, et al. Interindividual variability in gut microbiome mediates the efficacy of resistant starch on MASLD. Cell Metabolism. 2025;37(12):2342-2361.e9. https://doi.org/10.1016/j.cmet.2025.10.017 · FREE FULL TEXT
9. Kelly CJ, Zheng L, Campbell EL, et al. Crosstalk between microbiota-derived short-chain fatty acids and intestinal epithelial HIF augments tissue barrier function. Cell Host & Microbe. 2015;17(5):662-671. https://doi.org/10.1016/j.chom.2015.03.005 · FREE FULL TEXT
10. Byndloss MX, Olsan EE, Rivera-Chávez F, et al. Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. Science. 2017;357(6351):570-575. https://doi.org/10.1126/science.aam9949 · FREE FULL TEXT
11. Litvak Y, Byndloss MX, Bäumler AJ. Colonocyte metabolism shapes the gut microbiota. Science. 2018;362(6418):eaat9076. https://doi.org/10.1126/science.aat9076 · FREE FULL TEXT
12. Ribeiro Castro P, Corrêa RO, Sérvulo Cruz Angelim MK, et al. HIF-1 attenuates high-fiber diet-mediated proliferation and stemness of colonic epithelium. Gut Microbes. 2025;17(1). https://doi.org/10.1080/19490976.2025.2543123 · FREE FULL TEXT
13. Kroon S, Malcic D, Weidert L, et al. Sublethal systemic LPS in mice enables gut-luminal pathogens to bloom through oxygen species-mediated microbiota inhibition. Nature Communications. 2025;16. https://doi.org/10.1038/s41467-025-57979-0 · FREE FULL TEXT
14. Arpaia N, Campbell C, Fan X, et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature. 2013;504(7480):451-455. https://doi.org/10.1038/nature12726 · FREE FULL TEXT
15. Smith PM, Howitt MR, Panikov N, et al. The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis. Science. 2013;341(6145):569-573. https://doi.org/10.1126/science.1241165 · FREE FULL TEXT
16. Vinolo MA, Ferguson GJ, Kulkarni S, et al. SCFAs induce mouse neutrophil chemotaxis through the GPR43 receptor. PLoS One. 2011;6(6):e21205. https://doi.org/10.1371/journal.pone.0021205 · FREE FULL TEXT
17. Salvi PS, Cowles RA. Butyrate and the intestinal epithelium: modulation of proliferation and inflammation in homeostasis and disease. Cells. 2021;10(7):1775. https://doi.org/10.3390/cells10071775 · FREE FULL TEXT
18. Cuff MA, Lambert DW, Shirazi-Beechey SP. Substrate-induced regulation of the human colonic monocarboxylate transporter, MCT1. Journal of Physiology. 2002;539(Pt 2):361-371. https://doi.org/10.1113/jphysiol.2001.014241 · FREE FULL TEXT
19. van Wijck K, Lenaerts K, van Loon LJ, Peters WH, Buurman WA, Dejong CH. Exercise-induced splanchnic hypoperfusion results in gut dysfunction in healthy men. PLoS One. 2011;6(7):e22366. https://doi.org/10.1371/journal.pone.0022366 · FREE FULL TEXT
20. den Besten G, van Eunen K, Groen AK, Venema K, Reijngoud DJ, Bakker BM. The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. Journal of Lipid Research. 2013;54(9):2325-2340. https://doi.org/10.1194/jlr.R036012 · FREE FULL TEXT
21. Beisner J, Filipe Rosa L, Kaden-Volynets V, Stolzer I, Günther C, Bischoff SC. Prebiotic inulin and sodium butyrate attenuate obesity-induced intestinal barrier dysfunction by induction of antimicrobial peptides. Frontiers in Immunology. 2021;12:678360. https://doi.org/10.3389/fimmu.2021.678360 · FREE FULL TEXT
22. Clarke JM, Topping DL, Christophersen CT, et al. Butyrate esterified to starch is released in the human gastrointestinal tract. American Journal of Clinical Nutrition. 2011;94(5):1276-1283. https://doi.org/10.3945/ajcn.111.017228
23. Birkeland E, Gharagozlian S, Birkeland KI, et al. Prebiotic effect of inulin-type fructans on faecal microbiota and short-chain fatty acids in type 2 diabetes: a randomised controlled trial. European Journal of Nutrition. 2020;59(7):3325-3338. https://doi.org/10.1007/s00394-020-02282-5 · FREE FULL TEXT
24. Rath E, Moschetta A, Haller D. Mitochondrial function: gatekeeper of intestinal epithelial cell homeostasis. Nature Reviews Gastroenterology & Hepatology. 2018;15(8):497-516. https://doi.org/10.1038/s41575-018-0021-x

This post accompanies the Lit Review Friday episode of Learn Something with Thaena.