Do probiotics increase GLP-1?

A few specific strains have, in specific groups of people. In published human trials, VSL#3 raised GLP-1 in children with biopsy-confirmed fatty liver disease, and Bifidobacterium breve BBr60 raised both stool butyrate and GLP-1 in adults with obesity. Plenty of other strains have been tested and did nothing. The effect attaches to the individual strain, not to probiotics as a category, so a result for one strain says nothing about the one in your cupboard.

How does fiber affect GLP-1?

Fermentable fiber passes through the small intestine undigested and reaches the colon, where bacteria ferment it into short-chain fatty acids. Those acids are associated with GLP-1 release from L cells in the gut wall. The receptor step is genuinely unsettled, and the amounts of fiber used in the trials that moved GLP-1 were measured in grams per day, not milligrams.

Can a probiotic replace a GLP-1 medication?

No, and nothing in the research suggests otherwise. The GLP-1 your gut releases is cleared from the blood in minutes. The prescription medicines are engineered molecules designed to persist long enough for once-daily or once-weekly dosing, and they are prescribed and monitored by a clinician. Those are different things by orders of magnitude. If you take one of these medicines, talk to your prescriber or pharmacist before adding any supplement.

How much fiber does it take to change GLP-1?

More than most supplements contain. In one crossover trial, 10 grams of a fermentable dextrin raised GLP-1 and PYY while 5 grams did nothing at any timepoint, which is a dose floor measured inside a single study rather than guessed at across studies. The strongest fiber trial estimated that matching its effect with ordinary fermentable fiber would take more than 30 grams a day.

Has anyone measured GLP-1 with the strains in Shroombiosis?

Not in people. Our postbiotic, Bifidobacterium animalis subsp. lactis CECT 8145, has had GLP-1 measured exactly once anywhere, in a study of fifteen male Labrador retrievers. Our probiotic, Bacillus subtilis DE111, has never had GLP-1, appetite or satiety measured in any study we could find.

Do Probiotics or Fiber Raise Your Own GLP-1?

People keep asking me a version of the same question, so I want to answer it properly. Your body makes its own GLP-1. If fiber and bacteria influence the gut cells that release it, can the right supplement do something worth having?

The honest answer is that the mechanism is real, parts of it have been shown in people, and the amounts involved are much larger than what sits in most supplements. I am a pharmacist, and the useful version of this answer is the one with the doses in it.

What GLP-1 is before any medicine is involved

GLP-1 is a hormone released by L cells in the lining of your gut after you eat. It is part of normal digestion and everybody has it.

The important physical fact is how briefly it lasts. Native GLP-1 is broken down by an enzyme called DPP-4 almost immediately. Deacon and colleagues, working on human plasma, described DPP-4 as the primary mechanism of GLP-1 degradation in vitro and said it may have a role in inactivating the peptide in the body. That hedge is theirs and it matters, but either way the hormone is a signal measured in minutes.

The prescription medicines are a different kind of object. They are engineered so they are not cleared quickly, which is what allows once-daily or once-weekly dosing. Anything your gut does on its own operates on a completely different timescale, and that is worth holding onto for the rest of this piece.

The fiber pathway, and where it gets shaky

The proposed chain goes like this. Fermentable fiber survives the small intestine, reaches the colon, and gut bacteria ferment it into short-chain fatty acids. Those acids are then associated with GLP-1 release from nearby L cells.

Measured directly in human colonic contents, total short-chain fatty acids run about 131 mmol/kg in the caecum, falling to around 80 mmol/kg by the descending colon, with acetate the most abundant throughout.

The receptor step is where I would push back on the tidy version of this story. In mice, L cells are enriched for two short-chain fatty acid receptors, FFAR2 and FFAR3, and mice bred without either one show a blunted GLP-1 response. But in an isolated perfused rat colon, a preparation that keeps blood supply and nerves intact, acetate and butyrate raised GLP-1 only after intracellular cAMP had been boosted, propionate did nothing, and a drug that activates those receptors far more potently than the fatty acids themselves had no effect at all. Those authors concluded the fatty acids looked like fuel for colon cells rather than receptor signals.

So the mechanism most articles state as settled is, in the animal work, actively contested.

The best human fiber trial, including the part people skip

The clearest human result did not use ordinary fiber. Researchers bonded propionate to inulin so the propionate is released only once gut bacteria break the inulin down. Isotope tracing showed 82.9% of a 10 gram dose reached the colon.

In twenty healthy volunteers, that dose raised the GLP-1 area under the curve between 240 and 420 minutes to 10,801 min x pmol/L (95% CI 5,897 to 15,704), against 3,495 (95% CI minus 1,567 to 8,558) for the inulin control. PYY rose to 3,349 (95% CI 841 to 5,857) against 429 (95% CI minus 543 to 1,400). Both differences reached significance. Acute food intake at a following meal fell 13.8% on average, about 162 calories, in 16 of the 20 participants.

Here is the part that rarely gets quoted. The same team ran the same supplement for 24 weeks. At the end, GLP-1 had changed by 3.69% (95% CI minus 4.48 to 12.33, p = 0.361), which is to say not at all. The authors themselves raised the possibility of desensitisation over time. They also estimated that reproducing their effect with ordinary fermentable fiber would take more than 30 grams a day.

An acute hormone bump and a sustained change are not the same claim, and the same study produced one and not the other.

The dose floor, measured rather than estimated

The most useful dosing citation I found is a randomised crossover where 10 grams of a fermentable dextrin significantly raised GLP-1 and PYY, and 5 grams did nothing at any timepoint. That floor sits inside a single trial, so it is not an artefact of comparing across studies with different methods.

Our own blend contains 750 mg of acacia fiber per serving. Searching for acacia and GLP-1 together returns two records, both in rats. There is no human GLP-1 data for acacia fiber at any dose.

Acacia has been studied for satiety, with mixed results that track who paid. An industry-run trial found 5 and 10 grams reduced three-hour food intake by more than 60 calories. An independent academic trial of 48 people found effects at 40 grams and not at 20. A 12-week trial in 65 people using an acacia blend found no change in stool short-chain fatty acids at all.

The lowest amount that did anything in a person is around five grams. Ours is 750 mg, and it is in the formula as a prebiotic fiber that feeds the bacteria you already have, which is a different job. Anyone telling you a sub-gram dose of fiber is doing something to your GLP-1 is guessing.

Probiotics: some strains, some people, not a category

This is where the marketing gets loosest, so here is what has actually been measured in humans.

A handful of strains have moved GLP-1 in trials. VSL#3 raised GLP-1 and activated GLP-1 in 44 children with biopsy-proven fatty liver disease. Bifidobacterium breve BBr60 raised stool butyrate and GLP-1 in 65 adults with obesity, which is the clearest human demonstration of the fiber-to-fatty-acid-to-hormone chain working through a bacterium. Both of those are populations with a diagnosed condition, and neither result transfers to a healthy person by default.

Plenty of strains have been tested and done nothing, and the most instructive example is a failure. Lactobacillus casei W8 raised GLP-1 in an isolated pig intestine and raised the GLP-1 gene in piglets. In humans, the same strain did nothing to GLP-1, acutely or across four weeks.

That is the whole problem with this category in one study. A mechanism can work in tissue, work in an animal, and vanish in people. It is also why a result for one strain tells you nothing about another. Two strains of the same species can behave completely differently, which is why the research attaches to strain designations and why a label that names only a species is not telling you much.

Can something that is not alive do this?

Yes, once, in people. A pasteurised, non-living Akkermansia muciniphila preparation increased the GLP-1 rise after a glucose load compared with placebo in 142 adults with metabolic syndrome, at p less than 0.01. The trial's own primary endpoint, a measure of insulin sensitivity, did not differ between groups.

That is a real and interesting finding, and it is also the entire human evidence base for a non-living bacterium moving GLP-1. Worth noting alongside it: the earlier and better-known Akkermansia trial, the one usually cited for this organism, improved insulin sensitivity in 32 completers but never measured GLP-1 and found no significant weight difference.

What has been measured with our own strains

Our postbiotic is Bifidobacterium animalis subsp. lactis CECT 8145, at 100 mg delivering 10 billion cells. Across every study of that strain, GLP-1 has been measured exactly once, in fifteen male Labrador retrievers.

Our probiotic is Bacillus subtilis DE111, at 20 mg delivering 1 billion CFU. GLP-1, appetite and satiety have never been measured with it in any study I could find. Its stool short-chain fatty acids have been measured in humans once, where acetate came out higher than placebo mainly because the placebo group declined, and there was no effect on propionate or butyrate.

A different strain of the same species as our postbiotic did raise GLP-1 in people with type 2 diabetes. That is a species-level result. It is not evidence about our strain.

Nothing in our product has been shown to raise GLP-1 in a person. The biotics are in the formula for gut support, at the amounts their own research used. If you want the reasoning behind those choices, it is in what a tri-biotic actually is and in the difference between prebiotics, probiotics and postbiotics.

The bottom line

Fermentable fiber and a few specific bacterial strains can raise GLP-1 in people, by a modest amount, in trials that used grams of fiber a day and strains with their own evidence. The effect is real at the mechanism level and unreliable at the product level.

If you are taking a prescription GLP-1 medicine, none of this is a substitute for it or an addition to it, and you should talk to your prescriber or pharmacist before adding any supplement, including ours. If you are not, the boring advice is still the best supported one: eat more fermentable fiber from food, where the doses come in grams without anyone having to make a claim about them.

References

Deacon CF, Johnsen AH, Holst JJ. Degradation of glucagon-like peptide-1 by human plasma in vitro yields an N-terminally truncated peptide that is a major endogenous metabolite in vivo. J Clin Endocrinol Metab 1995;80(3):952-7. PMID: 7883856. https://pubmed.ncbi.nlm.nih.gov/7883856/ (opens in new tab) — source for DPP-4 degradation. The paper's own wording is "in vitro" with "may have a role" in vivo.
Cummings JH, Pomare EW, Branch WJ, Naylor CP, Macfarlane GT. Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut 1987;28(10):1221-7. PMID: 3678950. https://pubmed.ncbi.nlm.nih.gov/3678950/ (opens in new tab) — source for the 131 and 80 mmol/kg figures and for acetate being most abundant. It gives no propionate fraction.
Tolhurst G, Heffron H, Lam YS, et al. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes 2012;61(2):364-71. PMID: 22190648. https://pubmed.ncbi.nlm.nih.gov/22190648/ (opens in new tab) — Mouse and cell-culture work.
Christiansen CB, Gabe MBN, Svendsen B, et al. The impact of short-chain fatty acids on GLP-1 and PYY secretion from the isolated perfused rat colon. Am J Physiol Gastrointest Liver Physiol 2018;315(1):G53-G65. PMID: 29494208. https://pubmed.ncbi.nlm.nih.gov/29494208/ (opens in new tab) — the contested receptor step. The cAMP condition is essential to the finding.
Chambers ES, Viardot A, Psichas A, et al. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut 2015;64(11):1744-54. PMID: 25500202. https://pubmed.ncbi.nlm.nih.gov/25500202/ (opens in new tab) — source for the isotope recovery, both area-under-curve figures with their confidence intervals, the 13.8% acute intake reduction, the null 24-week GLP-1 result, and the more-than-30-grams-a-day estimate. The control intervals cross zero, so the areas under the curve are reported side by side rather than as a ratio.
Ye Z, Arumugam V, Haugabrooks E, Williamson P, Hendrich S. Soluble dietary fiber (Fibersol-2) decreased hunger and increased satiety hormones in humans when ingested with a meal. Nutr Res 2015;35(5):393-400. PMID: 25823991. https://pubmed.ncbi.nlm.nih.gov/25823991/ (opens in new tab) — the within-trial dose floor: 10 g raised GLP-1 and PYY, 5 g did not.
Calame W, Thomassen F, Hull S, Viebke C, Siemensma AD. Evaluation of satiety enhancement, including compensation, by blends of gum arabic. Appetite 2011;57(2):358-64. PMID: 21683750. https://pubmed.ncbi.nlm.nih.gov/21683750/ (opens in new tab) — acacia satiety at 5 and 10 g. Industry-run.
Larson R and colleagues. Acacia gum satiety trial. PMID: 33672963. https://pubmed.ncbi.nlm.nih.gov/33672963/ (opens in new tab) — independent academic trial, n=48, satiety effects at 40 g and not at 20 g. The contrast with the industry-run Calame trial, which found an effect at 5 g, is more informative than either result alone.
Eveleens Maarse BC and colleagues. Acacia blend trial. PMID: 38499450. https://pubmed.ncbi.nlm.nih.gov/38499450/ (opens in new tab) — 65 people, 12 weeks, no change in stool short-chain fatty acids.
Alisi A, Bedogni G, Baviera G, et al. Randomised clinical trial: the beneficial effects of VSL#3 in obese children with non-alcoholic steatohepatitis. Aliment Pharmacol Ther 2014;39(11):1276-85. PMID: 24738701. https://pubmed.ncbi.nlm.nih.gov/24738701/ (opens in new tab) — children with biopsy-proven disease. Does not transfer to healthy adults.
Bifidobacterium breve BBr60 trial. PMID: 41455007. https://pubmed.ncbi.nlm.nih.gov/41455007/ (opens in new tab) — 65 adults with obesity; stool butyrate and GLP-1 both rose. The clearest human version of the fiber-to-fatty-acid-to-hormone chain running through a bacterium.
Bjerg AT and colleagues. Lactobacillus paracasei subsp. paracasei W8 work. Appetite 2014;82:111-8 (PMID: 25049132) and Beneficial Microbes 2015;6(1):29-39 (PMID: 25245572). https://pubmed.ncbi.nlm.nih.gov/25049132/ (opens in new tab) and https://pubmed.ncbi.nlm.nih.gov/25245572/ (opens in new tab) — raised the GLP-1 response in an isolated pig intestine and raised GCG expression in piglets, then did nothing to GLP-1 in 21 humans, acutely or across four weeks. The animal-to-human failure described above.
Pasteurised Akkermansia muciniphila trial. PMID: 42343233. https://pubmed.ncbi.nlm.nih.gov/42343233/ (opens in new tab) — 142 adults with metabolic syndrome; the only human trial in which a non-living bacterium moved GLP-1. The post-glucose GLP-1 excursion beat placebo at p less than 0.01, but the trial's pre-specified primary endpoint did not differ between groups.
Depommier C, Everard A, Druart C, et al. Supplementation with Akkermansia muciniphila in overweight and obese human volunteers: a proof-of-concept exploratory study. Nat Med 2019;25(7):1096-1103. PMID: 31263284. https://pubmed.ncbi.nlm.nih.gov/31263284/ (opens in new tab) — insulin sensitivity improved in 32 completers, weight difference not significant, GLP-1 never measured.
Bifidobacterium animalis subsp. lactis MN-Gup trial. PMID: 39719724. https://pubmed.ncbi.nlm.nih.gov/39719724/ (opens in new tab) — same species as our postbiotic, different strain.
CECT 8145 canine study. PMID: 41594449. https://pubmed.ncbi.nlm.nih.gov/41594449/ (opens in new tab) — fifteen male Labrador retrievers; the only GLP-1 measurement that exists for our postbiotic's strain.
Freedman KE, Hill JL, Wei Y, et al. Examining the gastrointestinal and immunomodulatory effects of the novel probiotic Bacillus subtilis DE111. Int J Mol Sci 2021;22(5):2453. PMID: 33671071. https://pubmed.ncbi.nlm.nih.gov/33671071/ (opens in new tab) — the human stool short-chain fatty acid measurement for DE111, including that the acetate difference rested on a decline in the placebo group.