Scientific References

About this page

This page summarizes published, peer-reviewed research on ingredient categories used in gut-health supplements positioned for appetite and metabolic support: probiotic strains, prebiotic fibers, postbiotic compounds, pasteurized bacteria and botanical extracts. It also describes, separately and with its design stated, one company-sponsored laboratory study of the ingredient combination. It does not describe results of any finished product. No finished product has been tested in a published clinical trial.

Effects reported in clinical trials depend on the strain, the dose, the form in which an ingredient was given, the duration and the population studied, and are typically modest. Where a study tested a single named strain or a specific dose, the strain and dose are identified; results obtained with one strain or dose should not be assumed to apply to other strains, lower doses or other forms. Where the amount studied differs from amounts commonly used in supplements, this is stated. The literature was searched through November 2026; statements that no study exists refer to that search.

About amounts. Clinical trials often use larger amounts of an ingredient than are practical or customary in a multi-ingredient supplement, and several of the ingredients described here have been studied in people only at amounts higher than those used in the formulation described on this page. This page reports the amounts used in each study next to the amount in the formulation so that readers can judge the difference for themselves. A result obtained at a higher amount has not been shown to occur at a lower amount, and this page does not claim that it does. The formulation was designed as a combination of ingredients acting on the same gut pathways; the only evidence on the combination itself is the laboratory fermentation study described below, which did not involve people. Where human evidence at the formulation’s amount is lacking, this is stated in the relevant section.

GLP-1 (glucagon-like peptide-1) is a hormone released by intestinal L-cells after meals; it slows gastric emptying, stimulates insulin release and increases satiety. Dietary supplements do not contain GLP-1 and are not GLP-1 receptor agonist medicines. Studies cited here that measured GLP-1 measured the body's own hormone response to a food component, under the conditions described in each study.

These statements have not been evaluated by the Food and Drug Administration. The ingredients described are not intended to diagnose, treat, cure or prevent any disease.

GLP-1 and the gut: what human studies show

The body's own GLP-1 release can be influenced by what reaches the lower gut. Short-chain fatty acids (SCFA: acetate, propionate, butyrate) produced when gut bacteria ferment fiber and other substrates are one of the signals that stimulate the L-cells that release GLP-1 and PYY. This has been shown in human colonic cells and, under specific conditions, in people [1–3].

Delivering SCFA to the human colon. In a randomized crossover study, a single 10 g dose of inulin-propionate ester, designed to release propionate in the colon, increased postprandial plasma PYY and GLP-1 and reduced energy intake in overweight adults; over 24 weeks, 10 g/day reduced weight gain and intra-abdominal fat compared with inulin alone (n = 60) [1]. In a small crossover study in six hyperinsulinaemic women, plasma GLP-1 and PYY rose more after acetate than after saline, and more after rectal infusions (60 mmol, about 4.9 g sodium acetate) than after intravenous ones (20 mmol); rectal infusion of saline alone also raised these hormones, so part of the effect reflects distension of the rectum rather than acetate itself [2]. In 12 overweight or obese men, rectal infusions of SCFA mixtures high in acetate, propionate or butyrate increased PYY, fasting fat oxidation and (for acetate and propionate) resting energy expenditure; GLP-1 was not reported as a significant outcome [3]. These studies used gram-level amounts of SCFA or SCFA precursors delivered directly to the colon; they did not test oral supplements.

Capsaicin and GLP-1. In a crossover study of 30 adults, a lunch containing 1.03 g red pepper (80,000 Scoville heat units) produced a higher plasma GLP-1 concentration at one early time point than a control lunch (p < 0.05); the GLP-1 area under the curve, PYY, ghrelin, satiety ratings and energy expenditure did not differ significantly [4]. This is a single-meal effect with culinary amounts of pepper; see the cayenne section for amounts.

Company-sponsored laboratory study of the ingredient combination. The combination of the probiotic blend (B. animalis subsp. lactis B420 and L. gasseri SBT2055, 15 billion CFU) with the substrate blend (Sukré 400 mg, triacetin 200 mg, cayenne 50 mg, pasteurized Akkermansia muciniphila 10 mg) was tested on the company’s behalf by a contract laboratory (Cryptobiotix, Belgium; the same laboratory conducted the supplier-funded triacetin study cited below) in an ex vivo gut-fermentation model (SIFR®) using stool microbiota from six adults with obesity, incubated for 24 hours [5]. Compared with an untreated control, the substrate blend increased acetate, propionate (+47%) and butyrate (+123%) and reduced branched-chain fatty acids; the full combination increased butyrate further (+146%, significantly more than the substrate blend alone) and propionate (+52%, not significantly different). A synergistic increase in the amino-acid metabolite 2-aminoadipic acid was also observed. The findings are described in a US provisional patent application filed in September 2026 (patent pending) and have not been peer-reviewed or published in a journal.

What this does and does not show. The laboratory study shows that the ingredient combination increases SCFA production by human gut microbiota in a fermentation model. It did not involve people taking the ingredients, did not measure GLP-1, and cannot show effects on appetite or body weight. Whether the SCFA increase seen in the model occurs in the gut of a person taking these amounts, and whether it is large enough to change GLP-1 release, has not been tested. No human study has measured GLP-1 after intake of this ingredient combination.

Probiotics and body weight

Probiotic supplementation has been tested in dozens of randomized controlled trials in adults with overweight or obesity, with small average effects. An umbrella review pooling 29 meta-analyses (14,366 participants) estimated average reductions of about 0.4 kg in body weight and 0.2 kg/m² in BMI versus control [6]. A systematic review of 105 articles on randomized trials (6,826 subjects), several of whose authors were affiliated with a dairy company, found that in overweight (but not obese) subjects probiotics reduced body weight (−0.94 kg), BMI, waist circumference, fat mass (−0.96 kg) and visceral adipose tissue, mainly with mixtures containing bifidobacteria and certain lactobacilli [7]. A meta-analysis of 15 trials (957 subjects) found reductions in weight (−0.60 kg), BMI and fat percentage, which the authors described as small [8].

Bifidobacterium animalis subsp. lactis B420 (HOWARU® Shape). One randomized, double-blind, placebo-controlled trial has tested this strain in people: 225 adults with BMI 28–35 took B420 (10 billion CFU/day), polydextrose fiber (12 g/day), both, or placebo for 6 months with no diet or lifestyle intervention [9]. In the pre-specified intention-to-treat analysis, no group differed from placebo on the primary outcome, DXA body fat mass. In the per-protocol analysis (134 participants), B420 with polydextrose reduced body fat by 1.4 kg versus placebo (−4.5%, p = 0.02); B420 alone reduced it by about 1.0 kg, which was not statistically significant (p = 0.28). Participants taking B420, with or without fiber, reported eating about 230–320 kcal/day less than at baseline (per-protocol, food diaries). A post-hoc analysis pooling both B420 groups reported lower body fat (−4%), trunk fat and waist circumference (−2.4 cm). Stool analyses from the same trial showed increases in Lactobacillus and Akkermansia with B420 [10]. The manufacturer funded the trial and employed several of its authors; a company review summarizes the program [11]. We found no human B420 study that measured GLP-1 or other appetite hormones. A second, larger trial (418 adults, B420 10 billion CFU/day with a lifestyle program, completed 2022) has not been published [12].

Lactobacillus gasseri SBT2055. Two randomized, double-blind, placebo-controlled trials in Japanese adults with abdominal obesity, both using fermented milk made by the strain's manufacturer, found reductions in visceral fat measured by CT. In 87 adults taking 200 g/day for 12 weeks (about 2 × 10¹⁰ CFU/day), visceral fat area fell by 4.6% and body weight by 1.4% from baseline, with no significant change in the control group [13]. In 210 adults taking 200 g/day for 12 weeks at 10⁶ or 10⁷ CFU/g (about 2 × 10⁸ to 2 × 10⁹ CFU/day), visceral fat area fell by 8.5% and 8.2% from baseline at week 12 with no significant change in the control group; BMI, waist, hip and body fat also decreased, and the effects diminished within 4 weeks of stopping [14]. A 7-day study in 30 healthy adults (about 5 × 10⁹ CFU/day) found a within-group increase in fecal fat excretion that was not significantly different from placebo (p = 0.086) [15]. The strain's manufacturer employed most authors of these studies. We found no human SBT2055 study that measured GLP-1 or appetite hormones.

Amounts and combinations. The tested formulation provides 10 billion CFU of B420 and 5 billion CFU of SBT2055 per day in capsules. The B420 amount matches the trial dose, but the trial's significant result was obtained with 12 g/day of polydextrose added, which the formulation does not contain. The SBT2055 amount falls within the range used in the 2013 trial, but all SBT2055 trials used fermented milk rather than capsules and were conducted in Japanese adults. We found no study that tested B420 and SBT2055 together. Results obtained with one strain do not apply to other strains of the same species.

Pasteurized Akkermansia muciniphila

Akkermansia muciniphila is a mucus-dwelling gut bacterium whose abundance is lower in people with obesity and metabolic disease. Heat-killed (pasteurized) cells have been tested in three randomized, placebo-controlled trials in people, all at 10–30 billion cells per day.

In a 3-month pilot trial in 40 overweight or obese, insulin-resistant adults (32 completed, about 11 per group across placebo, live and pasteurized arms), 10 billion pasteurized cells/day improved insulin sensitivity (+28.6%, p = 0.002), lowered fasting insulin (−34%, p = 0.006) and total cholesterol (−8.7%, p = 0.02); body weight (−2.27 kg, p = 0.091), fat mass and hip circumference decreased without reaching statistical significance [16]. In a 16-week trial in 143 adults with metabolic syndrome, 30 billion pasteurized cells/day did not improve the primary outcome, whole-body insulin sensitivity; exploratory analyses reported a larger GLP-1 response to an oral glucose load and better hepatic insulin sensitivity in some subgroups, findings the authors describe as hypothesis-generating [17]. In a 2026 trial, 90 adults with overweight or obesity first followed an 8-week low-energy diet; those who lost at least 8% of their weight (80 completed the study) then took pasteurized A. muciniphila (30 billion cells/day, the dose reported by the manufacturer) or placebo for 24 weeks. Weight regain was 1.2 kg with A. muciniphila versus 3.2 kg with placebo (p = 0.012), the diet-induced gain in insulin sensitivity was preserved, and GLP-1 concentrations did not differ between groups [18]. The strain's manufacturer (The Akkermansia Company) employed or advised authors of all three trials. The European Food Safety Authority considers pasteurized A. muciniphila safe for adults, other than pregnant and breastfeeding women, at up to 34 billion cells/day [19].

Amounts. The tested formulation provides 10 mg of pasteurized A. muciniphila, which the manufacturer specifies as about 1 billion total fluorescent units (cells) per day. This is one-tenth of the dose used in the 2019 pilot trial and one-thirtieth of the dose used in the 2026 trials. We found no human trial of 1 billion cells/day, so the results above cannot be assumed to apply at this amount.

L-arabinose (Sukré™)

Sukré™ is purified L-arabinose, a naturally occurring five-carbon sugar produced by hydrolysing acacia gum [20]. L-arabinose inhibits sucrase, the intestinal enzyme that splits table sugar; when it is eaten together with sucrose, less sucrose is digested in the upper small intestine, the rise in blood glucose and insulin is smaller, and more sugar reaches the lower gut, where it stimulates GLP-1 release. All human studies are single-meal studies; none has tested L-arabinose on appetite, energy intake or body weight over time.

In 15 healthy men, adding 1, 2 or 3 g L-arabinose to a drink containing 75 g sucrose reduced the glucose and insulin peaks dose-dependently; at 3 g the insulin peak was about a third lower and the GLP-1 response significantly higher than with sucrose alone, with no effect on appetite ratings or energy intake at the next meal [21]. In 23 healthy adults, 5 g L-arabinose in a 50 g sucrose drink tripled the GLP-1 response (area under the curve 268 vs 803 pM·min, p < 0.001), lowered the glucose peak by 15% and the insulin peak by 52%, and did not change appetite or ad libitum food intake [22]. In Japanese adults, L-arabinose at 3–4% of the sucrose in a sucrose-containing food (about 0.9–1.2 g with 30 g sucrose) blunted the post-meal glucose rise; 2% did not [23]. When L-arabinose was added to solid mixed meals (5–10% of carbohydrate), glucose and insulin responses were unchanged [24], and in a drink without sucrose it had no effect on glucose [25].

Amounts. The tested formulation provides 400 mg L-arabinose per day in a capsule. The lowest amount that changed GLP-1 in a human study is 3 g, taken together with 75 g sucrose; the lowest amount that changed post-meal glucose is about 0.9 g with 30 g sucrose. We found no human study of 400 mg, or of L-arabinose taken on its own in a capsule. The published effects depend on a large sucrose load consumed at the same time in liquid form; taken apart from such a meal, L-arabinose has no demonstrated effect.

Triacetin (TriBiome™)

Triacetin (glycerol triacetate) is an ester of glycerol and acetic acid that releases acetate, a short-chain fatty acid, when hydrolysed. It is affirmed by the US FDA as GRAS (generally recognized as safe) for specified uses in foods, as a flavoring agent, formulation aid, humectant and solvent [26] and has an acceptable daily intake “not specified” from the WHO/FAO expert committee, which notes that it is hydrolysed rapidly in the digestive tract [27]. We found no human study of oral triacetin for any metabolic, appetite, hormone or body-weight outcome.

The rationale for its use rests on three separate lines of evidence. First, acetate and other short-chain fatty acids stimulate GLP-1 release from mouse intestinal cells through the receptor FFAR2 (GPR43) [28]; in one small study in people, rectal infusion of acetate in gram amounts was followed by higher GLP-1 and PYY, although rectal infusion of saline alone had a similar effect [2]. Second, in an ex vivo fermentation study using stool microbiota from eight adults with irritable bowel syndrome, a simulated 400 mg dose of encapsulated triacetin (twice the amount in the formulation described here) increased acetate and butyrate production and improved barrier integrity in a gut-cell model; the study was funded by the ingredient supplier and conducted by a contract laboratory, and it did not measure GLP-1 [29]. Third, in the company-sponsored fermentation study described above, the substrate blend containing triacetin increased acetate, propionate and butyrate [5].

Amounts and open questions. The tested formulation provides 200 mg triacetin per day, which can yield at most about 160 mg (2.75 mmol) of acetate. Whether intact triacetin reaches the colon after oral intake has not been shown in people; the WHO/FAO review and animal data indicate hydrolysis and absorption in the upper digestive tract. Human studies in which acetate changed gut hormones used 60 mmol delivered rectally, about 22 times more acetate than 200 mg triacetin can provide. Triacetin itself has no known receptor on intestinal cells; any effect on GLP-1 would be indirect, through acetate, and has not been demonstrated.

Capsaicinoids from cayenne pepper

Capsaicinoids, the pungent compounds in chili peppers, have small, short-term effects on energy intake and energy expenditure in human trials. A meta-analysis of 8 trials (191 participants) found that taking capsaicinoids before a meal reduced energy intake at that meal by about 74 kcal (310 kJ) on average, and concluded that a minimum of 2 mg capsaicinoids is needed for this effect [30]. A meta-analysis of 9 trials found that capsaicin or capsiate raised daily energy expenditure by about 59 kcal (245 kJ) and lowered the respiratory quotient, indicating more fat oxidation; the effect was seen in people with BMI over 25 (about 70 kcal/day) and not in leaner participants [31]. An earlier review of trials in people found that red pepper doses ranged from 0.2 mg to 33 mg per day in foods and up to 130–150 mg of pure capsaicin in capsules, with inconsistent results in people with overweight [32]. In a single-meal study, a lunch containing 1.03 g red pepper (80,000 Scoville heat units) raised GLP-1 at one early time point without changing GLP-1 overall, PYY, satiety or energy expenditure [4].

Amounts. The tested formulation provides 50 mg cayenne pepper powder per day. Cayenne powder is typically rated at 30,000–50,000 Scoville heat units; because pure capsaicin is rated at about 16 million units, such powder contains roughly 0.2–0.3% capsaicinoids, so 50 mg supplies on the order of 0.1–0.15 mg capsaicinoids. This is about 13–21 times less than the 2 mg minimum identified in the energy-intake meta-analysis, and about 35–50 times less capsaicinoid than the 1.03 g of 80,000-unit pepper (roughly 5 mg capsaicinoids) in the single-meal GLP-1 study. A capsaicinoid assay of the cayenne used would replace this estimate. The results above should not be assumed to apply at this amount.

References

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2. Freeland KR, Wolever TMS. Acute effects of intravenous and rectal acetate on glucagon-like peptide-1, peptide YY, ghrelin, adiponectin and tumour necrosis factor-α. Br J Nutr. 2010;103(3):460–466. https://pubmed.ncbi.nlm.nih.gov/19818198/
3. Canfora EE, et al. Colonic infusions of short-chain fatty acid mixtures promote energy metabolism in overweight/obese men: a randomized crossover trial. Sci Rep. 2017;7:2360. https://pubmed.ncbi.nlm.nih.gov/28539646/
4. Smeets AJ, Westerterp-Plantenga MS. The acute effects of a lunch containing capsaicin on energy and substrate utilisation, hormones, and satiety. Eur J Nutr. 2009;48(4):229–234. https://pubmed.ncbi.nlm.nih.gov/19238310/
5. Cryptobiotix (Ghent, Belgium) for Bioma Health, UAB. Ex vivo SIFR® study of a probiotic blend, a substrate blend and their synbiotic combination on the gut microbiota of six adults with obesity. Study report, 2026; described in US provisional patent application “Synbiotic Compositions for Modulating Gut Microbial Metabolism”, filed September 15, 2026. Unpublished, company-sponsored.
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9. Stenman LK, et al. Probiotic with or without fiber controls body fat mass, associated with serum zonulin, in overweight and obese adults – randomized controlled trial. EBioMedicine. 2016;13:190–200. https://pmc.ncbi.nlm.nih.gov/articles/PMC5264483
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11. Uusitupa H-M, et al. Bifidobacterium animalis subsp. lactis 420 for metabolic health: review of the research. Nutrients. 2020;12(4):892. https://doi.org/10.3390/nu12040892 (authors employed by the strain’s manufacturer)
12. ClinicalTrials.gov NCT03934229. The effect of the probiotic B420 on body fat mass in overweight and obese individuals following healthy lifestyle intervention. Completed January 2022; no results posted. https://clinicaltrials.gov/study/NCT03934229
13. Kadooka Y, et al. Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial. Eur J Clin Nutr. 2010;64(6):636–643. https://pubmed.ncbi.nlm.nih.gov/20216555/ (authors employed by the strain’s manufacturer)
14. Kadooka Y, et al. Effect of Lactobacillus gasseri SBT2055 in fermented milk on abdominal adiposity in adults in a randomised controlled trial. Br J Nutr. 2013;110(9):1696–1703. https://doi.org/10.1017/S0007114513001037 (authors employed by the strain’s manufacturer)
15. Ogawa A, et al. Lactobacillus gasseri SBT2055 suppresses fatty acid release through enlargement of fat emulsion size in vitro and promotes fecal fat excretion in healthy Japanese subjects. Lipids Health Dis. 2015;14:20. https://pmc.ncbi.nlm.nih.gov/articles/PMC4391304/
16. Depommier 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. https://doi.org/10.1038/s41591-019-0495-2
17. Suenaert P, Segers A, Rymenans L, et al. Effect of pasteurized Akkermansia muciniphila MucT on insulin sensitivity, body composition, and GLP-1 production in subjects with metabolic syndrome: impact of low baseline gut Akkermansia levels. Gut Microbes. 2026;18(1):2690689. https://doi.org/10.1080/19490976.2026.2690689 (registration NCT05114018; authors employed by the strain’s manufacturer)
18. Mount S, Canfora EE, Jocken JW, et al. Pasteurized Akkermansia muciniphila MucT for weight loss maintenance in people with overweight and obesity: a controlled randomized trial. Nat Med. 2026;32(6):2107–2116. https://pubmed.ncbi.nlm.nih.gov/42120725/
19. EFSA Panel on Nutrition, Novel Foods and Food Allergens. Safety of pasteurised Akkermansia muciniphila as a novel food pursuant to Regulation (EU) 2015/2283. EFSA J. 2021;19(9):6780. https://doi.org/10.2903/j.efsa.2021.6780
20. Dziwenka M, Emmel KV. Genotoxicity and repeat-dose 28-day oral toxicological evaluation of Sukré™, a purified L-arabinose from acacia hydrolysate. Int J Toxicol. 2026;45(2):190–197. https://doi.org/10.1177/10915818251380681 (rat and in vitro safety study; test article supplied by the ingredient’s manufacturer)
21. Krog-Mikkelsen I, Hels O, Tetens I, Holst JJ, Andersen JR, Bukhave K. The effects of L-arabinose on intestinal sucrase activity: dose-response studies in vitro and in humans. Am J Clin Nutr. 2011;94(2):472–478. https://pubmed.ncbi.nlm.nih.gov/21677059/
22. Pol K, Puhlmann M-L, Mars M. Efficacy of L-arabinose in lowering glycemic and insulinemic responses: the modifying effect of starch and fat. Foods. 2022;11(2):157. https://pmc.ncbi.nlm.nih.gov/articles/PMC8774789
23. Inoue S, Sanai K, Seri K. Effect of L-arabinose on blood glucose level after ingestion of sucrose-containing food in human. J Jpn Soc Nutr Food Sci. 2000;53(6):243–247. https://www.jstage.jst.go.jp/article/jsnfs1983/53/6/53_6_243/_article
24. Halschou-Jensen K, Bach Knudsen KE, Nielsen S, Bukhave K, Andersen JR. A mixed diet supplemented with L-arabinose does not alter glycaemic or insulinaemic responses in healthy human subjects. Br J Nutr. 2015;113(1):82–88. https://doi.org/10.1017/S0007114514003407
25. Pol K, de Graaf K, Diepeveen-de Bruin M, Balvers M, Mars M. The effect of replacing sucrose with L-arabinose in drinks and cereal foods on blood glucose and plasma insulin responses in healthy adults. J Funct Foods. 2020;73:104114. https://doi.org/10.1016/j.jff.2020.104114
26. US Food and Drug Administration. 21 CFR §184.1901 Triacetin (GRAS affirmation). https://www.ecfr.gov/current/title-21/chapter-I/subchapter-B/part-184/subpart-B/section-184.1901
27. Joint FAO/WHO Expert Committee on Food Additives (JECFA). Triacetin: toxicological evaluation. WHO Food Additives Series 8, 1975. https://inchem.org/documents/jecfa/jecmono/v08je12.htm
28. Tolhurst G, et al. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes. 2012;61(2):364–371. https://pmc.ncbi.nlm.nih.gov/articles/PMC3266401/ (mouse tissue and cell study)
29. Van den Abbeele P, Poppe J, Baudot A, Vu LD. Triacetin and a mushroom blend restore butyrate production by IBS microbiomes ex vivo, thus promoting barrier integrity. Int J Mol Sci. 2025;26(19):9388. https://www.mdpi.com/1422-0067/26/19/9388 (ex vivo; supplier-funded)
30. Whiting S, Derbyshire EJ, Tiwari B. Could capsaicinoids help to support weight management? A systematic review and meta-analysis of energy intake data. Appetite. 2014;73:183–188. https://pubmed.ncbi.nlm.nih.gov/24246368/
31. Zsiborás C, et al. Capsaicin and capsiate could be appropriate agents for treatment of obesity: a meta-analysis of human studies. Crit Rev Food Sci Nutr. 2018;58(9):1419–1427. https://pubmed.ncbi.nlm.nih.gov/28001433/
32. Ludy M-J, Moore GE, Mattes RD. The effects of capsaicin and capsiate on energy balance: critical review and meta-analyses of studies in humans. Chem Senses. 2012;37(2):103–121. https://pubmed.ncbi.nlm.nih.gov/22038945/