Science & Results

Everything we claim, documented.

The mechanism, the trial data, and the peer-reviewed study behind GLP-1 Biotic Matrix. Written for the curious, with the science intact.

560
subjects in the published cohort study
2024
peer-reviewed, Acta Scientific Medical Sciences
IRB
approved randomized crossover trial
3
clinical studies in the active pipeline

First, what GLP-1 actually does

GLP-1 (glucagon-like peptide-1) is an incretin hormone secreted by intestinal L-cells in response to nutrient intake. It is your body's own post-meal satiety and glucose-regulating signal, acting on four fronts:

Suppresses appetite

Signals the hypothalamus to reduce hunger and food intake (central satiety).

Regulates glucose

Potentiates glucose-dependent insulin secretion, attenuating postprandial spikes.

Slows gastric emptying

Delays nutrient transit, prolonging satiety after a single meal.

Mobilizes fat

Supports lipolysis in white adipose tissue, releasing stored triglycerides.

GLP-1 receptor agonist drugs (semaglutide, tirzepatide) deliver a synthetic analog of this hormone by injection. GLP-1 Biotic Matrix takes the opposite approach: stimulating endogenous (your body's own) GLP-1 secretion via the gut.

The mechanism, step by step

Step 1

Substrates reach the distal gut

One serving delivers a heat-treated postbiotic, fermentable prebiotics, and apple polyphenols to the lower intestine.

Step 2

Fermentation yields SCFAs

Gut microbiota ferment the substrates into short-chain fatty acids (acetate, propionate, butyrate), the endogenous trigger for incretin release.

Step 3

L-cells are activated

SCFAs bind free fatty-acid receptors (FFAR2/3) on enteroendocrine L-cells, the cells that synthesize GLP-1 and its partner peptide PYY.

Step 4

Endogenous GLP-1 is secreted

In vitro, the formula raised GLP-1 secretion by 51.8% and expression of the appetite-suppressing gene PYY by 79.8%.

Step 5

Central satiety, peripheral glucose control

Circulating GLP-1 signals satiety while gastric emptying slows; postprandial glucose excursion is attenuated. Fullness holds 4 to 6 hours.

Step 6

The loop is reinforced daily

Continued substrate feeding sustains microbial SCFA production, maintaining endogenous secretion over time.

Gut to brain: SCFAs activate L-cells, which secrete your own GLP-1.
Human clinical trial

A randomized, controlled, crossover design

Each subject served as their own control, tested on two visits (water vs. formula) 30 minutes before a 75 g oral glucose load, with plasma sampled across 270 minutes.

Design
Randomized, controlled, crossover
Oversight
IRB-approved protocol
Cohort
25 adults, body fat > 25%
Dose
2.15 g formula, 30 min pre-load

Plasma GLP-1 response

Fold-change vs. fasting baseline.

030607590120150270 min +16% pre-meal 4.7x peak vs. control

Endpoints: +16% at 30 min pre-load; 3.8x at 75 min; 4.7x at 90 min vs. water control.

Postprandial glucose, mg/dL

75 g glucose administered at minute 30.

15011080 030607590120150270 min -9.7% at 90 min

Glucose excursion vs. control: 8.0% lower at 60 min; 5.0% at 75 min; 9.7% at 90 min.

Subjects also reported lower postprandial hunger and craving scores in the formula condition, consistent with the hormonal response.

The evidence, at a glance

4.7x
peak plasma GLP-1 vs. control
See data
-9.7%
postprandial glucose excursion
See data
10.8 lbs
mean loss, 8 weeks, 560 subjects
See study
+79.8%
PYY expression in vitro
See data

The 560-subject cohort study

A real-world study of overweight and obese adults using the formula daily, peer-reviewed and published in 2024.

Mean reduction of 4.9 kg (10.8 lbs) over two months, with no adverse events reported.

Equivalent to an approximate weekly energy deficit of 4,725 kcal, achieved without digestive distress or reported side effects.

Chi-Fu C, Yung-Hsiang L, Chen-Chen F, et al. Efficacy of GLP-1 formula on body weight in overweight and obese adults. Acta Scientific Medical Sciences. 2024;8(10):62-67.

In-vitro cell studies

Gene-expression shifts from storage to oxidation

In cell-model testing, the formula up-regulates fat-oxidation pathways and down-regulates lipid-storage regulators. Measured change in relative gene expression:

GLP-1 secretionthe incretin hormone itself
+51.8%
PYYpeptide YY, appetite suppression
+79.8%
UCP1 / UCP2uncoupling proteins, thermogenesis
+4.35x
ATGLadipose triglyceride lipase, first step of lipolysis
+38.8%
GLUT4glucose transporter, uptake into muscle
+20.4%
Lipolysismeasured glycerol release
+20.6%
PLIN1perilipin-1, lipid-droplet shield
-82.3%
PPARG2adipogenesis / fat-storage regulator
-81.2%

Significance vs. untreated control: *p<0.05, **p<0.01, ***p<0.001. In-vitro findings describe mechanism and do not by themselves predict human outcomes; see human data above.

Adipocyte and colonic cell-model assays.

The actives, and the science behind each

A bio-synergetic system: a postbiotic, fermentable prebiotics, and a polyphenol-rich plant extract.

Bifidobacterium breve TC1761 (postbiotic)

A heat-treated, shelf-stable postbiotic. Its cell fragments and metabolites interact with the intestinal epithelium to stimulate L-cell incretin output. In vitro: +51.8% GLP-1 secretion, +79.8% PYY expression.

Kombucha black tea + hydrolyzed soy protein (prebiotics)

Rapidly fermentable substrates that drive microbial production of short-chain fatty acids (acetate, propionate, butyrate), the FFAR2/3 ligands that trigger endogenous GLP-1 release.

Rockit™ apple fruit extract (polyphenols)

Rich in phloridzin and procyanidins. Acts as a natural alpha-glucosidase inhibitor (slowing carbohydrate absorption), directly stimulates GLP-1 release, and up-regulates fat-oxidation genes in adipose tissue.

Gum acacia, erythritol, indigestible maltodextrin (fiber)

Soluble-fiber carriers and osmolytes that mechanically delay gastric emptying, prolonging postprandial satiety.

Made to clinical standards

Third-party testedIdentity and purity verified
Certified facilityStrict quality control
Clean labelNon-GMO, gluten-free, no artificial colors or preservatives
Shelf-stableStable 18 months without preservatives, no cold chain

Where the research goes next

2026

Acute GLP-1 response

IRB-approved crossover study, 25 subjects. Publication submitted.

Completed
2026 Q4

Glycemic control

Randomized, double-blind, placebo-controlled, 100 subjects.

In progress
2027 Q4

Weight management

Randomized, double-blind, placebo-controlled, 300 subjects.

Planned

"We did not set out to mimic the drug. We set out to make the gut do what it already knows how to do, and then measure it honestly."

Keepp formulation team

References

  • 1. Chi-Fu C, Yung-Hsiang L, Chen-Chen F, et al. Efficacy of GLP-1 formula on body weight in overweight and obese adults. Acta Scientific Medical Sciences. 2024;8(10):62-67.
  • 2. GLP-1 Formula IRB human study: instant GLP-1 boosting. Clinical Trial & Claim Lab (C&C Lab), 2026. Acute crossover response, n=25.
  • 3. In-vitro evaluation of GLP-1, PYY, UCP1/2, ATGL, GLUT4, PLIN1 and PPARG2 expression in colonic and adipocyte cell models.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare practitioner before use if pregnant, nursing, taking medication, or managing a medical condition.

The science is published. The jelly is ready.

One stick a day, 30 minutes before your largest meal.

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