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Metabolism

Natural GLP-1: What Actually Raises It, and What Is Getting Companies Sued

Half the supplement aisle now claims to raise your GLP-1. Some of those companies are in court over it. Here is what the human research really shows.

A glass of clear liquid on a dark kitchen counter beside a torn supplement sachet and a folded newspaper, lit by a single hard window light.

GLP-1 went from a hormone almost nobody could name to the most talked about molecule in health. Prescription drugs that act on its receptor changed what weight loss looks like, and the supplement industry noticed fast.

Now every third product on the shelf claims to raise your GLP-1 naturally. Some of the companies making those claims are in court over them.

Here is the verdict up front. You do make your own GLP-1, and certain foods and ingredients genuinely increase how much of it your gut releases after a meal. That is real, and it is measurable in humans. What is not real is the idea that any powder or capsule does what an injection does. The gap between those two statements is where the lawsuits live, and it is where most of the marketing you are reading has quietly parked itself.

What GLP-1 actually is

GLP-1 stands for glucagon-like peptide-1. It is a hormone released by L-cells in the lining of your intestine when food arrives. It does a few things at once: it tells your pancreas to release insulin when blood sugar is up, it slows how fast your stomach empties, and it signals your brain that you have had enough.

That last part is why it matters for appetite. GLP-1 is one of the switches that turns eating off.

Every healthy person releases GLP-1 after every meal. The hormone is broken down within minutes. The prescription drugs work by being resistant to that breakdown and by hitting the receptor far harder and for far longer than your own hormone ever does. Keep that distinction in your head, because everything below depends on it.

The claim that is getting companies sued

In 2025 a wave of class actions hit supplement brands over GLP-1 marketing.

Two proposed class actions were filed over a single celebrity-backed GLP-1 capsule, one in California Superior Court in February 2025 and one in the Southern District of New York in March 2025. The shared theory: promoting the product as a natural route to GLP-1 driven weight loss ran ahead of the evidence. Another suit targeted a supplement marketed as behaving like prescription GLP-1s without the side effects, arguing the product was never shown to produce clinically meaningful GLP-1 agonist outcomes. A third went after a patch brand for claiming effects comparable to name-brand prescriptions.

The legal issue is not that these products do nothing. It is the comparison. The Federal Trade Commission expects competent and reliable scientific evidence behind a health claim, which in practice means human randomized trials on the actual product. Saying an ingredient nudges a hormone is one thing. Implying it substitutes for a drug is a different thing, and that is the line these complaints are built on.

So when you read a label, the question is not whether GLP-1 appears on it. The question is what exactly is being promised.

Allulose has the cleanest human data

Allulose is a rare sugar. It tastes close to table sugar, and your body absorbs it but largely does not use it for energy, so it barely registers on blood glucose.

The relevant study here is a randomized, controlled, double-blind crossover trial in 18 people. Researchers delivered 25 g of allulose, 50 g of erythritol, or plain tap water directly to the stomach across six separate sessions, then tracked gut hormones. Allulose produced a significant release of GLP-1, PYY, and CCK compared with water, with large effect sizes across the board (Teysseire, 2022).

PYY and CCK are two more satiety hormones, so this is not a single-target effect. Interestingly, blocking the gut sweet taste receptor did nothing to the response, meaning allulose is not simply being detected as sweet. Something else is triggering the release.

The mechanism work backs this up. In animal models, oral allulose released GLP-1, activated vagal nerve signaling from the gut to the brain, reduced food intake, and improved glucose tolerance. Those effects disappeared when GLP-1 receptor signaling was genetically or pharmacologically blocked, which is strong evidence that the GLP-1 pathway is doing the work rather than riding along (Iwasaki, 2018). That study was in mice and rats, so treat it as mechanism, not proof in people.

Here is the part the megadose crowd skips. That 25 g is not a free lunch. Allulose is a rare sugar your gut does not fully absorb, so at high single doses it pulls water into the intestine and ferments, which means gas, bloating, and loose stools. A gastrointestinal tolerance study put the ceiling for a single dose at about 0.4 g per kg of body weight, roughly 25 to 30 g for most adults, with severe diarrhea showing up at 0.5 g per kg (Han, 2018). A separate 30 day study found close to half of people reported mild gut symptoms at 24 to 36 g per day (Qi, 2026). So the dose that lights up the hormone response is the same dose that sends a lot of people to the bathroom. The smart play is not to chase 25 g. It is to sit below it, where you keep the sugar swap and a real gut hormone nudge while the side effect risk stays near zero. The dose you actually take every day beats the megadose you quit in a week.

Butyrate is the other half of the story

Butyrate is a short-chain fatty acid. Your gut bacteria make it when they ferment dietary fiber, and it is the main fuel source for the cells lining your colon. It also supports the gut barrier by promoting mucus production and tight junctions between cells (Hajjar, 2021).

The link to GLP-1 runs through those same L-cells. Short-chain fatty acids stimulate them.

The cleanest human demonstration comes from a study that engineered a way to carry a short-chain fatty acid past the small intestine and release it in the colon, using an inulin-propionate ester. It is worth being precise here, because this number gets misread constantly. The 10 g was the ester, which is mostly the inulin carrier by weight, built to drop a small amount of the fatty acid exactly where it counts. It is not 10 g of the fatty acid, and nobody swallows 10 g of butyrate in one go, because it would taste and behave terribly. What the study proves is the principle, not a dose target. In the controlled crossover it raised postprandial GLP-1 and PYY and cut how much people ate, and over 24 weeks in 60 overweight adults the supplemented group gained less weight, carried less fat around the organs and in the liver, and held onto the insulin sensitivity the control group lost (Chambers, 2015).

That is propionate rather than butyrate, but it establishes the principle in humans: get a short-chain fatty acid to the right place and gut hormones respond.

For butyrate specifically, a randomized double-blind placebo-controlled trial gave 60 adults with type 2 diabetes sodium butyrate, inulin, both, or placebo for 45 days. GLP-1 rose significantly in the butyrate group and in the butyrate plus inulin group compared with placebo. The combination group was also the only one to significantly reduce fasting blood sugar and waist-to-hip ratio (Roshanravan, 2017).

Sixty people for 45 days is a small trial, and it was in a diabetic population rather than healthy men. But it is a real human randomized trial pointing the same direction as the mechanism.

Why butyrate plus a prebiotic fiber makes sense together

Notice which group did best in that last study. Not butyrate alone. Butyrate plus inulin.

There is a logic to that. Supplemental butyrate delivers the signal directly. A prebiotic fiber like inulin feeds the bacteria that produce butyrate in your colon on their own. One is the direct route, one builds the supply line. Pairing them is the most defensible version of this idea, and it is why the better formulations use both instead of one.

Allulose sits alongside that rather than inside it. It works through the gut hormone response to what you drink. The butyrate side works through the gut environment and the L-cells over time. Different levers, same destination.

What does not hold up

A neutral read means reporting the misses too.

Glucomannan, the konjac fiber in a lot of appetite products, is a good example. It absorbs water and creates real physical fullness, and a meta-analysis of six randomized trials in people with type 2 diabetes found meaningful improvements in total cholesterol, LDL, fasting blood glucose, and fasting insulin (Zhang, 2023). Useful. But a separate meta-analysis of eight randomized trials looking specifically at weight found no statistically significant difference versus placebo, a mean difference of just 0.22 kg (Onakpoya, 2014). Fullness is not the same as fat loss.

Psyllium is another one people reach for. It is a soluble fiber that swells into a gel and makes you feel full, and the flagship satiety trial did find it cut hunger between meals (Brum, 2016). Two things to notice. That trial was run and authored by the maker of the leading psyllium brand, and fullness is not the same as fat loss. Psyllium is a fine fiber for regularity and cholesterol. It is not a gut hormone story, and at higher doses it brings its own gas and bloating.

Lemon and citrus extracts are the newer entry, usually sold on a flavonoid called eriocitrin. To their credit, small trials did find it raised GLP-1 by around 15 to 17 percent in people with high blood sugar (Cesar, 2022; Ribeiro, 2019). Here is the catch. Those same trials found no change in body weight or body measurements, and they trace back to a single research group tied to the branded ingredient. A hormone marker moved. The scale did not. That gap, between a number on a lab report and a result you can see, is the whole game.

If a product tells you every ingredient in it is proven, that product is lying to you.

The ceiling, stated plainly

Here is the part that separates honest products from the ones getting served papers.

Raising your own GLP-1 through food and ingredients is a nudge to a natural system. It shows up as somewhat better appetite control and somewhat steadier blood sugar after meals. Prescription GLP-1 receptor agonists are a different category of intervention entirely, producing sustained receptor activation at levels your own hormone never reaches.

A supplement that supports your natural GLP-1 response is a real thing. A supplement that replaces a prescription is not a thing that exists. Any brand blurring those two is selling you the drug's reputation using the supplement's evidence.

What to actually do

  • Eat protein and fiber at every meal. This is the unglamorous foundation and it moves gut hormones without costing you anything.
  • For allulose, a moderate daily dose in the single digit grams is the sweet spot. It stays under the point where allulose causes gas and diarrhea while still swapping out sugar and nudging your gut hormones. Chasing the 25 g used in the lab mostly buys you a bathroom problem.
  • For butyrate, the form and delivery matter more than a giant dose, since only a small fraction reaches your bloodstream. Look for a version built to absorb, paired with a prebiotic fiber rather than either alone.
  • Read the claim, not the buzzword. Support and increase are defensible. Comparisons to prescriptions are the red flag.
  • Check whether the brand publishes its doses. If a label hides behind a proprietary blend, you cannot compare it to any study, which is usually the point.
  • If you are on a prescription GLP-1 or any diabetes medication, talk to your prescriber before adding anything that affects blood sugar.

A product that gets the framing right

Disclosure: Ozzi is operated by the same people who publish The Fitness Verdict. We are telling you that up front because an article about companies overstating their evidence has no business hiding its own connections.

With that on the table, Ozzi is a reasonable example of the approach described above. It is a drink stick built on 8 g of allulose, 500 mg of L-lysine butyrate, and chicory root inulin, which is the direct-plus-prebiotic pairing the Roshanravan trial pointed at. The doses are printed rather than buried in a blend, and the marketing language stays on supporting your natural GLP-1 rather than claiming to imitate a prescription. Their full explanation of the mechanism is on their GLP-1 page.

The dosing is the part worth understanding, because it is a choice, not a shortfall. The 8 g of allulose sits on purpose below the 25 g point where the gut hormone bump comes bundled with gas and diarrhea, so it is a dose you can take every day without the tradeoff. The butyrate is L-lysine butyrate, a tasteless, sodium-free form. In a small 2025 human crossover it reached peak serum butyrate in about 20 minutes, roughly five times the peak of tributyrin (La Monica, 2025). That is a pilot in ten men, absorption only, so hold it lightly. But the logic is sound. With a short-chain fatty acid, only a fraction ever reaches your bloodstream, so the form you can actually absorb matters more than a big number on the label. Dosed for tolerance and delivery, not for a screenshot.

The verdict

Natural GLP-1 support is a legitimate idea wrapped in some of the least legitimate marketing in the supplement industry. The hormone is real, you can influence it, and allulose and short-chain fatty acids have human trials behind them rather than vibes.

What you cannot do is buy an injection in powder form. The companies currently in court learned that the expensive way. Judge everything you read by whether it respects that line.

That is the verdict.

This is general education, not medical advice. Nothing here is intended to diagnose, treat, cure, or prevent any disease. If you have diabetes, take medication that affects blood sugar, or are already using a prescription GLP-1, talk to your prescriber before changing anything.

References

  1. Teysseire F, Bordier V, Budzinska A, et al. The Role of D-allulose and Erythritol on the Activity of the Gut Sweet Taste Receptor and Gastrointestinal Satiation Hormone Release in Humans: A Randomized, Controlled Trial. J Nutr. 2022. https://pubmed.ncbi.nlm.nih.gov/35135006/
  2. Iwasaki Y, Sendo M, Dezaki K, et al. GLP-1 release and vagal afferent activation mediate the beneficial metabolic and chronotherapeutic effects of D-allulose. Nat Commun. 2018. https://pubmed.ncbi.nlm.nih.gov/29317623/
  3. 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. https://pubmed.ncbi.nlm.nih.gov/25500202/
  4. Roshanravan N, Mahdavi R, Alizadeh E, et al. Effect of Butyrate and Inulin Supplementation on Glycemic Status, Lipid Profile and Glucagon-Like Peptide 1 Level in Patients with Type 2 Diabetes: A Randomized Double-Blind, Placebo-Controlled Trial. Horm Metab Res. 2017. https://pubmed.ncbi.nlm.nih.gov/28962046/
  5. Hajjar R, Richard CS, Santos MM. The role of butyrate in surgical and oncological outcomes in colorectal cancer. Am J Physiol Gastrointest Liver Physiol. 2021. https://pubmed.ncbi.nlm.nih.gov/33404375/
  6. Zhang Z, Zhang Y, Tao X, Wang Y, Rao B, Shi H. Effects of Glucomannan Supplementation on Type II Diabetes Mellitus in Humans: A Meta-Analysis. Nutrients. 2023. https://pubmed.ncbi.nlm.nih.gov/36771306/
  7. Onakpoya I, Posadzki P, Ernst E. The efficacy of glucomannan supplementation in overweight and obesity: a systematic review and meta-analysis of randomized clinical trials. J Am Coll Nutr. 2014. https://pubmed.ncbi.nlm.nih.gov/24533610/
  8. Han Y, Choi BR, Kim SY, et al. Gastrointestinal Tolerance of D-Allulose in Healthy and Young Adults. A Non-Randomized Controlled Trial. Nutrients. 2018. https://pubmed.ncbi.nlm.nih.gov/30572580/
  9. Qi L, Ning J, Han J, et al. D-Allulose as a Low-Calorie Sweetener: A 30-Day Randomized, Double-Blind Study on Gastrointestinal Tolerance and Systemic Safety. Food Sci Nutr. 2026. https://pubmed.ncbi.nlm.nih.gov/42375569/
  10. Brum JM, Gibb RD, Peters JC, Mattes RD. Satiety effects of psyllium in healthy volunteers. Appetite. 2016. https://pubmed.ncbi.nlm.nih.gov/27166077/
  11. Cesar TB, Ramos FMM, Ribeiro CB. Nutraceutical Eriocitrin (Eriomin) Reduces Hyperglycemia by Increasing Glucagon-Like Peptide 1 and Downregulates Systemic Inflammation: A Crossover-Randomized Clinical Trial. J Med Food. 2022. https://pubmed.ncbi.nlm.nih.gov/35796695/
  12. Ribeiro CB, Ramos FM, Manthey JA, Cesar TB. Effectiveness of Eriomin in managing hyperglycemia and reversal of prediabetes condition: A double-blind, randomized, controlled study. Phytother Res. 2019. https://pubmed.ncbi.nlm.nih.gov/31183921/
  13. La Monica MB, et al. Pharmacokinetics of lysine butyrate, sodium butyrate, and tributyrin in healthy men (pilot crossover). J Exerc Nutr. 2025;8(1):4. Trial NCT06700785. https://clinicaltrials.gov/study/NCT06700785

Common questions

Can a supplement really raise your GLP-1?

Some ingredients can increase how much GLP-1 your gut releases after a meal, and that has been measured in humans. In a randomized controlled crossover trial in 18 people, 25 g of allulose produced a significant release of GLP-1, PYY, and CCK compared with water (Teysseire, 2022). What no supplement does is reproduce what a prescription GLP-1 receptor agonist does. That is a different scale of effect entirely.

Why are GLP-1 supplement companies getting sued?

Not for saying their ingredients affect GLP-1. For implying the products work like the prescription drugs. In 2025 two proposed class actions were filed over one celebrity-backed GLP-1 capsule, in California Superior Court in February and the Southern District of New York in March, along with suits over a metabolism supplement and a patch brand. The shared argument is that the marketing outran the evidence, since the FTC expects human trial data behind health claims.

Does butyrate increase GLP-1?

There is human evidence pointing that way. In a randomized double-blind placebo-controlled trial in 60 adults with type 2 diabetes, GLP-1 rose significantly in the sodium butyrate group and in the butyrate plus inulin group compared with placebo (Roshanravan, 2017). Separately, delivering a short-chain fatty acid directly to the colon significantly raised GLP-1 and PYY and cut energy intake in humans (Chambers, 2015). The trials are small and still early, which is exactly why the delivery form matters, since only a fraction of butyrate ever reaches your bloodstream to begin with.

How much allulose do you actually need?

The trial that found a strong gut hormone response used 25 g (Teysseire, 2022). Here is what that number hides. 25 g is also right at the edge of what your gut tolerates. A tolerance study put the single dose ceiling near 0.4 g per kg of body weight, with severe diarrhea at 0.5 g per kg (Han, 2018), and about half of people reported mild gut symptoms at 24 to 36 g per day (Qi, 2026). So a lower daily dose is not under-dosing. It is trading a little of the hormone signal for near-zero side effects and a dose you will actually keep taking.

Is glucomannan worth taking for appetite?

For fullness and blood sugar, there is a case. A meta-analysis of six randomized trials in type 2 diabetes found improvements in cholesterol, LDL, fasting glucose, and fasting insulin (Zhang, 2023). For weight specifically, a meta-analysis of eight randomized trials found no statistically significant difference versus placebo, a mean difference of 0.22 kg (Onakpoya, 2014). It makes you feel full. That is not the same as making you lose fat.

What is the best natural way to support GLP-1?

Protein and fiber at every meal, consistently. It is unglamorous and it is the foundation. If you want to add an ingredient on top, the ones with actual human data behind them are allulose at a real dose and a short-chain fatty acid paired with a prebiotic fiber rather than either alone. Talk to your prescriber first if you take anything that affects blood sugar.