Akkermansia muciniphila is the gut bacterium most often tied to GLP-1, and low Akkermansia on a stool test is one of the more useful findings to have in hand before a patient starts a GLP-1 receptor agonist. Most of the marketing around "GLP-1 probiotics" is, in practice, marketing around this one organism.
GLP-1 is also a hormone the gut already makes, and the microbiome has a direct hand in how much of it gets made. This post covers what Akkermansia does, what a low result means, how the gut produces its own GLP-1, and how practitioners approach a dysbiotic pattern before and during GLP-1 therapy. It draws on the US BioTek™ webinar Beyond the Scale: Uncovering the Metabolic and Gut Health Impact of GLP-1s, presented by Dr. Racheal Onah, including the pre- and post-testing case she walked through.
"Lower levels of Akkermansia are linked to elevated HbA1c, high BMI, increased visceral fat, adipose inflammation, and also insulin resistance. And that's the reason why there's a lot of probiotics out there that say 'GLP-1 probiotics,' but when you actually look at what's inside, it's mainly Akkermansia."
Dr. Racheal Onah, Beyond the Scale webinar, at 19:59. Watch the webinar
Webinar recording now available. Beyond the Scale: Uncovering the Metabolic and Gut Health Impact of GLP-1s, presented by Dr. Racheal Onah, ND MRN. A 42-year-old case followed from baseline through nine months of semaglutide, with the metabolic, cortisol, and stool results at each point.
Akkermansia muciniphila is a mucin-degrading commensal bacterium that lives in the mucus layer of the intestinal lining. It is the main representative of the Verrucomicrobia phylum on a stool report, so a composition chart with no Verrucomicrobia usually means Akkermansia is below detectable limits.
In the webinar, Dr. Onah summarized the roles that make it relevant to metabolic health (Si et al., 2022): it increases mucin turnover, which supports the gut barrier; it is associated with reduced intestinal inflammation; it improves bile acid metabolism through deconjugation, and bile acids are one of the signals that prompt L cells to secrete GLP-1; and it produces microbial metabolites that help stimulate GLP-1 production.
Akkermansia is reported with the microbiome composition on every US BioTek GI profile, so a low result is read against inflammation, digestion, and mucosal immunity rather than on its own.
Low Akkermansia is not a diagnosis. It is a marker of a microbiome that is less able to maintain the mucus layer and the GLP-1 signaling that depends on it. Lower levels have been linked to elevated HbA1c, higher BMI, increased visceral fat, adipose tissue inflammation, and insulin resistance (Si et al., 2022).
On the GI report in the webinar case, the Verrucomicrobia phylum measured 0.000 percent against a reference range of 0.000 to 2.400 percent and was missing from the composition chart entirely. A result flagged low, or a phylum that does not appear at all, points to reduced capacity for mucin turnover and barrier maintenance, and is one more reason to look at the rest of the microbiome before relying on medication alone.
Low Akkermansia does not produce a symptom of its own. In the webinar case it sat alongside fatigue after meals, poor exercise tolerance, bloating, gas, constipation, gradual weight gain, and laboratory evidence of insulin resistance. The symptoms belong to the whole pattern, not to one organism, which is why a stool test is read as a panel.
Dr. Onah's position was that low Akkermansia is a reason to support the gut before or alongside the prescription, not a reason to withhold it, because the more dysfunction a stool test shows, the harder a patient is likely to find GLP-1 therapy.
"The more dysfunction on the test, the more I would suspect that they will have a harder time. If they had leaky gut, if they had severe GI overgrowths, I would be a bit concerned with them being on there. ... Constipation is one of the big side effects of GLP-1s, so if they're already experiencing some of those, it's most likely going to get worse while they're on a GLP-1."
Dr. Racheal Onah, Beyond the Scale webinar Q&A, at 42:42. Watch the webinar
| Organism or group | Role described in the webinar | What Dr. Onah wants to see |
|---|---|---|
| Akkermansia muciniphila | Mucin turnover, barrier support, bile acid deconjugation, metabolites that support GLP-1 secretion | Present, not low or undetectable |
| Faecalibacterium and Roseburia | Butyrate producers; higher Faecalibacterium prausnitzii correlates with lower fasting glucose in GLP-1 treated patients (Anachad et al., 2023) | Adequate levels |
| Clostridium species | Propionate and indole propionic acid production | Within range, not too high |
| Bacteroides species | Carbohydrate fermentation, propionate, bile acid metabolism | Within range: too low is linked to obesity and type 2 diabetes, too high to a high-fat, low-fiber diet |
| Gram-negative LPS producers (Citrobacter, Proteus) | Endotoxin and intestinal inflammation | Low, and cleared before fiber is added |
| Proteobacteria to Actinobacteria ratio | A high ratio has been linked to inflammation | Proteobacteria low, Actinobacteria present |
GLP-1 is secreted by enteroendocrine L cells in the ileum and colon. It increases satiety, slows gastric emptying, and improves the insulin response to a meal (Müller et al., 2019). Several gut-derived signals prompt L cells to secrete it, and each depends on the microbiome (Arora et al., 2021; Anachad et al., 2023):
LPS from gram-negative overgrowth can also trigger GLP-1 release, but it drives inflammation at the same time, which is why clearing LPS producers comes first. For a visual walk through GLP-1 secretion in the L cell, see the interactive L-cell explainer.
"The GI microbiome on its own naturally produces it, and helping with the functionality of your gut can definitely help with it naturally being produced."
Dr. Racheal Onah, Beyond the Scale webinar Q&A, at 46:21. Watch the webinar
Clinical case presented by Dr. Racheal Onah, ND MRN in the webinar Beyond the Scale. Patient details have been limited to protect identity.
A 42-year-old premenopausal woman presented with obesity: 205 pounds at 5 feet 6 inches, a BMI of 33.1, with gradual weight gain since age 35. She took no medications and ate a standard Western diet. She reported fatigue, poor exercise tolerance, tiredness after meals, bloating, gas, constipation, and waking one to two times per night. Her family doctor had recommended semaglutide, and she wanted support for her health before starting it.
A fasting NutriStat Metabolic Profile showed glucose of 103 mg/dL (reference 70 to 99), insulin of 20 µIU/mL (reference 1 to 17), HbA1c of 6.0 percent (reference 4.4 to 5.6), and a HOMA-IR of 5.1 against a reference of under 2.0. Dr. Onah reads a HOMA-IR of 3.0 and above as significant insulin resistance, so the picture was prediabetes with insulin resistance. Liver function was in range. Total cholesterol (203 mg/dL) and LDL (109 mg/dL) were flagged, but with HDL and triglycerides in range the triglyceride to HDL ratio was 0.56, well under the 3.0 threshold associated with insulin resistance (Shin et al., 2017).
Because she was waking at night, Dr. Onah ran a cortisol awakening response. Instead of rising 30 to 50 percent in the first 30 minutes, her salivary cortisol fell from 45.2 nmol/L at waking to 22.4 at 60 minutes, and the evening value of 16.6 nmol/L was high: HPA axis dysfunction with a significant stress component.
"She had high levels of inflammation with the calprotectin, very low pancreatic elastase, really low secretory IgA, which gives me an idea that most likely [there is] poor immune defense, but also could be a sign of poor mucosal support, because secretory IgA lives in the mucosal lining of the gut."
Dr. Racheal Onah, Beyond the Scale webinar, at 22:01. Watch the webinar
The sequence Dr. Onah described is to reduce the microbial load first, then build, with one framing question for every patient: "Is it that they need the GLP-1, or do they just need to fix the dysfunction?" (at 43:58). The interventions below are from her presentation and are applied at the practitioner's discretion.
Clear the overgrowths before adding fiber. Berberine and grapefruit seed extract, a binder during the antimicrobial phase only (binders can also bind nutrients), and magnesium.
Feed Akkermansia and the butyrate producers. A Mediterranean and anti-inflammatory diet with refined carbohydrate and high fat intake reduced, dietary polyphenols for Akkermansia, soluble fiber increased slowly once overgrowths are addressed, dietary protein increased gradually to feed indole propionic acid production, and supplemental butyrate for the mucosal membrane.
Support digestion and the mucosal lining. Digestive enzymes, bitters, and betaine HCl where elastase and stomach acid are low; immunoglobulins, vitamin A, and zinc carnosine for the gut lining and secretory IgA; vitamin B6 and ginger as needed for GLP-1 nausea.
Metabolic and lifestyle supports. A 10 to 20 minute walk after the largest meal, 5,000 to 7,000 steps a day built up from about 2,000, resistance training working from one session a week toward three, cinnamon with meals, and curcumin with an EPA-forward omega-3.
Retest on a realistic timeline. Toxin screening, if not done at baseline, belongs in the first three months, when weight loss is fastest. For the metabolic markers, Dr. Onah set expectations in the Q&A:
"I would say maybe slight changes after three months. I would say after six months is a good time point where you should start to notice differences."
Dr. Racheal Onah, Beyond the Scale webinar Q&A, at 38:14. Watch the webinar
Follow-up on the case above, presented by Dr. Racheal Onah, ND MRN.
After nine months on semaglutide 2 mg weekly alongside the support above, the patient had lost 25 pounds and her BMI had moved from 33.1 to 29. She reported better exercise tolerance, less fatigue around meals, no bloating after food, and one
regular bowel movement daily.
On the repeat NutriStat Metabolic Profile, fasting glucose, insulin, and HbA1c were back in range and HOMA-IR had improved from 5.1 to 3.2 but remained flagged. Total cholesterol was no longer flagged; LDL had lowered but stayed above the reference. Evening cortisol had fallen to 5.9 nmol/L, although the awakening response still lacked a full morning rise, so HPA axis support is the next phase of her plan.
On the stool test, Bacteroidetes had fallen from 79.45 to 52.36 percent and Firmicutes had risen from 17.49 to 46.30 percent, close to the reference split. Proteobacteria dropped to 0.614 percent, and the Verrucomicrobia phylum appeared for the first time at 0.504 percent: Akkermansia muciniphila was now detectable.
| Measure | Baseline | Nine months | Reference |
|---|---|---|---|
| Fasting glucose | 103 mg/dL (high) | 87 mg/dL | 70 to 99 mg/dL |
| Fasting insulin | 20 µIU/mL (high) | 15 µIU/mL | 1 to 17 µIU/mL |
| HOMA-IR | 5.1 (high) | 3.2 (high) | Under 2.0 |
| HbA1c | 6.0% (high) | 5.6% | 4.4 to 5.6% |
| LDL cholesterol | 109 mg/dL (high) | 106 mg/dL (high) | Under 100 mg/dL |
| Evening cortisol | 16.6 nmol/L (high) | 5.9 nmol/L | Evening range on report |
| Proteobacteria phylum | 2.984% | 0.614% | 0.250 to 5.000% |
| Verrucomicrobia phylum (Akkermansia) | 0.000% (below detectable limits) | 0.504% | 0.000 to 2.400% |
Dr. Onah was careful about attribution: the improvement could be the semaglutide, the lifestyle changes, or the treatment of the underlying gut dysfunction. The pre- and post-testing is what made it possible to see which markers had moved and which had not.
Weight is not the only outcome measure. GLP-1 receptor agonists act on the pancreas, liver, brain, and adipose tissue (Boer and Holst, 2020; Zhang et al., 2025; D'Marco et al., 2021), and the webinar's monitoring list follows those targets:
Dr. Onah would not recommend a GLP-1 with a family history of thyroid cancer or MEN2, past pancreatitis, gallstones, bulimia or anorexia, hypersensitivity reactions, or a patient unwilling to change diet and activity, because, in her words, "GLP-1s are meant to be supplemental. They're not corrective." (at 47:30). Stepping off is a stepwise reduction in frequency and dose, never an abrupt stop.
Akkermansia muciniphila is reported with the microbiome composition on every US BioTek GI profile. The GI Standard Profile and GI Advanced Profile add the GIT Functional Markers that gave this case its context, and the GI Advanced Profile adds culture and antimicrobial sensitivities, which matters where an overgrowth such as Citrobacter or Proteus needs clearing before fiber is introduced. The metabolic side of the case was run on the NutriStat Metabolic Profile at baseline and at nine months, which reports the glycemic markers, lipid fractions, liver function, and CVD inflammatory markers shown in the report crops above.
Presented by Dr. Racheal Onah, ND MRN, medical advisor to US BioTek, RealTime Labs, and NutriPATH. The recording covers the full baseline and nine-month results from the case above, how GLP-1 receptor agonists act on the brain, pancreas, liver, stomach, and adipose tissue, which gut metabolites and bacteria support endogenous GLP-1 secretion, and audience Q&A on testing timelines, toxin screening, binders, nutrient deficiencies, contraindications, and stepping off therapy.
US BioTek brings more than thirty years of laboratory science to functional gastrointestinal and metabolic testing.
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Talk to our team to learn more about using the GI profiles and the NutriStat Metabolic Profile with patients on GLP-1 therapy.
Low Akkermansia answers a specific question: is the microbiome in a position to support the mucus layer and the GLP-1 signaling that a receptor agonist is about to amplify? An undetectable result does not forbid the prescription, but it predicts a harder road and points at the work that needs to happen alongside it: clearing overgrowths, feeding the commensals in the right order, and supporting digestion and the mucosal lining. In Dr. Onah's case, Akkermansia moved from 0.000 to 0.504 percent over nine months while HOMA-IR fell from 5.1 to 3.2 and HbA1c returned to range. For practitioners seeing more GLP-1 patients every quarter, the stool test is where the monitoring starts, not where it ends.
"Don't use weight as the only outcome measure. ... GI symptoms deserve active monitoring, especially in a patient with pre-existing SIBO or GI dysfunction. ... Pre and post testing is most valuable when it changes clinical decision making."
Dr. Racheal Onah, Beyond the Scale webinar conclusion, at 37:18. Watch the webinar
Akkermansia muciniphila is a mucin-degrading commensal bacterium that lives in the mucus layer of the intestinal lining and is the main member of the Verrucomicrobia phylum on a stool report. It increases mucin turnover, supports gut barrier function, is associated with reduced intestinal inflammation, improves bile acid metabolism through deconjugation, and produces metabolites that help stimulate GLP-1 secretion.
What does low Akkermansia mean on a stool test?Low Akkermansia means the microbiome has reduced capacity to maintain the mucus layer and support GLP-1 signaling. Lower levels have been linked to elevated HbA1c, higher BMI, increased visceral fat, adipose tissue inflammation, and insulin resistance. A composition chart with no Verrucomicrobia phylum usually means Akkermansia is below detectable limits.
What are the symptoms of low Akkermansia?Low Akkermansia does not cause a symptom of its own. It tends to appear alongside a wider metabolic and digestive pattern. In the webinar case it sat with fatigue after meals, poor exercise tolerance, bloating, gas, constipation, gradual weight gain, and insulin resistance. Those symptoms belong to the whole picture, which is why a stool test is read as a panel.
How is Akkermansia connected to GLP-1?GLP-1 is secreted by L cells in the ileum and colon in response to short-chain fatty acids, bile acids, and tryptophan metabolites. Akkermansia produces metabolites that help stimulate that secretion and improves bile acid metabolism, which is another GLP-1 signal. This is why many products marketed as GLP-1 probiotics are mainly Akkermansia.
How do you increase Akkermansia muciniphila?The approach described in the webinar is to clear LPS-producing overgrowths first, then feed the commensals: a Mediterranean and anti-inflammatory diet, dietary polyphenols, soluble fiber increased slowly, gradual increases in dietary protein, and supplemental butyrate for the mucosal membrane. Digestive and mucosal support are added where pancreatic elastase and secretory IgA are low.
Should you test the gut microbiome before starting a GLP-1 receptor agonist?Dr. Onah's view is yes where possible. The more dysfunction a stool test shows, the harder a patient is likely to find GLP-1 therapy, and pre-existing constipation, bloating, and dysbiosis tend to worsen because slowed gastric emptying is part of the mechanism. Baseline testing also makes the follow-up meaningful, since pre- and post-testing is most valuable when it changes clinical decision making.
Which gut bacteria should be present before starting GLP-1 therapy?Dr. Onah looks for adequate beneficial bacteria rather than one organism: Akkermansia, the butyrate producers Faecalibacterium and Roseburia, propionate producers such as Clostridium within range, and a low level of LPS-producing gram-negative bacteria such as Citrobacter and Proteus, which drive inflammation.
How long does it take to see lab changes on a GLP-1 receptor agonist?In Dr. Onah's experience, slight changes appear at three to four months and six months is a reasonable point to expect measurable differences in metabolic markers. In the webinar case, nine months of semaglutide with gut and lifestyle support brought fasting glucose, insulin, and HbA1c back into range and lowered HOMA-IR from 5.1 to 3.2, although it remained elevated.
Which US BioTek tests report Akkermansia and the metabolic markers in this case?Akkermansia muciniphila is reported with the microbiome composition on every US BioTek GI profile. The GI Standard Profile and GI Advanced Profile add calprotectin, pancreatic elastase, secretory IgA, and the other GIT Functional Markers. The metabolic markers in this case, including HOMA-IR and HbA1c, were run on the NutriStat Metabolic Profile. Environmental toxin, hormone, and nutritional panels cover the rest of the GLP-1 monitoring list.