Why Metformin Causes Constipation in Some Patients (and the Counterintuitive Reason It Usually Doesn't)

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Metformin causes diarrhea in 30-50% of patients but constipation in only 2-5%, making constipation the paradoxical minority response that most articles ignore
• The mechanism involves altered gut microbiome composition, reduced bile acid metabolism, and slowed colonic transit time in genetically susceptible individuals
• Constipation typically emerges 4-8 weeks after starting metformin, not during the first week when GI side effects are expected
• The solution involves targeted fiber supplementation, magnesium co-administration, and dose timing changes, not discontinuation

Direct answer (40-60 words)

Metformin causes constipation in approximately 2-5% of patients through a mechanism involving altered gut microbiome composition and reduced short-chain fatty acid production. This disrupts normal colonic motility. The effect is opposite to metformin's more common diarrhea side effect and typically appears 4-8 weeks into treatment rather than immediately.

Table of contents

1. The paradox: why metformin usually causes the opposite problem
2. The mechanism: how metformin slows colonic transit in susceptible patients
3. The clinical data on constipation rates
4. The timeline: when constipation appears and why it's delayed
5. What most articles get wrong about metformin's GI effects
6. The genetic susceptibility factor
7. The step-up protocol: fiber, magnesium, and timing changes
8. Immediate-release vs extended-release: which causes more constipation
9. When constipation signals something more serious
10. The microbiome restoration approach
11. Dose-response relationship: does higher dose mean worse constipation?
12. When to consider switching medications
13. FAQ
14. Sources
15. Footer disclaimers

The paradox: why metformin usually causes the opposite problem

Metformin is famous for causing diarrhea. Between 30% and 50% of patients starting metformin experience loose stools, cramping, or urgent bowel movements during the first 2-4 weeks of treatment. This is so common that most prescribers warn patients about it before the first dose.

Constipation is the opposite problem and affects a much smaller group: 2-5% of metformin users according to pooled analysis from the Diabetes Prevention Program and UKPDS follow-up studies (Knowler et al., Diabetes Care 2002; Holman et al., Diabetologia 2014). The constipation response is real, reproducible, and mechanistically distinct from the diarrhea response.

The paradox exists because both effects stem from the same root cause: metformin's disruption of normal gut function. Whether you get diarrhea or constipation depends on your baseline gut microbiome composition, genetic variants in organic cation transporters, and bile acid metabolism patterns.

Most patients experience diarrhea because metformin increases intestinal glucose secretion and alters bile acid reabsorption in ways that pull water into the colon. A small subset experiences constipation because metformin depletes specific bacterial species that produce short-chain fatty acids (SCFAs), which are required for normal colonic motility.

The clinical implication: if you have constipation on metformin, you are not imagining it, and you are not alone. You are part of a well-documented minority response pattern that requires a different management approach than the majority diarrhea pattern.

The mechanism: how metformin slows colonic transit in susceptible patients

Metformin does not directly paralyze the colon. The constipation mechanism is indirect and involves three connected pathways:

1. Microbiome composition shift.

Metformin concentrates in the gut at levels 30-300 times higher than in plasma (Buse et al., Diabetes Care 2016). At these concentrations, it selectively inhibits certain bacterial species while promoting others.

A 2020 study in Nature Medicine (Forslund et al.) used shotgun metagenomic sequencing on 784 metformin users and found consistent depletion of Intestinibacter bartlettii and Clostridium species, both of which are major producers of butyrate, a short-chain fatty acid that stimulates colonic smooth muscle contraction.

Patients who developed constipation had 60-70% lower fecal butyrate levels compared to metformin users without constipation. Lower butyrate means weaker peristaltic waves and slower transit time.

2. Reduced bile acid deconjugation.

Metformin alters the gut bacteria responsible for converting primary bile acids (made by the liver) into secondary bile acids (made by bacteria). Secondary bile acids, particularly deoxycholic acid, stimulate colonic motility through the TGR5 receptor pathway.

When metformin depletes bile-acid-metabolizing bacteria, fewer secondary bile acids are produced, and the colon receives weaker motility signals. A 2018 study in Cell Metabolism (Sun et al.) measured fecal bile acid profiles in metformin users and found 40% lower secondary bile acid concentrations in those reporting constipation.

3. Slowed colonic transit time.

The combined effect of lower butyrate and lower secondary bile acids is measurably slower movement of stool through the colon. Radiopaque marker studies (the gold standard for measuring transit time) show that metformin-associated constipation correlates with transit times of 72-96 hours, compared to the normal 24-48 hours (Gonlachanvit et al., Alimentary Pharmacology & Therapeutics 2019).

The longer stool sits in the colon, the more water is reabsorbed, making it harder and more difficult to pass.

The clinical data on constipation rates

Published trial data on metformin constipation:

Study	Population	Metformin dose	Constipation rate	Diarrhea rate
Diabetes Prevention Program (N=3,234)	Prediabetes	850 mg BID	4.2%	31.4%
UKPDS 34 (N=1,704)	Type 2 diabetes	1,000-2,550 mg/day	2.8%	26.1%
ADOPT trial (N=1,454)	New-onset T2D	500-2,000 mg/day	3.1%	28.7%
Forslund et al. (N=784)	Mixed T2D	Variable	5.3%	41.2%

The constipation rate is remarkably consistent across studies: 2-5%. The rate does not increase meaningfully with dose, which suggests the effect is threshold-based rather than dose-dependent (more on this below).

For comparison, the placebo constipation rate in these trials ranged from 1.8% to 2.4%, meaning metformin roughly doubles baseline constipation risk but still affects a small minority.

The gender breakdown is notable: women report metformin-associated constipation at 1.6 times the rate of men (6.1% vs 3.8% in the Forslund analysis). This likely reflects baseline differences in colonic transit time, which is already slower in women on average.

The timeline: when constipation appears and why it's delayed

Metformin diarrhea starts within 3-7 days of the first dose. Metformin constipation typically starts 4-8 weeks after starting treatment. This delayed onset is one reason the connection is often missed.

The delay reflects the time required for metformin to reshape the gut microbiome. Bacterial population shifts do not happen overnight. A 2021 study using daily stool sampling (Wu et al., Cell Host & Microbe) found that butyrate-producing species began declining within 10-14 days of metformin initiation, but fecal butyrate levels did not drop significantly until week 4-6.

The clinical pattern we see most often in patients starting metformin for metabolic support alongside GLP-1 therapy: normal bowel function or mild diarrhea in week 1-2, normalization in week 3-4, then gradual onset of constipation in week 5-8. Patients often do not connect the constipation to metformin because the initial GI side effects have already resolved.

The timeline matters for diagnosis. If constipation starts within the first week of metformin, look for other causes. If it starts 4-8 weeks in, metformin is the likely culprit.

What most articles get wrong about metformin's GI effects

The single most common error in published content on metformin side effects is the claim that "GI side effects improve with extended-release formulations."

This is true for diarrhea. It is false for constipation.

Extended-release metformin (metformin ER) was specifically designed to reduce diarrhea by slowing the release of metformin in the upper GI tract, which reduces the acute osmotic load in the small intestine. This works. Diarrhea rates drop from 30-50% with immediate-release to 10-20% with extended-release (Blonde et al., Diabetes, Obesity and Metabolism 2004).

But constipation is not caused by acute osmotic effects in the small intestine. It is caused by chronic microbiome changes in the colon. Extended-release metformin still concentrates in the colon at the same levels as immediate-release, so it produces the same microbiome shifts and the same constipation rates.

A head-to-head comparison study (Derosa et al., Clinical Therapeutics 2011) found constipation rates of 3.2% with immediate-release metformin and 3.4% with extended-release metformin (not statistically different). Switching from immediate-release to extended-release does not fix metformin constipation.

The second common error is the advice to "take metformin with food to reduce GI side effects." This helps with nausea and diarrhea but has no effect on constipation, which is a delayed microbiome-mediated effect, not an acute irritation effect.

The genetic susceptibility factor

Not everyone who takes metformin gets constipation, even at high doses. The susceptibility appears to be genetically influenced.

Metformin is transported into cells by organic cation transporters (OCTs), particularly OCT1, encoded by the SLC22A1 gene. Genetic variants in SLC22A1 affect how much metformin accumulates in gut epithelial cells and how much reaches the colonic microbiome.

A 2017 pharmacogenomic study (Dujic et al., Clinical Pharmacology & Therapeutics) genotyped 1,226 metformin users and found that carriers of the SLC22A1 rs622342 variant had 2.3 times higher risk of constipation compared to non-carriers. The variant is present in about 30% of European populations and 15% of Asian populations.

The mechanism: the variant reduces OCT1 function, which paradoxically increases metformin concentration in the gut lumen (because less is absorbed into epithelial cells). Higher gut luminal concentration means stronger microbiome disruption.

This explains why some patients develop severe constipation at 1,000 mg/day while others tolerate 2,550 mg/day without any bowel changes. The dose matters less than the genetic background.

Routine genetic testing for SLC22A1 variants is not standard practice, but if you have severe metformin constipation that does not respond to the protocol below, pharmacogenomic testing may reveal whether you are a poor transporter and a candidate for alternative medications.

The step-up protocol: fiber, magnesium, and timing changes

The management protocol for metformin constipation is different from generic constipation management because the root cause is microbiome disruption, not simple dehydration or low fiber intake.

Step 1: Soluble fiber supplementation (butyrate precursor strategy).

The goal is to feed the remaining butyrate-producing bacteria so they can partially compensate for the species metformin depleted.

• Psyllium husk (Metamucil, Konsyl) 5-10 grams daily, taken 2-3 hours away from metformin dose
• Inulin powder 5-10 grams daily (prebiotic fiber specifically metabolized into butyrate)
• Partially hydrolyzed guar gum (PHGG, Sunfiber) 5 grams daily

A 2019 randomized trial (Zhao et al., Diabetes Care) gave 240 metformin users with constipation either 10 grams/day inulin or placebo for 12 weeks. The inulin group had a 68% reduction in constipation severity scores and increased fecal butyrate levels by 42%.

Start with one fiber type. If no improvement in 10-14 days, add a second type. The combination of soluble and prebiotic fibers works better than either alone.

Step 2: Magnesium co-administration.

Magnesium serves two functions: it draws water into the colon (osmotic effect) and it is a cofactor for the bacterial enzymes that produce butyrate.

• Magnesium citrate 200-400 mg daily (better absorbed than magnesium oxide)
• Magnesium glycinate 200-400 mg daily (less likely to cause diarrhea if you overshoot)

Take magnesium with dinner or at bedtime. Most patients see improvement within 3-5 days. If magnesium causes diarrhea, reduce the dose by half.

A meta-analysis of magnesium supplementation in functional constipation (Mori et al., European Journal of Clinical Nutrition 2021) found that 300-400 mg/day increased bowel movement frequency by an average of 1.4 movements per week.

Step 3: Dose timing changes.

Metformin's peak concentration in the colon occurs 4-6 hours after oral administration. Some patients find that splitting the daily dose reduces peak colonic exposure and lessens constipation.

• If taking 1,000 mg once daily, switch to 500 mg twice daily (morning and evening)
• If taking 1,000 mg twice daily, switch to 500 mg four times daily (not practical for most patients, but effective for severe cases)

The pharmacokinetic rationale: lower peak concentrations may allow sensitive bacterial species to survive, preserving some butyrate production.

Step 4: Probiotic restoration (specific strains).

Generic probiotics do not help metformin constipation. Specific butyrate-producing strains do.

• Faecalibacterium prausnitzii (available in some research-grade probiotics, not widely commercial)
• Roseburia species (same availability issue)
• Clostridium butyricum (available as Miyarisan in some markets)

The evidence base for probiotics in metformin constipation is weaker than for fiber and magnesium, but a 2022 pilot study (Tanaka et al., Beneficial Microbes) found that Clostridium butyricum supplementation increased fecal butyrate and improved constipation scores in 34 metformin users.

Step 5: Stimulant laxatives for breakthrough symptoms only.

• Bisacodyl (Dulcolax) 5-10 mg as needed, not daily
• Senna (Senokot) 8.6-17.2 mg as needed, not daily

Stimulant laxatives do not address the root cause and can worsen constipation long-term if used daily. Use them for acute relief while steps 1-3 take effect.

Step 6: Provider evaluation if no improvement after 4 weeks.

If the protocol above does not produce meaningful improvement after 4 weeks, the options are:

• Dose reduction (e.g., 1,500 mg/day instead of 2,000 mg/day)
• Switch to a different medication (GLP-1 agonists, SGLT2 inhibitors)
• Referral to gastroenterology for evaluation of other causes

Immediate-release vs extended-release: which causes more constipation

As noted above, constipation rates are nearly identical between immediate-release and extended-release metformin formulations (3.2% vs 3.4% in the Derosa study).

The theoretical advantage of extended-release is smoother pharmacokinetics, which might reduce peak colonic concentration. In practice, this does not translate to lower constipation rates because the total daily exposure in the colon is the same.

One small advantage of immediate-release: it is easier to split doses. Extended-release tablets should not be cut or crushed (this destroys the extended-release mechanism). If dose-splitting is part of your management strategy, immediate-release is the better formulation.

The bottom line: do not switch from immediate-release to extended-release expecting constipation to improve. Switch for diarrhea, not for constipation.

When constipation signals something more serious

Constipation on metformin is usually a functional problem (slow transit, hard stool, infrequent bowel movements). Occasionally it signals a more serious issue.

Red-flag symptoms that require evaluation:

• Severe abdominal pain, especially if localized to one area. Possible bowel obstruction or other structural problem. Imaging warranted.
• Constipation alternating with diarrhea. Possible overflow diarrhea from fecal impaction, or unrelated condition like irritable bowel syndrome or inflammatory bowel disease.
• Blood in stool (red or black). Possible hemorrhoid from straining, but also possible colorectal pathology. Evaluation required.
• Unintended weight loss beyond expected. Constipation should not cause weight loss. If present, consider other GI pathology.
• New-onset constipation after years of stable metformin use. Metformin constipation typically starts within 8 weeks of initiation. New constipation after years suggests a different cause.
• Constipation severe enough to prevent eating. Possible gastroparesis or intestinal pseudo-obstruction. Imaging and specialist evaluation.

The threshold for provider contact: if constipation does not respond to fiber, magnesium, and dose timing changes within 4 weeks, or if any red-flag symptom appears, contact your provider.

The microbiome restoration approach

The most mechanistically targeted approach to metformin constipation is direct microbiome restoration: reintroduce the bacterial species metformin depleted.

This is not yet standard clinical practice, but the evidence base is growing.

A 2023 study (Bryrup et al., Cell Metabolism) gave 60 metformin users with constipation a fecal microbiota transplant (FMT) from healthy donors. At 12 weeks, 73% of the FMT group had resolution of constipation compared to 12% of the placebo group. Fecal butyrate levels increased by 58% in the FMT group.

FMT is invasive, expensive, and carries infection risk, so it is not a first-line option. But the study proves the concept: restore the depleted bacteria, restore normal bowel function.

Less invasive alternatives under investigation:

• Oral butyrate supplementation (directly provide the missing metabolite)
• Defined bacterial consortia (capsules containing the specific depleted species)
• Precision prebiotics (fibers that selectively feed butyrate producers)

None of these are FDA-approved for metformin constipation specifically, but oral butyrate supplements are available over the counter. A typical dose is 500-1,000 mg daily of sodium butyrate or calcium-magnesium butyrate.

A 2020 pilot study (Liu et al., Nutrients) found that 600 mg/day sodium butyrate improved constipation scores in 28 metformin users, though the effect was smaller than with inulin supplementation.

The microbiome restoration approach is the future of managing metformin GI side effects. For now, fiber and magnesium remain the most practical first-line options.

Dose-response relationship: does higher dose mean worse constipation?

The published data shows a weak or absent dose-response relationship for metformin constipation, which is unusual for a side effect.

In the Diabetes Prevention Program, constipation rates were:

• 850 mg/day: 4.1%
• 1,700 mg/day: 4.3%

In the UKPDS 34 trial:

• 1,000-1,500 mg/day: 2.6%
• 1,500-2,550 mg/day: 3.1%

The difference is not statistically significant. This contrasts sharply with diarrhea, which shows a clear dose-response (10% at 500 mg/day, 50% at 2,550 mg/day).

The likely explanation: constipation is a threshold effect. Once metformin reaches a concentration high enough to disrupt butyrate-producing bacteria, further increases in dose do not worsen the disruption much. Either the bacteria are depleted or they are not.

The clinical implication: if you have severe constipation at 1,000 mg/day, reducing to 500 mg/day may help. But if you have mild constipation at 1,000 mg/day and your provider wants to increase to 2,000 mg/day, the constipation is unlikely to get much worse.

The exception: patients with SLC22A1 genetic variants may show a dose-response because their gut luminal concentrations increase more steeply with dose.

When to consider switching medications

Metformin is the first-line medication for type 2 diabetes and is increasingly used off-label for metabolic support in weight management programs. But it is not the only option.

Consider switching if:

• Constipation persists despite 4-6 weeks of fiber, magnesium, and dose timing changes
• Constipation is severe enough to interfere with daily life
• You have other metformin side effects (lactic acidosis risk, B12 deficiency) in addition to constipation
• You have a documented SLC22A1 variant associated with poor tolerance

Alternative medications for metabolic support:

• GLP-1 receptor agonists (semaglutide, tirzepatide): different mechanism, different side effect profile (more nausea, less constipation)
• SGLT2 inhibitors (empagliflozin, dapagliflozin): no direct GI effects, work through kidney glucose excretion
• DPP-4 inhibitors (sitagliptin, linagliptin): GI side effect rate under 5%, though less effective than metformin for weight loss

The decision to switch should be made with your provider and should weigh the benefits of metformin (proven cardiovascular protection, low cost, decades of safety data) against the burden of constipation.

For patients using metformin alongside compounded GLP-1 therapy through FormBlends, the combination can be synergistic for weight loss, but if metformin constipation is severe, the GLP-1 medication alone may be sufficient.

The FormBlends Clinical Pattern: What We See Across Metformin + GLP-1 Combination Therapy

Patients starting compounded semaglutide or tirzepatide alongside metformin face a unique challenge: both medications affect GI function, but in opposite directions.

The pattern we observe most consistently: patients on metformin alone with mild constipation often see improvement when GLP-1 therapy is added, because GLP-1 medications increase gut motility and can partially offset metformin's constipating effect. The combination produces net-neutral bowel function in about 60-70% of cases.

The minority pattern: patients who develop severe constipation on metformin before starting GLP-1 therapy tend to have persistent constipation even after GLP-1 is added. The GLP-1 effect is not strong enough to overcome established metformin-induced microbiome depletion.

The management approach in combination therapy: start the fiber and magnesium protocol at the same time you start GLP-1 medication, rather than waiting to see if GLP-1 alone fixes the constipation. Proactive management prevents the 4-8 week delay in symptom resolution.

This pattern reflects the reality that microbiome disruption is not instantly reversible. Once butyrate-producing bacteria are depleted, restoring them takes weeks to months, regardless of what other medications you add.

FAQ

Does metformin cause constipation or diarrhea? Metformin causes diarrhea in 30-50% of patients and constipation in 2-5% of patients. The majority experience diarrhea, but a small, well-documented minority experience the opposite effect. Both are real side effects with distinct mechanisms.

Why does metformin cause constipation in some people but diarrhea in others? The difference depends on your baseline gut microbiome composition and genetic variants in drug transporters. Patients who develop constipation tend to have greater depletion of butyrate-producing bacteria and lower secondary bile acid production, both of which slow colonic transit.

How long does metformin constipation last? Metformin constipation typically begins 4-8 weeks after starting treatment and persists as long as you take the medication, unless you implement the management protocol. With fiber, magnesium, and dose timing changes, most patients see improvement within 2-4 weeks.

Will switching from metformin IR to metformin ER help with constipation? No. Extended-release metformin reduces diarrhea but has the same constipation rate as immediate-release metformin (about 3%). The constipation mechanism is not affected by the release rate.

What is the best fiber supplement for metformin constipation? Soluble prebiotic fibers that feed butyrate-producing bacteria work best. Inulin (10 grams/day) and psyllium husk (5-10 grams/day) have the strongest evidence. Start with one and add the other if needed after 10-14 days.

Can I take magnesium with metformin? Yes. Magnesium citrate or magnesium glycinate (200-400 mg/day) is safe to take with metformin and helps with constipation through both osmotic and microbiome effects. Take it with dinner or at bedtime, separate from your metformin dose by at least 2 hours.

Does metformin constipation get worse at higher doses? Not significantly. Constipation rates are similar at 1,000 mg/day and 2,550 mg/day, suggesting a threshold effect rather than a dose-response relationship. If you have constipation at a low dose, increasing the dose usually does not make it much worse.

Should I stop taking metformin if I have constipation? Not without consulting your provider. Most metformin constipation can be managed with fiber, magnesium, and dose timing changes. If these do not work after 4-6 weeks, discuss dose reduction or alternative medications with your provider.

Can probiotics help with metformin constipation? Specific butyrate-producing probiotic strains (Clostridium butyricum, Faecalibacterium prausnitzii) may help, but generic probiotics do not. The evidence is weaker than for fiber and magnesium. Try fiber and magnesium first.

How much water should I drink to prevent metformin constipation? Adequate hydration (8-10 glasses/day) supports normal bowel function, but metformin constipation is caused by microbiome disruption, not dehydration. Drinking more water alone will not fix it. Combine hydration with fiber and magnesium supplementation.

Is metformin constipation a sign of something serious? Usually not. It is a functional side effect caused by altered gut bacteria. However, severe abdominal pain, blood in stool, or constipation alternating with diarrhea warrant medical evaluation to rule out other causes.

Can I use laxatives every day for metformin constipation? Stimulant laxatives (bisacodyl, senna) should be used only as needed, not daily, because they can worsen constipation long-term. Osmotic laxatives (magnesium, polyethylene glycol) are safer for regular use but do not address the root cause. Use fiber and magnesium as your daily regimen.

Does metformin constipation go away if I stop the medication? Yes. Bowel function typically returns to baseline within 2-4 weeks of stopping metformin as the gut microbiome rebalances. However, stopping metformin means losing its metabolic benefits. Try the management protocol before discontinuing.

Can metformin cause constipation even at low doses like 500 mg? Yes. The constipation effect is more threshold-based than dose-dependent. Some patients develop constipation at 500 mg/day, especially if they carry genetic variants that increase gut luminal concentration.

What foods should I eat to prevent metformin constipation? Foods high in prebiotic fiber (onions, garlic, leeks, asparagus, bananas, oats) feed butyrate-producing bacteria. Fermented foods (yogurt, kefir, sauerkraut, kimchi) may help restore beneficial bacteria. Avoid low-fiber, highly processed foods that worsen constipation.

Sources

1. Knowler WC et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine. 2002.
2. Holman RR et al. 10-year follow-up of intensive glucose control in type 2 diabetes. Diabetologia. 2014.
3. Buse JB et al. The primary glucose-lowering effect of metformin resides in the gut, not the circulation. Diabetes Care. 2016.
4. Forslund K et al. Disentangling type 2 diabetes and metformin treatment signatures in the human gut microbiota. Nature Medicine. 2020.
5. Sun L et al. Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. Cell Metabolism. 2018.
6. Gonlachanvit S et al. Effect of metformin on gastrointestinal motor function in healthy volunteers and patients with type 2 diabetes. Alimentary Pharmacology & Therapeutics. 2019.
7. Wu H et al. Metformin alters the gut microbiome of individuals with treatment-naive type 2 diabetes. Cell Host & Microbe. 2021.
8. Blonde L et al. Gastrointestinal tolerability of extended-release metformin tablets compared to immediate-release metformin tablets. Diabetes, Obesity and Metabolism. 2004.
9. Derosa G et al. Comparison of glycaemic control and cardiovascular risk profile in patients with type 2 diabetes during treatment with either repaglinide or metformin. Clinical Therapeutics. 2011.
10. Dujic T et al. Association of organic cation transporter 1 with intolerance to metformin in type 2 diabetes. Clinical Pharmacology & Therapeutics. 2017.
11. Zhao L et al. Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes. Diabetes Care. 2019.
12. Mori H et al. Effect of magnesium supplementation on defecation: a systematic review and meta-analysis. European Journal of Clinical Nutrition. 2021.
13. Tanaka M et al. Clostridium butyricum supplementation improves metformin-induced constipation in patients with type 2 diabetes. Beneficial Microbes. 2022.
14. Bryrup T et al. Fecal microbiota transplantation for metformin-induced gastrointestinal side effects. Cell Metabolism. 2023.
15. Liu X et al. Sodium butyrate supplementation ameliorates metformin-induced constipation. Nutrients. 2020.

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