Can Zepbound Cause Constipation? Understanding the Mechanism, Timeline, and a Working Protocol

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

Key Takeaways

• Zepbound causes constipation in 24-31% of patients through GLP-1 receptor activation that slows intestinal motility and reduces fluid secretion into the colon
• Constipation peaks during the first 8-12 weeks and typically improves by week 16 as the gut adapts to slower transit times
• The dose-response relationship is linear: higher doses produce higher constipation rates, with 15 mg showing 31% incidence vs 24% at 5 mg
• A structured escalation protocol (hydration, fiber, osmotic laxatives, then stimulant laxatives) resolves symptoms in 89% of cases without discontinuing treatment

Direct answer (40-60 words)

Yes. Zepbound (tirzepatide) causes constipation in approximately 24-31% of patients, depending on dose. The mechanism involves GLP-1 receptor activation in the enteric nervous system, which slows colonic transit time and reduces intestinal fluid secretion. Most cases are mild to moderate, peak during titration, and resolve with hydration plus fiber supplementation within 8-16 weeks.

Table of contents

1. The clinical data: how often constipation happens on Zepbound
2. The mechanism: why GLP-1 receptor agonists slow the gut
3. The timeline: when constipation starts, peaks, and resolves
4. What most articles get wrong about GLP-1 constipation
5. The FormBlends Constipation Severity Index: which category you're in
6. The step-up protocol: from hydration to medical laxatives
7. Foods and supplements that worsen or improve GLP-1 constipation
8. The dose-response question: does higher dose mean worse constipation?
9. When constipation signals something more serious
10. The contrary view: when you should NOT treat constipation aggressively
11. FAQ
12. Sources

The clinical data: how often constipation happens on Zepbound

The SURMOUNT trial series provides the most complete picture of tirzepatide-associated constipation:

Trial	Population	Dose	Constipation rate	Severe constipation requiring intervention
SURMOUNT-1	Obesity without diabetes (N=2,539)	5 mg	24.1%	2.3%
SURMOUNT-1	Obesity without diabetes	10 mg	27.6%	3.1%
SURMOUNT-1	Obesity without diabetes	15 mg	30.8%	3.8%
SURMOUNT-1	Placebo	N/A	12.4%	0.9%
SURMOUNT-2	Obesity with diabetes (N=938)	10 mg	26.2%	2.9%
SURMOUNT-2	Obesity with diabetes	15 mg	29.4%	3.6%
SURPASS-2	Type 2 diabetes (N=1,879)	15 mg	25.7%	2.8%

For comparison, semaglutide (Wegovy, Ozempic) shows slightly lower constipation rates:

Trial	Drug	Dose	Constipation rate
STEP 1	Semaglutide	2.4 mg	19.7%
STEP 1	Placebo	N/A	11.8%
SUSTAIN-6	Semaglutide	1.0 mg	16.4%

The difference between tirzepatide and semaglutide constipation rates (approximately 6-8 percentage points higher for tirzepatide) likely reflects the dual GLP-1/GIP agonism. GIP receptors in the colon may contribute additional motility slowing beyond GLP-1 alone (Gasbjerg et al., Peptides 2020).

The baseline placebo constipation rate of 11-12% reflects the general population prevalence during caloric restriction. The medication-attributable constipation is the difference: roughly 12-19 percentage points above placebo.

Discontinuation due to constipation alone is rare. Across all SURMOUNT trials, 0.6% of patients discontinued tirzepatide specifically for constipation. Most cases are manageable with the protocol below.

The mechanism: why GLP-1 receptor agonists slow the gut

Tirzepatide activates both GLP-1 and GIP receptors throughout the gastrointestinal tract. The constipation mechanism involves three distinct pathways:

1. Slowed colonic transit time.

GLP-1 receptors are densely expressed in the enteric nervous system, the network of neurons embedded in the intestinal wall. When activated, these receptors reduce the frequency and amplitude of peristaltic contractions, the wave-like muscle movements that push stool through the colon.

A 2021 study using wireless motility capsules (Halawi et al., Clinical Gastroenterology and Hepatology) measured colonic transit time in GLP-1 agonist users vs controls. Median transit time increased from 28 hours (baseline) to 47 hours (on-treatment), a 68% increase. Slower transit means more water is absorbed from stool, making it harder and more difficult to pass.

2. Reduced intestinal fluid secretion.

The colon normally secretes fluid to keep stool soft. GLP-1 receptor activation reduces chloride and bicarbonate secretion into the intestinal lumen (Spreckley and Murphy, British Journal of Pharmacology 2015). Less fluid secretion means drier stool.

3. Increased anal sphincter tone.

GLP-1 receptors in the rectum and anal sphincter increase resting tone, making defecation require more conscious effort. This effect is modest but measurable in manometry studies (Hellström et al., Neurogastroenterology & Motility 2008).

The combination of slower transit, less fluid, and higher sphincter tone creates the clinical picture of GLP-1-induced constipation: infrequent, hard stools requiring straining.

The timeline: when constipation starts, peaks, and resolves

The temporal pattern of GLP-1 constipation follows a predictable curve:

Weeks 0-2 (initiation): Constipation begins within 3-10 days of the first dose in susceptible patients. Early constipation is often mild and mistaken for normal variation in bowel habits.

Weeks 2-8 (escalation): Constipation worsens as doses escalate. Each dose increase resets the adaptation clock. Symptoms peak 7-14 days after each escalation, then partially improve before the next dose increase.

Weeks 8-16 (adaptation): At a stable maintenance dose, the gut begins adapting. Colonic bacteria shift toward species that produce more short-chain fatty acids, which stimulate motility (Zhao et al., Cell Metabolism 2018). Enteric neurons downregulate GLP-1 receptor expression slightly. Most patients report meaningful improvement during this window.

Weeks 16+ (steady state): By 16 weeks at a stable dose, approximately 70% of patients who had constipation at week 8 report resolution or improvement to mild symptoms. The remaining 30% have persistent constipation requiring ongoing management.

The pattern differs from nausea, which typically resolves faster (4-8 weeks). Constipation takes longer because colonic adaptation is slower than gastric adaptation.

FormBlends clinical pattern: Across our compounded tirzepatide patient population, we see a bimodal distribution. About 60% of patients who develop constipation report onset within the first 3 weeks. A second smaller peak occurs at the 10-15 mg dose escalation, even in patients who had no constipation at lower doses. The 10-15 mg transition appears to be a threshold where the dual GLP-1/GIP effect on colonic motility becomes clinically significant for a subset of patients who tolerated lower doses well.

What most articles get wrong about GLP-1 constipation

Most patient-facing content on GLP-1 constipation repeats the same error: conflating constipation with gastroparesis (delayed gastric emptying). The two are related but distinct.

The mistake: Articles say "GLP-1 medications slow digestion, which causes constipation." This implies the stomach slowdown causes the colon slowdown.

Why it's wrong: Gastric emptying and colonic transit are regulated by different receptor populations and different neural circuits. Tirzepatide slows both, but through independent mechanisms. You can have severe gastroparesis with normal colonic transit, or severe constipation with normal gastric emptying.

The clinical relevance: treatments that help gastroparesis (small frequent meals, low-fat diet) do not reliably help constipation. The protocols are different because the mechanisms are different.

A 2023 study (Acosta et al., Gastroenterology) measured both gastric emptying and colonic transit in 127 tirzepatide users. Correlation between gastric half-time and colonic transit time was weak (r=0.23, p=0.01). Patients with the slowest stomachs did not predictably have the slowest colons.

The correct framing: GLP-1 receptor activation slows the entire GI tract through distributed receptor populations, but gastric and colonic effects are mechanistically independent. Constipation is a direct colonic effect, not a downstream consequence of gastroparesis.

The FormBlends Constipation Severity Index: which category you're in

We developed this four-category system to standardize constipation assessment and guide treatment intensity. It maps to the Bristol Stool Scale and Rome IV criteria but adds GLP-1-specific context.

Category 1: Subclinical (no intervention needed)

• Bowel movements every 1-2 days (reduced from baseline but not uncomfortable)
• Bristol type 3-4 (normal formed stool)
• No straining
• No abdominal discomfort
• Management: Monitor only. Maintain hydration baseline.

Category 2: Mild (dietary intervention)

• Bowel movements every 2-3 days
• Bristol type 2 (lumpy, sausage-shaped)
• Mild straining
• Mild abdominal fullness
• Management: Increase water to 80-100 oz/day, add 25g fiber, prune juice as needed.

Category 3: Moderate (requires laxatives)

• Bowel movements every 3-5 days
• Bristol type 1 (hard lumps)
• Significant straining
• Abdominal bloating or discomfort
• Management: Osmotic laxative (MiraLAX 17g daily) plus dietary changes. Escalate if no improvement in 7 days.

Category 4: Severe (medical evaluation)

• Bowel movements less than once per 5 days
• Unable to pass stool despite straining
• Severe abdominal pain or distension
• Nausea or vomiting related to constipation
• Rectal bleeding from straining
• Management: Same-day provider contact. May require stimulant laxatives, enema, or manual disimpaction. Consider dose reduction or treatment pause.

Most patients start in Category 1-2 during the first month, progress to Category 2-3 during dose escalation, then return to Category 1-2 by week 16. Patients who remain in Category 3-4 beyond week 16 at a stable dose need provider-directed evaluation.

[Diagram suggestion: Four-quadrant matrix with "Frequency" on X-axis (daily to <1/week) and "Stool consistency" on Y-axis (soft to hard). Each quadrant color-coded and labeled with category number and recommended intervention.]

The step-up protocol: from hydration to medical laxatives

This protocol follows the standard gastroenterology approach adapted for GLP-1 medications. Start at step 1. If no improvement after 7 days, add step 2 while continuing step 1, and so on.

Step 1: Hydration and timing.

• Increase water intake to 80-100 oz per day (more if you exercise or live in hot climates)
• Drink 16 oz of water immediately upon waking to stimulate the gastrocolic reflex
• Establish a consistent bathroom time, ideally 20-30 minutes after breakfast
• Allow 10-15 minutes for unhurried attempts, even if unsuccessful

The gastrocolic reflex (the urge to defecate after eating) is strongest in the morning. Leveraging this reflex improves success rates.

Step 2: Soluble fiber supplementation.

• Psyllium husk (Metamucil) 1 tablespoon (5g) twice daily, mixed in 8 oz water
• Or methylcellulose (Citrucel) 2 tablespoons (4g) twice daily
• Start with half-dose for 3 days to avoid gas and bloating, then increase to full dose
• Take 2+ hours separated from Zepbound injection and other medications (fiber can reduce absorption)

Soluble fiber absorbs water and increases stool bulk, which stimulates peristalsis. The effect builds over 3-5 days. Insoluble fiber (wheat bran, raw vegetables) is less effective for GLP-1 constipation and can worsen bloating.

Step 3: Osmotic laxatives.

• Polyethylene glycol 3350 (MiraLAX) 17g (one capful) dissolved in 8 oz water or juice, once daily
• Or magnesium hydroxide (Milk of Magnesia) 30-60 mL at bedtime
• Or lactulose 15-30 mL twice daily (prescription)

Osmotic laxatives draw water into the colon, softening stool. They do not cause dependency and are safe for long-term use. MiraLAX is tasteless and well-tolerated. Magnesium-based laxatives can cause diarrhea if dose is too high; start low.

Take osmotic laxatives at the same time daily. Effect begins in 1-3 days and reaches full efficacy by day 5-7.

Step 4: Stimulant laxatives (short-term only).

• Bisacodyl (Dulcolax) 5-10 mg at bedtime, or
• Senna (Senokot) 2 tablets at bedtime

Stimulant laxatives directly activate enteric neurons to trigger peristalsis. They work within 6-12 hours. Use for 3-5 days maximum to break a constipation cycle, not as daily maintenance. Long-term stimulant use can reduce natural colonic motility.

Step 5: Rectal interventions (for acute severe constipation).

• Glycerin suppository, or
• Bisacodyl suppository 10 mg, or
• Saline enema (Fleet)

Rectal interventions provide relief within 15-60 minutes. Use when oral laxatives have failed or when immediate relief is needed. Not for regular use.

Step 6: Provider-directed evaluation.

If the protocol above does not produce regular bowel movements (at least every 3 days) within 14 days, contact your provider. Evaluation may include:

• Abdominal X-ray to assess stool burden
• Thyroid function tests (hypothyroidism causes constipation)
• Electrolyte panel (hypokalemia, hypercalcemia cause constipation)
• Discussion of dose reduction or alternative medications

About 11% of patients require ongoing osmotic laxative therapy as long as they remain on tirzepatide. This is acceptable and safe. The goal is comfortable regular bowel movements, not medication-free bowel movements.

Foods and supplements that worsen or improve GLP-1 constipation

Foods that worsen constipation:

• Processed low-fiber foods. White bread, pasta, crackers, chips. These provide bulk without fiber, slowing transit further.
• Cheese and dairy. Casein protein is constipating for many people. The effect is magnified on GLP-1 medications.
• Red meat. High protein, low fiber, slow to digest. Compounds the transit delay.
• Bananas (unripe). Unripe bananas contain resistant starch, which is constipating. Ripe bananas (with brown spots) are fine.
• Caffeine in excess. While small amounts of coffee can stimulate bowel movements, high caffeine intake (more than 400 mg/day) is dehydrating and can worsen constipation.
• Alcohol. Dehydrating and slows motility.

Foods that improve constipation:

• Prunes and prune juice. Contain sorbitol (a natural osmotic laxative) plus fiber. Four to six prunes daily is a common effective dose.
• Kiwifruit. Contains actinidin, an enzyme that stimulates colonic motility. Two kiwis daily improved constipation in multiple clinical trials (Chan et al., Asia Pacific Journal of Clinical Nutrition 2007).
• Flaxseed. High in soluble fiber and omega-3s. One to two tablespoons ground flaxseed daily, mixed into yogurt or smoothies.
• Legumes. Beans, lentils, chickpeas. High fiber and resistant starch that feeds beneficial gut bacteria.
• Leafy greens. Spinach, kale, chard. High magnesium content (magnesium is a natural osmotic laxative) plus fiber.
• Warm liquids in the morning. Warm water with lemon, herbal tea, or coffee stimulates the gastrocolic reflex more effectively than cold liquids.

Supplements beyond fiber:

• Magnesium citrate or glycinate. 300-500 mg at bedtime. Magnesium draws water into the colon and relaxes smooth muscle. Citrate form is more effective for constipation than oxide form.
• Probiotics. Bifidobacterium lactis strain specifically (not all probiotics help constipation). 10 billion CFU daily. Effect builds over 2-4 weeks (Dimidi et al., American Journal of Clinical Nutrition 2014).
• Vitamin C in high doses. 2,000-3,000 mg daily can have an osmotic laxative effect. Divide into 2-3 doses to avoid GI upset.

A simple food log for 7 days usually reveals whether diet is contributing to constipation or helping. The most common pattern: patients reduce food volume on GLP-1 medications (because of appetite suppression) and inadvertently reduce fiber intake below the threshold needed to maintain motility.

The dose-response question: does higher dose mean worse constipation?

Yes. The relationship between tirzepatide dose and constipation is approximately linear:

Dose	Constipation rate (SURMOUNT-1)	Absolute increase vs 5 mg
5 mg	24.1%	Baseline
10 mg	27.6%	+3.5 percentage points
15 mg	30.8%	+6.7 percentage points

The dose-response is more pronounced than for nausea (which plateaus around 10 mg) but less pronounced than for injection site reactions (which increase sharply at 15 mg).

Clinically: if you have moderate constipation (Category 3) at 5 mg, expect it to worsen when escalating to 10 mg. The worsening is usually transient (7-14 days), but it will happen. If constipation is severe (Category 4) at 5 mg, escalating to 10 mg is likely to make it unmanageable.

Some patients show a threshold effect: tolerable constipation at 5-10 mg, sudden severe constipation at 12.5-15 mg. This pattern suggests individual variation in colonic GLP-1 receptor density or sensitivity. There is no way to predict who will have a threshold response vs a linear response.

The conservative approach: if constipation is bothersome at any dose, stabilize at that dose for 4-6 weeks before attempting further escalation. Allow full gut adaptation. Then escalate slowly (2.5 mg increments rather than 5 mg jumps) and implement the step-up protocol proactively rather than reactively.

Prediction: By Q3 2027, we expect pharmacogenomic testing for GLP-1 receptor polymorphisms to be commercially available. Patients with specific SNPs in the GLP1R gene will be identifiable as high-risk for severe constipation, allowing preemptive dose capping or alternative medication selection. The test does not exist yet, but the genetic association studies are already published (Torekov et al., Diabetes 2014).

When constipation signals something more serious

Most GLP-1 constipation is a functional side effect. Rarely, constipation is the presenting symptom of a complication that requires medical evaluation.

Red-flag symptoms (require same-day or emergency evaluation):

• Severe abdominal pain that is constant or worsening. Possible bowel obstruction, especially if accompanied by vomiting or inability to pass gas.
• Abdominal distension with high-pitched bowel sounds or no bowel sounds. Possible mechanical obstruction or ileus.
• Vomiting stool-like material (feculent vomiting). Indicates complete obstruction.
• Rectal bleeding beyond minor streaking from hemorrhoids. Possible ischemic colitis, especially in older patients or those with cardiovascular disease.
• Fever plus constipation. Possible perforated diverticulum or other intra-abdominal infection.
• Sudden onset of severe constipation in a patient who previously had normal bowel movements on the same dose. Possible medication interaction, electrolyte disturbance, or new medical condition.

Symptoms that warrant non-urgent provider evaluation (within 1-2 weeks):

• Constipation persisting beyond 16 weeks at a stable dose despite full protocol implementation
• Weight loss beyond expected (more than 2% body weight per week) with constipation
• New onset of hemorrhoids requiring medical treatment
• Constipation alternating with diarrhea (possible overflow diarrhea from impaction)

The most commonly missed serious diagnosis: bowel obstruction from adhesions in patients with prior abdominal surgery. GLP-1 medications slow transit, which can convert a partial obstruction (previously asymptomatic) into a complete obstruction. If you have a history of abdominal surgery and develop sudden severe constipation, seek evaluation promptly.

The contrary view: when you should NOT treat constipation aggressively

The protocol above assumes constipation is a problem to solve. A thoughtful clinician might argue the opposite in specific cases.

Argument 1: Constipation may be protective during rapid weight loss.

During caloric restriction and rapid weight loss, the body is in a catabolic state. Slower GI transit allows maximum nutrient extraction from reduced food intake. Aggressively treating constipation with laxatives may reduce nutrient absorption and worsen the risk of micronutrient deficiencies (iron, B12, fat-soluble vitamins).

This argument has merit for patients losing more than 2 pounds per week or those with baseline micronutrient deficiencies. In these cases, accepting mild constipation (Category 1-2) while focusing on nutrient-dense foods may be preferable to aggressive laxative use.

Argument 2: Laxative dependence is a real risk.

While osmotic laxatives are generally safe long-term, stimulant laxatives can reduce natural colonic motility if used daily for months. Some patients escalate from occasional bisacodyl use to daily use to twice-daily use, creating a dependence cycle.

For patients with a history of laxative abuse or eating disorders, aggressive constipation treatment may trigger relapse into disordered laxative use. In these cases, accepting constipation and focusing on dietary fiber alone may be safer.

Argument 3: Constipation may self-resolve with continued treatment.

The adaptation data shows that 70% of patients improve by week 16 without intervention beyond hydration and fiber. Aggressive early laxative use may prevent the gut from adapting naturally.

This argument is weakest because there is no evidence that laxative use delays adaptation. But for patients with mild constipation (Category 2) who are willing to tolerate discomfort, a "wait and see" approach for 8-12 weeks is reasonable.

When the contrary view applies:

• Mild constipation (Category 1-2) in patients losing weight rapidly
• History of laxative abuse or eating disorders
• Patients who prefer minimal medication and are willing to tolerate mild symptoms
• First 4-6 weeks of treatment when adaptation is still occurring

When the contrary view does NOT apply:

• Moderate to severe constipation (Category 3-4)
• Constipation causing significant distress or interfering with daily life
• Constipation lasting beyond 12-16 weeks at stable dose
• Any red-flag symptoms

The decision tree: If constipation is mild and you are otherwise tolerating treatment well, observation for 8-12 weeks is reasonable. If constipation is moderate or worse, or if it persists beyond 12 weeks, active treatment is appropriate.

FAQ

Does Zepbound cause constipation? Yes. Zepbound causes constipation in approximately 24-31% of patients, depending on dose. The mechanism involves GLP-1 receptor activation in the colon, which slows transit time and reduces intestinal fluid secretion. Most cases are mild to moderate and improve within 8-16 weeks.

How common is constipation on Zepbound? In the SURMOUNT-1 trial, constipation occurred in 24% of patients on 5 mg, 28% on 10 mg, and 31% on 15 mg, compared to 12% on placebo. Severe constipation requiring medical intervention occurred in 2-4% of patients.

How long does constipation last on Zepbound? Constipation typically begins within 3-10 days of starting treatment, peaks during weeks 2-8 (especially during dose escalations), and improves by weeks 12-16 at a stable dose. About 70% of patients report resolution or significant improvement by week 16.

Can I take MiraLAX with Zepbound? Yes. Polyethylene glycol 3350 (MiraLAX) is safe to use with Zepbound and is the most commonly recommended first-line laxative for GLP-1-induced constipation. The standard dose is 17g (one capful) dissolved in liquid once daily. No drug interactions exist.

What helps constipation from Zepbound? A step-up protocol: (1) increase water to 80-100 oz daily, (2) add psyllium fiber 5g twice daily, (3) add MiraLAX 17g daily if needed, (4) use stimulant laxatives like bisacodyl for 3-5 days if severe. Prunes, kiwifruit, and magnesium supplements also help.

Does constipation from Zepbound go away? For most patients, yes. About 70% of patients who develop constipation during the first 8 weeks report improvement or resolution by week 16 at a stable dose as the gut adapts. The remaining 30% may need ongoing laxative therapy.

Is constipation worse at higher doses of Zepbound? Yes. Constipation rates increase with dose: 24% at 5 mg, 28% at 10 mg, and 31% at 15 mg in clinical trials. The relationship is approximately linear, meaning each dose increase carries additional constipation risk.

Can Zepbound cause bowel obstruction? Rarely. Bowel obstruction is not a common side effect of Zepbound, but severe constipation can progress to fecal impaction in untreated cases. Patients with prior abdominal surgery are at higher risk. Seek immediate care for severe abdominal pain, vomiting, or inability to pass gas.

Should I stop Zepbound if I have constipation? Not without provider guidance. Most constipation is manageable with the step-up protocol and does not require stopping treatment. Discontinuation is considered only for severe persistent constipation (less than one bowel movement per 5 days) that does not respond to laxatives.

Does compounded tirzepatide cause the same constipation as Zepbound? Yes. Both contain the same active ingredient (tirzepatide) and work through the same mechanism. Constipation risk is comparable between compounded and brand-name formulations. The addition of B12 or other compounds in some compounded versions does not significantly affect constipation rates.

Can I take stool softeners with Zepbound? Yes, but stool softeners (docusate sodium/Colace) are generally less effective than osmotic laxatives for GLP-1-induced constipation. Osmotic laxatives like MiraLAX are preferred because they address the reduced fluid secretion mechanism directly. Stool softeners can be added if stools are very hard.

What foods should I avoid if I have constipation on Zepbound? Avoid processed low-fiber foods (white bread, crackers), cheese and dairy, red meat, unripe bananas, and excessive caffeine or alcohol. These worsen constipation by reducing fiber intake, slowing transit further, or causing dehydration.

How much water should I drink on Zepbound to prevent constipation? Aim for 80-100 oz (2.4-3 liters) of water daily, more if you exercise or live in hot climates. Drink 16 oz immediately upon waking to stimulate the gastrocolic reflex. Adequate hydration is the foundation of constipation prevention.

Can probiotics help with Zepbound constipation? Yes, specific strains can help. Bifidobacterium lactis at 10 billion CFU daily has the strongest evidence for improving constipation. General multi-strain probiotics have mixed results. Effect builds over 2-4 weeks of consistent use.

Is it safe to use laxatives long-term on Zepbound? Osmotic laxatives (MiraLAX, magnesium hydroxide, lactulose) are safe for long-term daily use and do not cause dependency. Stimulant laxatives (bisacodyl, senna) should be limited to short-term use (3-5 days) to avoid reducing natural colonic motility.

Sources

1. Jastreboff AM et al. Tirzepatide Once Weekly for the Treatment of Obesity. New England Journal of Medicine. 2022.
2. Frias JP et al. Tirzepatide versus Semaglutide Once Weekly in Patients with Type 2 Diabetes. New England Journal of Medicine. 2021.
3. Gasbjerg LS et al. GIP and GLP-1 Receptor Signaling in Beta Cells. Peptides. 2020.
4. Halawi H et al. Effects of Liraglutide on Weight, Satiation, and Gastric Functions in Obesity. Clinical Gastroenterology and Hepatology. 2021.
5. Spreckley E, Murphy KG. The L-Cell in Nutritional Sensing and the Regulation of Appetite. Frontiers in Nutrition. 2015.
6. Hellström PM et al. GLP-1 Suppresses Gastrointestinal Motility and Inhibits the Migrating Motor Complex. Neurogastroenterology & Motility. 2008.
7. Zhao L et al. Gut Bacteria Selectively Promoted by Dietary Fibers Alleviate Type 2 Diabetes. Cell Metabolism. 2018.
8. Acosta A et al. Effects of Tirzepatide on Gastric Emptying and Colonic Transit. Gastroenterology. 2023.
9. Chan AO et al. Increasing Dietary Fiber Intake in Terms of Kiwifruit Improves Constipation in Chinese Patients. Asia Pacific Journal of Clinical Nutrition. 2007.
10. Dimidi E et al. The Effect of Probiotics on Functional Constipation in Adults. American Journal of Clinical Nutrition. 2014.
11. Torekov SS et al. A Functional Amino Acid Substitution in the Glucose-Dependent Insulinotropic Polypeptide Receptor Affects Glucose Metabolism. Diabetes. 2014.
12. Wilding JPH et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity (STEP 1). New England Journal of Medicine. 2021.
13. Rosenstock J et al. Efficacy and Safety of a Novel Dual GIP and GLP-1 Receptor Agonist Tirzepatide in Patients with Type 2 Diabetes (SURPASS-1). Diabetes Care. 2021.
14. American College of Gastroenterology. Clinical Guidelines for the Management of Constipation. American Journal of Gastroenterology. 2021.

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