Constipation in Diabetes: The Role of GLP-1–Based Therapies

By VETTAPHARMA reporter: For millions of adults living with diabetes mellitus, the focus often falls on blood sugar control, cardiovascular health, and neuropathy. Yet a growing body of evidence shows that chronic constipation affects a substantial portion of patients, significantly impacting quality of life. A narrative review published in Nutrients examines mechanisms, diagnosis, and management of constipation in diabetes, providing a comprehensive guide for clinicians and researchers.

The review by Fano et al. 2025, analyzed studies involving adults aged 18–75 years with type 1 or type 2 diabetes, noting that type 2 diabetes accounts for over 90% of adult cases. Using Rome IV criteria, constipation prevalence was estimated at 11%–60% in people with diabetes, compared with ~14% in the general population. The mean body mass index (BMI) of study participants ranged from 28 to 36 kg/m², reflecting overweight and obesity as common comorbidities.

This narrative review synthesized data from over 40 peer-reviewed studies, focusing on:

  • Pathophysiological mechanisms: Autonomic neuropathy, chronic hyperglycemia, and gut structural changes contribute to slowed colonic transit, with studies reporting transit times up to 72 hours in affected patients.
  • Clinical diagnosis: Rome IV criteria, patient questionnaires, and colonic transit measurements identified constipation in up to 60% of adults with diabetes.
  • Therapeutic approaches: Dietary fiber (25–30 g/day), osmotic laxatives, stimulant laxatives, and prokinetic agents; GLP‑1 receptor agonists were associated with constipation in 10–20% of users.
  • Quality-of-life impacts: Studies using validated instruments found that 30–40% of patients reported reduced physical functioning and vitality, while 20–25% reported significant social limitations due to constipation.
  • Research gaps: The review highlights the need for longitudinal studies to correlate glycemic control, neuropathy severity, and constipation-related functional impairment.

The authors observed that the biological mechanisms linking diabetes mellitus (DM) to chronic constipation remain incompletely understood, but current evidence supports a multifactorial origin. Structural alterations within the gastrointestinal (GI) tract wall—affecting smooth muscle, enteric neurons, and interstitial cells—combine with functional disturbances driven by chronic hyperglycemia, ultimately impairing colonic motility.

An additional and increasingly relevant contributor is pharmacologic. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), now widely used for glycemic control and for reducing cardiovascular and renal risk in type 2 diabetes, have been consistently associated with constipation as an adverse effect, further complicating bowel function in an already vulnerable population.

In clinical practice, the diagnosis of constipation remains largely symptom-based, relying on careful patient history and validated criteria, as objective assessments of colonic transit are invasive, costly, and typically restricted to specialized centers. As a result, constipation may be underrecognized or undertreated in routine diabetes care.

Management strategies focus on symptom relief and restoration of bowel function. First-line interventions emphasize dietary modification and increased physical activity. When these measures fail, laxatives are introduced, followed by newer pharmacologic agents or mechanical interventions in particularly severe or refractory cases.

Given the rising global prevalence of diabetes, the review underscores the importance for healthcare professionals to systematically recognize and address chronic constipation—especially in patients treated with GLP-1 RAs, where medication-induced effects may exacerbate underlying gastrointestinal dysfunction.

Source credit:

  1. De Fano, M., Baluganti, S., Manco, M., Porcellati, F., Fanelli, C. G., & Bassotti, G. (2025). The sweet side of constipation: Colonic motor dysfunction in diabetes mellitus. Nutrients, 17(19), 3038. Click here

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