Diabetic gastroparesis: what we have learned and had to unlearn in the past 5 years: Figure 1
Open accessAbstract
Diabetic gastroparesis is a disorder that occurs in both type 1 and type 2 diabetes. It is associated with considerable morbidity among these patients and with the resultant economic burden on the health system. It is primarily a disease seen in middle-aged women, although the increased predisposition in women still remains unexplained. Patients often present with nausea, vomiting, bloating, early satiety and abdominal pain. The pathogenesis of this complex disorder is still not well understood but involves abnormalities in multiple interacting cell types including the extrinsic nervous system, enteric nervous system, interstitial cells of Cajal (ICCs), smooth muscles and immune cells. The primary diagnostic test remains gastric scintigraphy, although other modalities such as breath test, capsule, ultrasound, MRI and single photon emission CT imaging show promise as alternative diagnostic modalities. The mainstay of treatment for diabetic gastroparesis has been antiemetics, prokinetics, nutritional support and pain control. In recent years, gastric stimulation has been used in refractory cases with nausea and vomiting. As we better understand the pathophysiology, newer treatment modalities are emerging with the aim of correcting the underlying defect. In this review, what has been learned about diabetic gastroparesis in the past 5 years is highlighted. The epidemiology, pathogenesis, diagnosis and treatment of diabetic gastroparesis are reviewed, focusing on the areas that are still controversial and those that require more studies. There is also a focus on advances in our understanding of the cellular changes that underlie development of diabetic gastroparesis, highlighting new opportunities for targeted treatment.
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Gastroparesis profoundly affects postprandial glycemic excursions, insulin requirements, and the overall management of diabetes.
“As a consequence, gastroparesis profoundly affects postprandial glycemic excursions, insulin requirements, and the overall management of diabetes [15, 19, 23, 88, 89].”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [89]
The Pathogenesis section says gastric-emptying rate is a major determinant of the initial postprandial glycemic response and that delayed emptying can cause hypoglycemia in insulin-treated people. The Treatment section says erratic emptying affects glycemic control, supporting its relevance to diabetes management. Neither passage states that gastroparesis changes insulin requirements. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe interplay between autonomic neuropathy, impaired enteric neurotransmission, and loss or dysfunction of interstitial cells of Cajal produces a motility disorder that disrupts the temporal coordination between meal ingestion, gastric processing, intestinal absorption, and insulin pharmacodynamics.
“The interplay between autonomic neuropathy, impaired enteric neurotransmission, and loss or dysfunction of interstitial cells of Cajal produces a motility disorder that disrupts the temporal coordination between meal ingestion, gastric processing, intestinal absorption, and insulin pharmacodynamics.”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [89]
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Research works printed but not linked: 1
- [65]McCallum RW Lin Z Damjanov I Interstitial cells of cajal in the stomach of patients with gastroparesis Neurogastroenterol Motil 2006 18 758 19614868
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Relationships Between Gastric Emptying, Postprandial Glycemia, and Incretin Hormones
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Diabetic gastroparesis: pathophysiology and impact on insulin timing choices
Galeano, F., Tumminia, A., Oteri, V., Le Moli, R., Piticchio, T., Scilletta, S., Di Marco, M., Di Pino, A., & Frasca, F. (2026) · Endocrine · doi:10.1007/s12020-026-04693-6
“As a consequence, gastroparesis profoundly affects postprandial glycemic excursions, insulin require - ments, and the overall management of diabetes [15, 19, 23, 88, 89].”
- Authors
- Kashyap, P., & Farrugia, G.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Farrugia, Gianrico
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2010-09-25
- Volume
- 59
- Issue
- 12
- Pages
- 1716-1726
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- PMC
- PMC2996823
- OpenAlex
- W2119082327
- Cited by
- 175
- References
- 120
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 6 · 2023: 10 · 2022: 10 · 2021: 7 · 2020: 14 · 2019: 6 · 2018: 14 · 2017: 10 · 2016: 12 · 2015: 6 · 2014: 17 · 2013: 23 · 2012: 20
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gut (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (U01DK074008, DK57061, DK-68055, P01DK068055, R01DK057061, U01DK074035)
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Gastroenterology › Gastroesophageal reflux and treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- diabetic gastroparesis, type 1 diabetes, type 2 diabetes, pathogenesis, interstitial cells of Cajal, enteric nervous system, gastric emptying scintigraphy, gastric emptying, antiemetics, prokinetic agents, gastric electrical stimulation, nausea and vomiting, sex differences, targeted therapy
- MeSH terms
- Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Gastroenterology, Humans, Sex Factors, Gastroparesis
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