Impaired insulin/IGF-1 is responsible for diabetic gastroparesis by damaging myenteric cholinergic neurones and interstitial cells of Cajal
Open accessAbstract
Diabetic gastroparesis is a common complication of diabetes mellitus (DM) that is characterized by decreased serum insulin and insulin-like growth factor-1 (IGF-1). Despite the fact that insulin treatment not glycemic control potently accelerated gastric emptying in type 1 DM patients, the role of insulin/InsR and IGF-1/IGF-1R signaling in diabetic gastroparesis remains incompletely elucidated. In the present study, type 1 DM mice were established and treated with insulin or Voglibose for 8 weeks. The gastric emptying was delayed from DM week 4 when the gastric InsR and IGF-1R were declined. Meanwhile, the gastric choline acetyltransferase (ChAT) was significantly reduced and the myenteric cholinergic neurones and their fibers were significantly diminished. The production of stem cell factor (SCF) was dramatically repressed in the gastric smooth muscles in DM week 6. TWereafter, interstitial cells of Cajal (ICC) were clearly lost and their networks were impaired in DM week 8. Significantly, compared with Voglibose, an 8-week treatment with insulin more efficiently delayed diabetic gastroparesis development by protecting the myenteric cholinergic neurones and ICC. In conclusion, diabetic gastroparesis was an aggressive process due to the successive damages of myenteric cholinergic neurones and ICC by impairing the insulin/InsR and IGF-1/IGF-1R signaling. Insulin therapy in the early stage may delay diabetic gastroparesis.
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In diabetes, insulin and IGF-1 deficiency causes muscle atrophy and reduced SCF production, leading to ICC depletion and impaired neuromuscular transmission.
“In diabetes, insulin and IGF-1 deficiency causes muscle atrophy and reduced SCF production, leading to ICC depletion and impaired neuromuscular transmission [52–60].”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [58]
The Results section (page unavailable) reports reduced gastric smooth-muscle SCF in diabetic mice at week 6, followed by ICC loss at week 8; the Discussion links these changes to reduced insulin/IGF-1 signaling. The Discussion also identifies ICC as mediators of neuronal transmission, but the paper does not report muscle atrophy or directly demonstrate impaired neuromuscular transmission. (LLM, conf=0.87)
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- Authors
- Yang, S., Wu, B., Sun, H., Sun, T., Han, K., Li, D., Ji, F., Zhang, G., & Zhou, D.
- Affiliations
- Capital Medical University (CN)
- Corresponding author
- Zhang, Guoquan
- Zhou, Deshan
- Venue
- Bioscience Reports
- Publisher
- Portland Press Ltd.
- Published
- 2017-10-27
- Volume
- 37
- Issue
- 5
- ISSN
- 0144-8463 (ISSN-L)
- 1573-4935
- PMC
- PMC5665615
- OpenAlex
- W2755494287
- Cited by
- 23
- References
- 35
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 4
- FWCI
- 2.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Bioscience Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31371220, 81300285, 81572322)
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Health Sciences › Medicine › Surgery › Congenital gastrointestinal and neural anomalies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- diabetic gastroparesis, insulin resistance, insulin-like growth factor I, insulin receptor, IGF1R signaling, interstitial cells of Cajal, choline acetyltransferase, stem cell factor, gastric smooth muscle, gastric emptying, type 1 diabetes, voglibose, insulin therapy
- MeSH terms
- Animals, Choline O-Acetyltransferase, Disease Models, Animal, Gene Expression Regulation, Humans, Inositol, Insulin, Insulin-Like Growth Factor I, Muscle, Smooth, Receptor, Insulin, Antigens, CD, Mice, Inbred NOD, Receptor, IGF Type 1, Gastroparesis, Stem Cell Factor, Diabetes Complications, Mice, Interstitial Cells of Cajal, Cholinergic Neurons
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