ArticleDigestive diseases and sciences2017
Enteric Glial Dysfunction Evoked by Apolipoprotein E Deficiency Contributes to Delayed Gastric Emptying.
Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Exploring the Mechanism of Medicated Thread Moxibustion of Zhuang Medicine in Diabetic Gastroparesis Rats Based on the Enteric Nervous System.Neurogastroenterology and motility · 2026Article
- Impact of Ammonia Exposure on the Enteric Nervous System in the Ileum of Pigs From Birth.Neurogastroenterology and motility · 2025Article
- A branching model of lineage differentiation underpinning the neurogenic potential of enteric glia.Nature communications · 2023Article
- Neutrophil-activating Protein Polymorphism of Helicobacter pylori Determines the Host Risk of Dyspepsia.Cellular and molecular gastroenterology and hepatology · 2019Article
- Co-expression of caspase-3 or caspase-8 with galanin in the human stomach section affected by carcinoma.Apoptosis : an international journal on programmed cell death · 2018Article
- MicroRNA 375 modulates hyperglycemia-induced enteric glial cell apoptosis and Diabetes-induced gastrointestinal dysfunction by targeting Pdk1 and repressing PI3K/Akt pathway.Scientific reports · 2018Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimDiabetes is the main cause of gastroparesis accompanying decreased neuronal nitric oxide synthase (nNOS) in myenteric ganglia of the stomach. Decreased nNOS expression in the stomach also results from defects in apolipoprotein E (ApoE), which is secreted by astrocytes and has neuroprotective effects on the central nervous system. However, the roles of ApoE and enteric glial cells on gastric motility are uncertain. In this study, ApoE and enteric glial cell alterations in gastroparesis were investigated.
methodsType 2 diabetic (db/db) mice and ApoE-knockout mice were analyzed. Gastric emptying was measured using the
resultsDelayed gastric emptying was observed in 27% of db/db mice with significant decreases in serum ApoE levels and GFAP expression in the gastric antrum. Gastric emptying was also delayed in ApoE-knockout mice, with a significant decrease in GFAP expression, but no change in PGP 9.5 expression. Transplantation of NSCs improved gastric emptying in ApoE-knockout mice through supplementation of GFAP-positive cells.
conclusionsOur results suggest that decreased enteric glial cells in ApoE-knockout mice are crucial for development of delayed gastric emptying, and NSC transplantation is effective in restoring myenteric ganglia and gastric motility.
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