ArticleNutrition & diabetes2019
Intestinal electrical stimulation attenuates hyperglycemia and prevents loss of pancreatic β cells in type 2 diabetic Goto-Kakizaki rats.
Article in Nutrition & diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 14 citations in OpenAlex.
- Duodenal myoelectrical hyperactivity drives diabetic remission in rat models of type 2 diabetes.Diabetologia · 2026Article
- Carbohydrate response element-binding protein (ChREBP) mediates decreased SNAP25 expression in islets from diabetic Goto-Kakizaki (GK) rats.FEBS open bio · 2024Article
- Article
- GLP-1 signaling-regulated SNAP25 is involved in improved insulin secretion in diabetic GK rats after Roux-en-Y gastric bypass surgery.Molecular biology reports · 2024Article
- An efficient online peak detection algorithm for synchronized intestinal electrical stimulation and its application for treating diabetes.Medical & biological engineering & computing · 2023Article
- A short review on the features of the non-obese diabetic Goto-Kakizaki rat intestine.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022Review
- Intestinal Electrical Stimulation Enhances Release of Postprandial Incretin Hormones Via Cholinergic Mechanisms.Obesity surgery · 2021Article
- Small intestine remodeling in male Goto-Kakizaki rats.Physiological reports · 2021Article
- Electroceuticals in the Gastrointestinal Tract.Trends in pharmacological sciences · 2020Review
- Integrated 16S rRNA Sequencing, Metagenomics, and Metabolomics to Characterize Gut Microbial Composition, Function, and Fecal Metabolic Phenotype in Non-obese Type 2 Diabetic Goto-Kakizaki Rats.Frontiers in microbiology · 2019Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveRecently, intestinal electrical stimulation (IES) has been reported to result in weight loss; however, it is unclear whether it has a therapeutic potential for diabetes. The aim of the present study was to explore the potential hypoglycemic effects of IES and its possible mechanisms involving β cells in diabetic rats. SUBJECTS/
methodsDiabetic Goto-Kakizaki (GK) rats were chronically implanted with one pair of electrodes in the duodenum. The oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed with or without IES, and plasma glucagon-like peptide-1 (GLP-1) and insulin level were measured. In the other two OGTT sessions, rats were treated with either Exendin (9-39) (GLP-1 antagonist) or Exendin (9-39) plus IES to investigate the underlying mechanism involving GLP-1. Gastric emptying and small intestinal transit were also measured with or without IES. In a chronic study, GK rats were treated with IES or Sham-IES for 8 weeks. Blood glucose, plasma GLP-1 and insulin level, body weight, and food intake were measured. Pancreas weight, islet β-cell apoptosis, and proliferation were also analyzed.
resultsAcute IES reduced blood glucose level from 60 to 120 min during OGTT by 16-20% (all p < 0.05, vs. Sham-IES). GLP-1 antagonist significantly blocked the inhibitory effect of IES on hyperglycemia from 15 to 120 min (all p < 0.05). IES accelerated the small intestinal transit by 15% (p = 0.004). After 8 weeks of chronic stimulation, IES significantly reduced blood glucose (p < 0.05) and body weight (p = 0.02) and increased the plasma GLP-1 concentration (p < 0.05). Furthermore, we observed that chronic IES reduced pancreatic β-cell apoptosis (p = 0.045), but showed no effects on β-cell proliferation.
conclusionsOur study firstly proved the hypoglycemic effect of IES in a rodent model of type 2 diabetes, possibly attributed to the increasing GLP-1 secretion and improvement in β-cell functions.
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