ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012
Glucose sensing by gut endocrine cells and activation of the vagal afferent pathway is impaired in a rodent model of type 2 diabetes mellitus.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 81 citations in OpenAlex.
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- Microbiota and enteric nervous system crosstalk in diabetic gastroenteropathy: bridging mechanistic insights to microbiome-based therapies.Frontiers in cellular and infection microbiology · 2025Review
- Autonomic neuromodulation for cardiomyopathy associated with metabolic syndrome - Prevention of precursors for heart failure with preserved ejection fraction.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Contribution of animal models to diabetes research: Its history, significance, and translation to humans.Journal of diabetes investigation · 2023Review
- Irritable bowel syndrome: Epidemiology, overlap disorders, pathophysiology and treatment.World journal of gastroenterology · 2023Review
- Impact of Metabolic Surgery on Gut Microbiota and Sera Metabolomic Patterns among Patients with Diabetes.International journal of molecular sciences · 2022Article
- Role of Proximal Intestinal Glucose Sensing and Metabolism in the Blood Glucose Control in Type 2 Diabetic Rats After Duodenal Jejunal Bypass Surgery.Obesity surgery · 2022Article
- Zucker Diabetic-Sprague Dawley (ZDSD) rat: Type 2 diabetes translational research model.Experimental physiology · 2022Review
- Tangshen Decoction Enhances Podocytes Autophagy to Relieve Diabetic Nephropathy through Modulation of p-AMPK/p-ULK1 Signaling.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Potential Roles of Enterochromaffin Cells in Early Life Stress-Induced Irritable Bowel Syndrome.Frontiers in cellular neuroscience · 2022Review
- Review
- Bariatric and Metabolic Endoscopy: A New Paradigm.Clinical and translational gastroenterology · 2021Review
- The evolving obesity challenge: targeting the vagus nerve and the inflammatory reflex in the response.Pharmacology & therapeutics · 2021Review
- The role of diet in the pathophysiology and management of irritable bowel syndrome.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2021Review
- Immunity and the carotid body: implications for metabolic diseases.Bioelectronic medicine · 2020Review
- Therapeutic potential of α7 nicotinic acetylcholine receptor agonists to combat obesity, diabetes, and inflammation.Reviews in endocrine & metabolic disorders · 2020Review
- Possible role of intestinal stem cells in the pathophysiology of irritable bowel syndrome.World journal of gastroenterology · 2020Review
- Recording and Decoding of Vagal Neural Signals Related to Changes in Physiological Parameters and Biomarkers of Disease.Cold Spring Harbor perspectives in medicine · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Glucose in the gut lumen activates gut endocrine cells to release 5-HT, glucagon-like peptide 1/2 (GLP-1/2), and glucose-dependent insulinotropic polypeptide (GIP), which act to change gastrointestinal function and regulate postprandial plasma glucose. There is evidence that both release and action of incretin hormones is reduced in type 2 diabetes (T2D). We measured cellular activation of enteroendocrine and enterochromaffin cells, enteric neurons, and vagal afferent neurons in response to intestinal glucose in a model of type 2 diabetes mellitus, the UCD-T2DM rat. Prediabetic (PD), recent-diabetic (RD, 2 wk postonset), and 3-mo diabetic (3MD) fasted UCD-T2DM rats were given an orogastric gavage of vehicle (water, 0.5 ml /100 g body wt) or glucose (330 μmol/100 g body wt); after 6 min tissue was removed and cellular activation was determined by immunohistochemistry for phosphorylated calcium calmodulin-dependent kinase II (pCaMKII). In PD rats, pCaMKII immunoreactivity was increased in duodenal 5-HT (P < 0.001), K (P < 0.01) and L (P < 0.01) cells in response to glucose; glucose-induced activation of all three cell types was significantly reduced in RD and 3MD compared with PD rats. Immunoreactivity for GLP-1, but not GIP, was significantly reduced in RD and 3MD compared with PD rats (P < 0.01). Administration of glucose significantly increased pCaMKII in enteric and vagal afferent neurons in PD rats; glucose-induced pCaMKII immunoreactivity was attenuated in enteric and vagal afferent neurons (P < 0.01, P < 0.001, respectively) in RD and 3MD. These data suggest that glucose sensing in enteroendocrine and enterochromaffin cells and activation of neural pathways is markedly impaired in UCD-T2DM rats.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.