ArticleBMC gastroenterology2018
Neuroprotective effects of vitamin D on high fat diet- and palmitic acid-induced enteric neuronal loss in mice.
Article in BMC gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Dietary Modulation of the Enteric Nervous System: From Molecular Mechanisms to Therapeutic Applications.Nutrients · 2025Review
- Mechanisms of enteric neuropathy in diverse contexts of gastrointestinal dysfunction.Neurogastroenterology and motility · 2025Review
- Effect of Sphingomyelin and Vitamin D3 Intake on the Rabbit Brain.International journal of molecular sciences · 2025Article
- Functional Analysis of TAAR1 Expression in the Intestine Wall and the Effect of Its Gene Knockout on the Gut Microbiota in Mice.International journal of molecular sciences · 2024Article
- Oxidative Stress and Histomorphometric Remodeling: Two Key Intestinal Features of Type 2 Diabetes in Goto-Kakizaki Rats.International journal of molecular sciences · 2024Article
- 1,25(OH)2D3 supplementation alleviates gut-vascular barrier disruption via inhibition of S100B/ADAM10 pathway.Tissue barriers · 2024Article
- Potential role for vitamin D vs. intermittent fasting in controlling aquaporin-1 and aquaporin-3 expression in HFD-induced urinary bladder alterations in rats.Frontiers in molecular biosciences · 2023Article
- Short-Chain Fatty Acids as Bacterial Enterocytes and Therapeutic Target in Diabetes Mellitus Type 2.Biomedicines · 2022Review
- Article
- Disorders of the enteric nervous system - a holistic view.Nature reviews. Gastroenterology & hepatology · 2021Review
- Small intestine remodeling in male Goto-Kakizaki rats.Physiological reports · 2021Article
- Vitamin D signaling maintains intestinal innate immunity and gut microbiota: potential intervention for metabolic syndrome and NAFLD.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Exosomes derived from mangiferin‑stimulated perivascular adipose tissue ameliorate endothelial dysfunction.Molecular medicine reports · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe role of vitamin D in obesity and diabetes is debated. Obese and/or diabetic patients have elevated levels of free fatty acids, increased susceptibility to gastrointestinal symptoms and are suggested to have altered vitamin D balance. The enteric nervous system is pivotal in regulating gastrointestinal activity and high fat diet (HFD) has been shown to cause loss of enteric neurons in ileum and colon. This study investigates the effect of vitamin D on HFD- and palmitic acid-induced enteric neuronal loss in vivo and in vitro.
methodsMice were fed either a normal diet (ND) or HFD supplemented with varying levels of vitamin D (from 0x to 20x normal vitamin D level) for 19 weeks. Ileum and colon were analyzed for neuronal numbers and remodeling. Primary cultures of myenteric neurons from mouse small intestine were treated with palmitic acid (4x10
resultsVitamin D supplementation had no effect on enteric neuronal survival in the ND group. HFD caused substantial loss of myenteric neurons in ileum and colon. Vitamin D supplementation between 0-2x normal had no effect on HFD-induced neuronal loss. Supplementation with 20x normal, prevented the HFD-induced neuronal loss. In vitro supplementation of VD prevented the palmitic acid-induced neuronal loss. The VD receptor (VDR) was not identified in enteric neurons. Enteric glia expressed the alternative VD receptor, protein disulphide isomerase family A member 3 (PDIA3), but PDIA3 was not found to mediate the VD response in vitro. Inhibition of peroxisome proliferator-activated receptor gamma (PPARγ) and immune neutralization of isocitrate lyase prevented the VD mediated neuroprotection to palmitic acid exposure.
conclusionsResults show that VD protect enteric neurons against HFD and palmitic acid induced neuronal loss. The mechanism behind is suggested to be through activation of PPARγ leading to improved neuronal peroxisome function and metabolism of neuronal lipid intermediates.
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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.