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Neuroprotective effects of vitamin D on high fat diet- and palmitic acid-induced enteric neuronal loss in mice. | LitMetric

Neuroprotective effects of vitamin D on high fat diet- and palmitic acid-induced enteric neuronal loss in mice.

BMC Gastroenterol

Unit of Neurogastroenterology, Department of Experimental Medical Science, Lund University, Sölvegatan 19, BMC B11, 22184, Lund, Sweden.

Published: November 2018

AI Article Synopsis

  • This study explores how vitamin D affects the loss of enteric neurons caused by a high-fat diet (HFD) and palmitic acid in both live mice and cultured cells.
  • In mice, vitamin D supplementation only prevented neuron loss when given at a very high level (20 times the normal amount) during a HFD, while lower doses had no impact.
  • In cell cultures, vitamin D also protected against palmitic acid-induced neuron loss, although the exact mechanisms involving vitamin D receptors in enteric neurons remain unclear.

Article Abstract

Background: The 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.

Methods: Mice 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 (4x10M) and/or 1α,25-hydroxy-vitamin D3 (VD, 10- 10M) with or without modulators of lipid metabolism and VD pathways. Cultures were analyzed by immunocyto- and histochemical methods.

Results: Vitamin 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.

Conclusions: Results 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249721PMC
http://dx.doi.org/10.1186/s12876-018-0905-9DOI Listing

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