AI Article Synopsis
- * Mice lacking VA (VAD) experienced decreased insulin secretion and reduced glucagon-like peptide-1 (GLP-1), but these levels could be restored by reintroducing VA into their diet.
- * The findings suggest that VA deficiency disrupts glucose metabolism via the retinoic acid receptor β (RARβ) pathway, offering potential strategies for treating glucose metabolism issues caused by VA deficiency.
Article Abstract
Background: This study aimed to investigate the impact of Vitamin A (VA) on intestinal glucose metabolic phenotypes.
Methods: Male C57BL/6 mice were randomized assigned to a VA-normal diet (VAN) or a VA-deficient diet (VAD) for 12 weeks. After12 weeks, the VAD mice were given 30 IU/g/d retinol for 10 days and VAN diet (VADN) for 10 weeks. By using glucose tolerance tests, immunofluorescence staining, quantitative polymerase chain reaction, siRNA transduction, and enzyme-linked immunosorbent assay, the glucose metabolic phenotypes as well as secretory function and intracellular hormone changes of STC-1 were assessed.
Results: VAD mice showed a decrease of glucose-stimulated insulin secretion and a loss of intestinal glucagon-like peptide-1 (GLP-1) expression. Through reintroducing dietary VA to VAD mice, the intestinal VA levels, GLP-1 expression and normal glucose can be restored. The incubation with retinol increased VA signaling factors expression within STC-1 cells, especially retinoic acid receptor β (RARβ). The activation of RARβ restored intracellular incretin hormone synthesis and secretory function.
Conclusions: VA deficiency leads to an imbalance of intestinal glucose metabolic phenotypes through a mechanism involving RARβ signaling pathway, suggesting a new method to achieve the treatment for VAD induced glucose metabolism impairment.
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| http://dx.doi.org/10.1016/j.jdiacomp.2024.108806 | DOI Listing |
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