{Reference Type}: Journal Article
{Title}: Vitamin A influences the incretin hormone profiles by activating the retinoic acid receptor β.
{Author}: Yu B;Chen J;Wang Y;Zhou J;Wang H;Li H;Cai T;Huang R;Zhou Y;Ma J;
{Journal}: J Diabetes Complications
{Volume}: 38
{Issue}: 8
{Year}: 2024 Aug 8
{Factor}: 3.219
{DOI}: 10.1016/j.jdiacomp.2024.108806
{Abstract}: <B>BACKGROUND: </B>This study aimed to investigate the impact of Vitamin A (VA) on intestinal glucose metabolic phenotypes.<BR><B>METHODS: </B>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.<BR><B>RESULTS: </B>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.<BR><B>CONCLUSIONS: </B>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.