Fig. 7: RA signaling and β-cell dysfunction.
From: Genetic and pharmacologic inhibition of ALDH1A3 as a treatment of β-cell failure
A Insulin secretion in islets from db/db mice following 3-day treatment with 10 μM KOTX1 or/and 50 nM atRA. Data are expressed as means ± SEM (n = 7 or 8 per condition). Two-way ANOVA with multiple comparison test was used for statistical analysis. B Insulin secretion assay as (A) using islets from β-Aldh1a3 KO_db/db mice. Data are expressed as means ± SEM (n = 10 per condition). Two-way ANOVA with multiple comparison test was used for statistical analysis. C qPCR analyses after atRA treatment of islets from β-Aldh1a3 KO_db/db mice. Results expressed as fold changes relative to expression levels in DMSO control. Data are expressed as means ± SEM for n = 3 biologically independent samples per group. Two-way ANOVA with multiple comparison test was used for statistical analysis. D Transcription factor motif analyses on DE gene promoters. E Schematic model of the effect of diet, genetic, or pharmacological ALDH1A3 inhibition in β-cells. Source data are provided as a Source Data file.
