Fig. 3: ChREBPβ expression and nuclear localization correlates with adaptive expansion of β-cells and with glucose toxicity in diabetes.
From: Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure
a The N-terminal or the C-terminal antibodies recognizing ChREBP were used to stain pancreatic tissue slices from C57Bl/6 mice fed on a standard chow diet, or fed a high-fat diet for 1 week, or from db/db diabetic mice. All micrographs represent at least 3 independent experiments. b Ratio of expression of ChREBPβ to ChREBPα FPKM from RNAseq performed from FACS-sorted human β-cells isolated from non-diabetic (n = 4) and Type 2 diabetic subjects (n = 7). Each data point represents a different donor. Data are means ± SEM; *p < 0.05 using one-way ANOVA. c, d The N-terminal or C-terminal antibody recognizing ChREBP were used to immunolabel pancreatic tissue slices from diabetic db/db mice treated with control AAV (GFP) or with AAV expressing adipsin for 24 weeks. Correlation between percentages of nuclear ChREBPβ in insulin-positive β-cells and blood glucose levels (e) or blood insulin levels (f), where each data point represents an individual mouse. All micrographs represent at least 3 independent experiments.
