Fig. 4: ChREBPβ nuclear localization correlates with blood glucose levels in β-cells from transplanted human islets.
From: Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure
a Schematic of experimental design using the STZ-diabetic immunocompromised marginal islet mass model (Created with BioRender.com). Three groups of mice each received human islets from the same four to five human islet donors: Cre-transduced 500 IEQs (n = 4), ChREBPα-transduced 500 IEQs (n = 5), or 1500 untreated control IEQs (n = 5). The 500 IEQ groups were treated with an adenovirus expressing either Cre as a negative control or ChREBPα 24 h prior to transplantation. Glucose tolerance test was performed at day 42, a unilateral nephrectomy was performed at day 43. b Glucose levels were measured. c Circulating insulin measured using a human insulin-specific assay. d Intraperitoneal glucose tolerance test. e Area under the curve (AUC) for the three groups in (d). Values are means ± SEM. *p < 0.05; **p < 0.01 compared to 1500 IEQ using two-way ANOVA. f Representative images of insulin and C-terminal ChREBP immunohistochemistry from islet grafts of at least 3 different mice. g Correlation between percentages of nuclear ChREBPβ from at least 1000 insulin-positive β-cells from the grafted human islets and blood glucose levels, where each data point represents an individual transplanted mouse.
