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. 2017 Dec 13;5(3):367–398. doi: 10.1016/j.jcmgh.2017.11.016

Figure 2.

Figure 2

Experimental design. (A, Study 1). In group (i), Nrf2+/+ C57BL/6 mice were first primed over a period of 15 weeks for NASH by feeding a HF55Fr diet before being transferred to the standard HF30Fr diet at the beginning of Week 16. In group (ii), an equal number of age-matched Nrf2+/+ mice were fed an RC diet along with unadulterated drinking water throughout. After being placed for 24 weeks on either of these 2 dietary regimens, mice in group (i) and group (ii) were treated with either TBE-31 (5 nmol/g body weight) or DMSO vehicle control, by oral gavage 3 times/week for a total of 6 weeks, while still being provided with the same HF30Fr diet or RC diet. Glucose homeostasis was monitored in all mice by ITT, GTT, and PTT at the times indicated. (B, Study 2). In group (i), Nrf2+/+ and Nrf2-/- C57BL/6 mice, of 8–10 weeks of age, were fed the standard HF30Fr diet for 10 weeks before being treated with either TBE-31 or DMSO for a total of 6 weeks while being maintained on the same diet. In group (ii), Nrf2+/+ and Nrf2-/- mice were fed the RC diet for 10 weeks, with no fructose in the drinking water, before being treated with either TBE-31 or DMSO for a further 6 weeks while being maintained on the same diet. Glucose homeostasis was monitored in all mice by ITT and PTT at the times indicated.