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. 2020 Apr 21;10(3):451–466. doi: 10.1016/j.jcmgh.2020.04.009

Figure 6.

Figure 6

NTCP inhibition by Myrcludex B stimulates fatty acid oxidation, stimulates fecal energy excretion, and mobilizes VL/L-derived TG. (A) Food intake of HFD-fed female KO-h1B1 mice during their daily treatment with placebo or Myrcludex B for 3.5 weeks. (B) Bomb calorimetry–assessed remaining calories in the feces of HFD-fed female Oatp1a/1b KO-h1B1 mice (n = 3). (C) Locomotor activity, (D) energy expenditure, and (E) respiratory quotient of chow-fed Oatp1a/1b KO mice, treated with placebo or Myrcludex B (2.5 μg/g), housed in calorimetric cages. Dashed line, 4PM, indicates injection with placebo or Myrcludex B (n = 8, crossover design). (F) Plasma cholesterol and (G) TG in male HFD-fed Oatp1a/1b KO mice treated daily with placebo or Myrcludex B for 3.5 weeks (n = 9–10). Hepatic VLDL secretion, determined after Poloxamer-407 (1 mg/kg) injection, measured by (H) serum TG accumulation and (I) calculated TG production rate (n = 7–8) in chow-fed Oatp1a/1b KO mice after Myrcludex B or placebo administration. (J) Volcano plot depicting the lipidomics data. Significance cutoff is shown in the legend (n = 8–9 mice per group, mice were treated with Myrcludex B for 5 consecutive days). (K) Principal component analysis (PCA) of the lipidomics analysis. Error bars show SEM, asterisk indicates significant changes.