Fig. 7: Genetic models of Slc25a1 gene deficiency partially recapitulate the activity of CTPI-2. | Cell Death & Differentiation

Fig. 7: Genetic models of Slc25a1 gene deficiency partially recapitulate the activity of CTPI-2.

From: Inhibition of the mitochondrial citrate carrier, Slc25a1, reverts steatosis, glucose intolerance, and inflammation in preclinical models of NAFLD/NASH

Fig. 7

a Body weight measurements of wild-type or Slc25a1 mice (n = 3–6), at different ages (indicated in weeks). b, c Body weight of wild-type and Slc25a1 mice in HFD conditions examined over time (b), or at the end of experiments (c) (n = 4). d. Immuno-blot experiments of different Slc25a1 mice (indicated from 1 to 4), in the liver and visceral adipose tissue (WAT). e Body weight gain (expressed in percentage) of all wild-type and Slc25a1 mice, and of mouse #4. f, g Quantification of liver steatosis (f), and representative H&E staining (g) of the livers of the indicated mice. ND not detected. h Immunoblot analysis with the indicated antibodies of the livers and WAT of Alb/Cre:Slc25a1 (fl/fl) and Alb/Cre:Slc25a1 (−/−) animals in CD and HFD. i Quantification of liver steatosis in Alb/Cre:Slc25a1 and Alb/Cre:Slc25a1 animals in HFD conditions. j Top panels: magnetic resonance imaging (MRI) of the livers (circled in red and indicated by arrows). Numbers in white indicate the percentage of liver fat calculated with MRI on all slices of the image dataset for each mouse. Bottom panels: representative H&E staining of the livers of Alb/Cre:Slc25a1 and Alb/Cre:Slc25a1 mice. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001.

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