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. Author manuscript; available in PMC: 2021 May 1.
Published in final edited form as: Nat Metab. 2020 Oct 26;2(11):1232–1247. doi: 10.1038/s42255-020-00296-1

Extended Data Fig. 2: Heart failure develops in CS-MPC2−/− mice, but not CS-MPC2+/− or mice treated with the MPC inhibitor MSDC-0602K.

Extended Data Fig. 2:

a-h, Serial echocardiography data of chow-fed mice at 6, 10, and 16 weeks of age. Left ventricular internal diameter at end diastole (LVIDd) and end systole (LVIDs), end systolic volume (ESV), fractional shortening (FS), relative wall thickness (RWT), stroke volume (SV), and cardiac output (CO) (n=7, 10, and 9 for fl/fl, +/−, and −/−, respectively). i, Heart weights from WT mice fed low fat (LF) diet or a high trans-fat, fructose, cholesterol (HTF-C) diet +/− 330 ppm MSDC-0602, an insulin-sensitizing MPC inhibitor (n=7, 9, and 9 for LF, HTF-C, and HTF-C+MSDC-0602K, respectively). j, Heart gene expression of hypertrophy gene markers from WT mice fed LF, HTF-C, or HTF-C + MSDC-0602 diets (n=6 for all groups). k-l, Heart gene expression for fatty acid transport and oxidation genes and PPAR⍺ target genes from chow-fed 16-week old mice after a 4 h fast (n= 7, 5, and 7 for fl/fl, +/−, and −/−, respectively). Data are presented as mean ± s.e.m., or mean ± s.e.m. within dot plot. Each data point represents one individual mouse or sample. Two-tailed unpaired Student’s t test.