p38γ and p38δ regulate postnatal cardiac metabolism through glycogen synthase 1
Fig 9
Maternal HFD feeding suppresses cardiac dysfunction in pups overexpressing p38γ/δact.
(A) Schematic protocol: CD1 females were crossed; after pregnancy confirmation by vaginal plug appearance, they were fed a HFD for the entire experiment (e.g., pregnancy and lactation). Neonates were IV injected at PD1 with AAV-cTnT-GFP-Luc (TnTGFP) or AAV-cTnT-p38γ/δact (TnTp38γ/δact); during their lactation, mother remained on the same diet (e.g., ND or HFD) as during pregnancy. Pups were killed at PD14. (B) Percentage of mice at PD14 with normal or abnormal mitral valve flow (E/A) as an indicator of diastolic dysfunction. (C) Echocardiography measured parameters. (D) BAT temperature chart and representative thermographic images from 2-week-old mice. Data are mean ± SEM (n = 9 or 10). *p < 0.05, **p < 0.01, ***p < 0.001 by one-way ANOVA coupled to Tukey posttest or chi-squared test. Raw data are given in S14 Fig. The figure was prepared using Servier Medical Art (https://smart.servier.com/). BAT, brown adipose tissue; FS, fractional shortening; HFD, high-fat diet; LVID; d, left ventricular internal diameter in diastole; LV mass, left vetricular mass; LVvol; d, left ventricular volume in diastole; ND, normal diet.