Figure 1. Paribs protect from HFD-induced metabolic complications.

Ten-wk-old male C57Bl/6J mice were challenged with HFD supplemented with either vehicle (DMSO; Veh) or MRL-45696 (50 mg/kg/day) (n=10/group). (A) Body weight gain during 18wks of HFD. (B) Fat mass was measured using Echo-MRI. (C–D) A comprehensive laboratory animal monitoring system was used to evaluate VO₂ (C) and activity (D) after 7wks of HFD. (E) Food intake measured by averaging weekly food consumption during HFD. (F) Liver 8-oxo-dG content, as indicator of DNA damage, (G) muscle lipid peroxidation-derived aldehyde, 4-hydroxy-2-nonenal, and (H) muscle total poly(ADP-ribose) (PAR) contents were measured in vehicle and MRL-45696-treated mice (n=7/group) (I–J) Total intracellular (I) and mitochondrial (J) NAD⁺ levels in gastrocnemius of refed vehicle and MRL-45696-treated mice (n=5–10/group). (K) SIRT1, acetylated FOXO1 and total FOXO1 protein levels were assessed in total homogenates from quadriceps of chow-diet fed mice. (L) The acetylation status of Ndufa9 immunoprecipates was tested as a marker of SIRT3 activity. Values are shown as mean+/−SEM. * indicates statistical significant difference vs. respective Veh group. *, p<0.05; **, p<0.01; ***, p<0.001. This figure is complemented by Figures S1 and S2, and Table S1.