Figure 1. Oral administration of indole-3-acetate (I3A) alleviates diet-induced hepatic steatosis and inflammation.

(A) Fecal, (B) liver, and (C) serum concentrations of I3A in male B6 129SF1/J mice in control low-fat diet (CN), Western diet (WD), WD with low-dose I3A (WD-50), and WD with high-dose I3A (WD-100) at week 16. (D) Serum alanine aminotransferase (ALT) levels in mice at weeks 10 and 16. (E) Liver triglyceride (TG) levels at week 16. Data shown are TG concentrations (mg/dl) normalized to corresponding tissue DNA contents (µg DNA). (F) Representative liver sections stained with hematoxylin-eosin (H&E). (G) Histology score for steatosis, hepatocyte ballooning, and lobular inflammation. H&E-stained liver sections were evaluated by an expert pathologist using the non-alcoholic steatohepatitis (NASH) CRN and fatty liver inhibition of progression (FLIP) consortia criteria. Data shown are mean ± SEM (n=10 per group). *: p<0.05, **: p<0.01, ***: p<0.001 using Wilcoxon rank sum test.

Figure 1—figure supplement 1. Overview of in vivo study.

(A) Three groups of male B6 129SF1/J mice (n=10 for each group) were fed ad libitum a Western diet (WD) and a sugar water (SW) solution while a fourth group was given normal chow diet. After 8 weeks, the three groups of WD-fed mice were randomly selected for treatment with vehicle (WD group) or low (WD-50 group) or high dose (WD-100 group) of I3A for an additional 8 weeks. The fourth group (control mice [CN]) was continued on low-fat diet calorie matched with the WD. (B) Sampling scheme. (C) Quantification of I3A in feces at week 8. (D) Weight increase and food intake of the four groups. Body weights were normalized to week 8 body weight when I3A administration was started. Food intakes were measured per cage and average food intake was calculated as per gram food intake per mouse per day. Data shown are mean ± SEM from a replicate study. **: p<0.01, WD group compared to CN group using Wilcoxon rank sum test.