The aim of this study was to analyze the effects of ethanol extract of sambiloto (Andrographis paniculata) on fatty liver percentage, serum glutamic oxaloacetic transaminase (SGOT) level and lipid profile of wistar strain white rat exposed to high fat diet. The study used randomized post test only control group design. Total sample was 50 male wistar strain rats (Rattus norvegicus) divided randomly into 5 groups (randomization). The normality test used was Kolmogorov Smirnov test (a=0.05). The homogeneity test used was Levene test (a=0.05). The comparative test was done using Anova test (analysis of variance) (a=0.05) or Brown-Forsythe test (a=0.05). The correlation test was done using Pearson test (a=0.05). The administration of sambiloto ethanol extract with doses of 100, 200 and 400 milligrams (mg)/kilogram (kg) body weight (BW) decreased the percentage of fatty liver (r=-0.950), SGOT (r=-0.964)/SGPT (r=(R=-0.973)/LDL (low-density lipoprotein) (r=-0.960) and increased HDL (high-density lipoprotein) levels (r=-0.923)=0.956) in white rats exposed to a high-fat diet. In conclusion, increased dose of ethanol extract of sambiloto can decrease the percentage of fatty liver, SGOT/SGPT and total cholesterol/TG/LDL and increase HDL level of white rats exposed to high fat diet.

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The modern dietary exposome is calorie dense and poor in nutritional quality resulting in a high prevalence of fatty liver disease and an increasing incidence of cardiometabolic disease and cancer. We investigated the impact of dietary composition on the interaction between the liver and haematopoietic systems in mice. Using xenograft and chemical-induced liver cancer models, we find that liver tumours per se have a minimal impact on haematopoietic stem and progenitor cell (HSPC) responses. In contrast, alterations in dietary composition had profound effects on the liver-bone marrow axis. Specifically, exposure to sucrose with or without dietary cholesterol had minimal impact on the HSPC response, while perturbations in bile acid biosynthesis synergises with dietary cholesterol to enhance HSPC responses. Pharmacological restoration of bile acid biosynthesis partially reversed these effects. We conclude that the crosstalk between the liver and bone marrow, and subsequent HSPC responses is regulated by bile acid biosynthesis.