Figure 4.

Histidine supplementation alleviates liver steatosis in different animal models

(A‒F) Effects of HAA supplementation in the ob/ob mice model.

(A) Representative macroscopic appearance of livers.

(B) Representative liver micrographs of H&E staining. Scale bar, 100 μm.

(C) Lipid droplet. Count.

(D) Lipid droplet surface field.

(E) Total hepatic lipid content.

(F) Hepatic mRNA expression of genes related to de novo hepatic lipogenesis (Acc1, Fasn, and Scd1), lipid transport (Fabp4), and inflammation (F4/80, Cd11c, Il1a, Tnfa, and Il10).

(G‒L) Effects of HAA supplementation in the OVX rat model.

(G) Liver weight.

(H) Representative liver micrographs of H&E staining. Scale bar, 100 μm.

(I) Lipid droplet count.

(J) Lipid droplet surface field.

(K) Total hepatic lipid content.

(L) Hepatic mRNA expression of genes related to de novo hepatic lipogenesis (Acc1, Fasn, and Scd1), lipolysis (Hsl), lipid transport (Fapt1 and Cd36), and inflammation (Mcp1, Il1b, Tnfa, and Il10).

(M and N) Effects of histidine supplementation (8 g/L) in the NAFLD fly model.

(M) Boxplots represent TG content per fly. TG levels were assessed in 10-day-old flies.

(N) RT-qPCR results of genes related to de novo hepatic lipogenesis (ACC, Desat2, FASN1, SREBP, and mdy), β-oxidation (Eip75B, EcR, whr, and Acoxd57d), lipid transport (Fabp), fatty acid mobilization (Lsd1 and bmm), and insulin receptors (InR and chico).

For all Drosophila experiments, samples contained a pool of 8 flies. Data are mean ± SEM. The p values were determined using Fisher’s least significant difference (LSD) ANOVA test (#p < 0.1, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).