Table 1.
Effects of lactoferrin on body, liver, and spleen weights, and weight gain in HFCS-induced murine HMMS.
Figure 1.
Gross and microscopic evaluation of the effect of lactoferrin on lipid accumulation by the mouse liver after HFCS challenge.
Liver sections (5 µm) were prepared using HE and Oil Red O stains to determine lipid accumulation. Lipid accumulation around the vein was minimal in normal mice (naïve group). Lipid accumulation was marked in HMMS mice (control group). Treatment with lactoferrin at 50, 100, and 200 mg/kg markedly suppressed lipid accumulation. The scale bar represents 0.5 mm in liver gross, 100 µm in HE-stained sections, and 50 µm in Oil Red O stained sections.
Figure 2.
Treatment with lactoferrin improved the histology of livers of HFCS-induced HMMS mice.
Immunohistochemical staining with 4-HNE, TLR-4, and TSLP show lipid peroxidation (4-HNE) and associated inflammatory markers (TLR-4 and TSLP). The control group showed lipid vascular accumulation and stained positive for 4-HNE, TLR-4, and TSLP, compared to the naïve group (indicated by arrows). Open arrows indicate negative staining for TLR-4 and TSLP, which indicate without infiltration of inflammatory cells. Treatment with lactoferrin at 50, 100, and 200 mg/kg markedly reduced 4-HNE, TLR-4, and TSLP expression. Scale bars represent 100 µm (4-HNE) and 50 µm (TLR-4 and TSLP).
Table 2.
Effect of lactoferrin on hepatic steatosis scores.
Table 3.
Effect of lactoferrin on liver lipid droplets in Oil Red O stain.
Table 4.
Effects of lactoferrin on serum mediators in HFCS-induced murine HMMS.
Table 5.
Effects of lactoferrin on hepatic mediators in HFCS-induced murine HMMS.
Figure 3.
Insulin resistance and OGTT determination in HFCS-induced insulin resistance in the murine model.
(A) Blood glucose determined by OGTT after oral administration of glucose (2%). (B) Area under curve (AUC) was calculated for the OGTT. The control group showed a significant increase compared to the naïve group, whereas lactoferrin at 50, 100, and 200 mg/kg markedly reduced the AUC. (C) Fasting serum insulin was determined by ELISA. Insulin levels were significantly increased in the control group compared to the naïve group, and lactoferrin at 50, 100, and 200 mg/kg markedly reduced blood insulin. (D) HOMA-IR insulin resistance calculated from fasting serum glucose and insulin levels. Lactoferrin at 50, 100, and 200 mg/kg markedly reduced blood insulin. Data are presented as mean ± SD (n = 10) and were analyzed using one-way ANOVAs and Duncan's multiple range test. a–d: Different letters indicate significant differences between groups (P<0.05).