Anti-obesity effect of robusta fermented with Leuconostoc mesenteroides in high-fat diet-induced obese mice

Abstract

Robusta beans cultivated with Monascus ruber (RMR) were successively fermented with Leuconostoc mesenteroides (LM) and the antiobesity effects were examined. To produce an obese mouse model to investigate the hypolipidemic effects, ICR mice were fed the same high-fat diet for 6 weeks. Treatment groups were given 10 or 20% RMR-LM. Body weight changes in the 20% RMR-LM group were lower compared with those in the control group. Visceral adipose tissue weight and adipose size were significantly lower in the 20% RMR-LM group compared with those in the control group. Significant improvement in glucose tolerance was observed in the 10 and 20% RMR-LM groups compared with the control group. The 20% RMR-LM group exhibited a significant reduction in serum glucose concentration. Hepatic mRNA levels of sterol regulatory element-binding protein 1, fas cell surface death receptor, and peroxisome proliferator-activated receptor γ, which are associated with lipid, and fatty acid metabolism, in the 20% RMR-LM group were significantly lower compared with those in the control group. The results of the present study demonstrated that 20% RMR-LM may be used to prevent obesity, and ameliorate diabetes and lipid metabolism imbalances.

Keywords: Leuconostoc mesenteroides; Monascus ruber; anti-obesity; high-fat diet; robusta.

Figure 1.

Body weight changes, average food intake levels, and total visceral fat weights. (A) Body weight changes; (B) Average food intake; (C) Total visceral fat/body weight. Average food intake calculated as g/day/mouse. Data are expressed as the mean ± SD (n=10 per group). *P<0.05 vs. control.

Figure 2.

Adipocyte size in visceral adipose tissue intraperitoneal glucose tolerance tests. (A) Adipocyte number; (B) Adipocyte size; (C) Control of visceral adipose tissue, hematoxylin and eosin (H&E) staining; (D) 10% RMR-LM of visceral adipose tissue, H&E staining; (E) 20% RMR-LM of visceral adipose tissue, H&E staining; (F) Intraperitoneal glucose tolerance test; (G) Area under the curve (AUC) of glucose tolerance test. Adipocyte size was calculated by dividing the number of adipocytes by the area counted. H&E staining. Data are shown as the mean ± SD (n=10 per group). *P<0.05 vs. control.

Figure 3.

Effects on serum lipid and hepatic profiles by biochemistry analysis. (A) TG level; (B) GLU level; (C) AST level; (D) ALT level. Values are expressed as the mean ± standard deviation (n=10 per group). *P<0.05 vs. control. TG, triglyceride; GLU, glucose; AST, aspartate aminotransferase; ALT, alanine aminotransferase.

Figure 4.

Effects of RMR-LM on relative mRNA expression in the liver. (A) sterol regulation element-binding protein (SREBP)-1; (B) fatty acid synthase (FAS); (C) acetyl-CoA carboxylase (ACC); (D) lipoprotein lipase (LPL); (E) peroxisome proliferator-activated receptor γ (PPARγ). β-actin was used as an internal control. Data are expressed as the mean ± standard deviation (n=10 per group). *P<0.05 vs. control.