L. fermentum CECT5716 administration reduced the inflammatory status in metabolic tissues
HFD-diet-induced obesity was associated with a systemic inflammatory status, as evidenced by increased mRNA expression in liver and fat tissues of pro-inflammatory cytokines, including Tnf-α andIl-6, as well as the chemokine monocyte chemotactic protein-1 (Mcp-1 ), when compared with those mice fed control diet (Figure 3A). L. fermentum administration to obese mice significantly ameliorated all these inflammatory markers, showing in most cases similar mRNA expression to control diet-fed mice (Figure 3A). Likewise, the expression of c-jun N-terminal kinase (Jnk)-1 protein in both tissues was significantly increased in control HFD-fed mice in comparison with the control diet group, whereas probiotic treatment reduced its expression (Figure 3A). Likewise, obese mice also manifested an altered expression of peroxisome proliferator-activated receptor α (Pparα ) in fat, which was significantly ameliorated after treatment with L. fermentum (Figure 3B).
Furthermore, the impairment in glucose and lipid metabolism in obese mice was associated with a decreased expression of the glucose transporter Glut-4 and AMP-activated protein kinase (Ampk ) in liver and fat tissue, which were ameliorated in HFD-fed mice treated with L. fermentum (Figure 3B). Moreover, the expression ofTlr4 in liver and adipose tissues was also altered in control HFD-fed mice, which was significantly restored by the treatment (Figure 3B).
In addition, and in comparison, with control diet-fed mice, HFD intake resulted in an imbalance expression of the adipokines leptin and adiponectin in fat tissue, in combination with a reduced expression of leptin receptor in both liver and fat tissues (Figure 4). The probiotic treatment significantly restored the expression of all these genes in fat tissue and increased the expression of leptin receptor in liver (Figure 4).