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).