Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose

Abstract

Gut microbiota are known to play an important role in obesity. Enterobacter cloacae, a Gram-negative bacterium, has been considered a pathogenic bacterium related to obesity in the gut. In this study, we established an obesity model of C. elegans by feeding E. cloacae combined with a high glucose diet (HGD), which significantly induced lipid accumulation. An anti-lipid mechanism study revealed that the fatty acid composition and the expression level of fat metabolism-related genes were altered by feeding E. cloacae to C. elegans under HGD conditions. Lactic acid bacteria that showed antagonistic activity against E. cloacae were used to screen anti-obesity candidates in this model. Among them, L. pentosus MJM60383 (MJM60383) showed good antagonistic activity. C. eleans fed with MJM60383 significantly reduced lipid accumulation and triglyceride content. The ratio of C18:1D9/C18:0 was also changed in C. elegans by feeding MJM60383. In addition, the expression level of genes related to fatty acid synthesis was significantly decreased and the genes related to fatty acid β-oxidation were up-regulated by feeding MJM60383. Moreover, MJM60383 also exhibited a high adhesive ability to Caco-2 cells and colonized the gut of C. elegans. Thus, L. pentosus MJM60383 can be a promising candidate for anti-obesity probiotics. To the best of our knowledge, this is the first report that uses E. cloacae combined with a high-glucose diet to study the interactions between individual pathogens and probiotics in C. elegans.

Caenorhabditis elegans as a Screening Model for Probiotics with Properties against Metabolic Syndrome

“…An interesting study performed by Gu et al [36] described the efficacy of a probiotic strain of Lactobacillus pentosus MJM60383 in an obese model of C. elegans (Table 1). In this work, they established a new obesity model by feeding this nematode with a culture of Enterobacter cloacae, a proposed pathogenic bacterium that induces obesity in germ-free mice, in combination with high-glucose (100 mM) conditions (HGD-E) [36]. The proposed C. elegans obese model was characterized by an increase in the lipogenic and a decrease in the β-oxidation genes.…”

“…The proposed C. elegans obese model was characterized by an increase in the lipogenic and a decrease in the β-oxidation genes. With this model, they demonstrated that supplementation with L. pentosus MJM60383 strain was able to significantly reduce C. elegans fat accumulation, counteracting the effect of the obesity-related pathogenic bacteria E. cloacae [36].…”

“…Gene expression analyses demonstrated the downregulation of lipid-accumulationrelated genes fat-6 and fat-7, which encode for a stearoyl-CoA desaturase (SCD) known to modulate the relative abundance of saturated and monounsaturated fatty acids in C. elegans [44]. Moreover, the fat-reducing activity of this probiotic strain was also mediated by the upregulation of the β-oxidation genes nhr-49 and acs-2 [36]. The gene nhr-49 encodes a transcription factor involved in the control of pathways regulating fat consumption and maintenance of the normal balance of fatty acid saturation by modulating the expression of genes involved in fatty acid beta-oxidation.…”

“…Consequently, MCB-fed worms exhibited smaller body length and size, lower fertility, lower fat content, and an extended lifespan in comparison to those fed with the standard diet [65]. Moreover, Gu et al demonstrated the differential fatty acid composition of C. elegans exposed to E. cloacae in comparison with E. coli OP50 [36].…”

“…E. coli OP50 (control group) or a combination of E. coli OP50 and each lactobacilli strain in a ratio of 25:75; 20 • C; L1 to L4/adult.↓ Fat content (Nile red and oil content)↓ ratio of C18:1∆9/C18:0 ↑ acs-2 and nhr-49 genes, enhancing fatty acid β-oxidation ↓ fat6 and fat7 and tub1[36] …”