Lactobacillus plantarum NA136 ameliorates nonalcoholic fatty liver disease by modulating gut microbiota, improving intestinal barrier integrity, and attenuating inflammation

Abstract

Gut microbiota dysbiosis, associated with insulin resistance, weak intestinal barrier integrity, and inflammation, may also play a role in the development of dietary-induced nonalcoholic fatty liver disease (NAFLD). This study investigates the effects of dietary Lactobacillus plantarum NA136 administration on gut microbiota composition in an insulin-resistant C57BL/6J mouse NAFLD model. Comparison of mice with and without L. plantarum NA136 treatment revealed that L. plantarum NA136 treatment not only relieved insulin resistance but also significantly increased relative proportions of Desulfovibrio, Alistipes, Prevotella, and Enterorhabdus in gut microbiota of NAFLD mice. Meanwhile, L. plantarum NA136 administration also inhibited pathogenic bacterial growth, while promoting growth of probiotics such as Allobaculum, Lactobacillus, and, most markedly, Bifidobacterium. Moreover, L. plantarum NA136 treatment of NAFLD mice improved intestinal barrier integrity and attenuated high-fat and fructose diet (HFD/F)-induced inflammation. These results implicate gut-liver-axis-dependent microbiota modulation as the underlying mechanism for L. plantarum NA136-induced amelioration of NAFLD. Key points • L. plantarum NA136 corrects gut microbiota disorders caused by a high-fat and fructose diet.• L. plantarum NA136 strengthens the intestinal barrier and reduces inflammation in the liver.• L. plantarum NA136 relieves NAFLD by improving the gut-liver axis.

Val‐Val‐Tyr‐Pro protects against non‐alcoholic steatohepatitis in mice by modulating the gut microbiota and gut‐liver axis activation

“…A recent research has indicated that MCD diet caused dysbiosis of gut microbiota and disrupted intestinal barrier function by down‐regulating expression of intestinal tight junction mRNA levels (claudin‐1 and ZO‐1) in mice 25 . Another study has reported that the levels of claudin‐1, ZO‐1 and occludin were decreased in high‐fat and fructose diet group 91 92 .…”

“…A recent research has indicated that MCD diet caused dysbiosis of gut microbiota and disrupted intestinal barrier function by down-regulating expression of intestinal tight junction mRNA levels (claudin-1 and ZO-1) in mice 25. Another study has reported that the levels of claudin-1, ZO-1 and occludin were decreased in high-fat and fructose diet group 91. Once this barrier was disrupted, overproduction of LPS induced by the overgrowth of gut Gram-negative bacterial would enter into blood and promote inflammation which impaired intestinal barrier integrity 92.…”

Desulfovibrio vulgaris, a potent acetic acid-producing bacterium, attenuates nonalcoholic fatty liver disease in mice

“…Desulfovibrio bacteria are capable of producing H 2 S in the mammalian intestinal tract and are usually found in a variety of habitats including soil, intestine and feces of animals, and both salt and fresh water. [45][46][47] In addition, either increased or decreased abundance of Desulfovibrio bacteria was observed in NAFLD animals, [48][49][50] therefore, the exact role of Desulfovibrio bacteria in NAFLD is not clear. Our results revealed Desulfovibrio bacteria were positively correlated with acetic acid levels and negatively correlated with metabolic disorders suggesting Desulfovibrio bacteria were beneficial rather than detrimental bacteria for metabolic disease.…”

Gut Microbiota Metabolites in NAFLD Pathogenesis and Therapeutic Implications

“…Lactobacillus plantarum has been revealed to be effective in ameliorating NAFLD. Zhao et al (2020) reported that Lactobacillus plantarum NA136 reduced severity of NAFLD in a mouse model established by a high-fat/high-fructose diet [ 75 ]. The probiotics changed the gut microbiota with an increase in Bifidobacteria .…”