(MDPI, 2022) Riezu Boj, José I.; Barajas Vélez, Miguel Ángel; Pérez Sánchez, Tania; Pajares Villandiego, María Josefa; Araña Ciordia, Miriam; Milagro Yoldi, F. I.; Urtasun Alonso, Raquel; Ciencias de la Salud; Osasun Zientziak
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver
disease, reaching epidemic proportions worldwide. Targeting the gut–adipose tissue–liver axis
by modulating the gut microbiota can be a promising therapeutic approach in NAFLD. Lactiplantibacillus plantarum, a potent lactic-acid-producing bacterium, has been shown to attenuate NAFLD.
However, to our knowledge, the possible effect of the Lactiplantibacillus plantarum strain DSM20174
(L.p. DSM20174) on the gut–adipose tissue axis, diminishing inflammatory mediators as fuel for
NAFLD progression, is still unknown. Using a NAFLD mouse model fed a high-fat, high-fructose
(HFHF) diet for 10 weeks, we show that L.p DSM20174 supplementation of HFHF mice prevented
weight gain, improved glucose and lipid homeostasis, and reduced white adipose inflammation and
NAFLD progression. Furthermore, 16S rRNA gene sequencing of the faecal microbiota suggested that
treatment of HFHF-fed mice with L.p DSM20174 changed the diversity and altered specific bacterial
taxa at the levels of family, genus, and species in the gut microbiota. In conclusion, the beneficial
effects of L.p DSM20174 in preventing fatty liver progression may be related to modulations in the
composition and potential function of gut microbiota associated with lower metabolic risk factors
and a reduced M1-like/M2-like ratio of macrophages and proinflammatory cytokine expression in
white adipose tissue and liver.
