Lactobacillus pentosus S-PT84 Prevents Low-Grade Chronic Inflammation-Associated Metabolic Disorders in a Lipopolysaccharide and High-Fat Diet C57/BL6J Mouse Model

J Agric Food Chem. 2020 Apr 15;68(15):4374-4386. doi: 10.1021/acs.jafc.0c00118. Epub 2020 Apr 6.

Abstract

A long-term exposure to lipopolysaccharides results in the gut inflammation and its impaired barrier function, leading to the development of metabolic disorders. In this study, the role of dietary heat killed Lactobacillus pentosus S-PT84 on preventing endotoxemia to maintain metabolic homeostasis was studied. We demonstrated that the treatment of L. pentosus S-PT84 improved the gut integrity by maintaining tight-junction protein expression, in order to suppress the infiltration of endotoxin into plasma. The systemic inflammatory responses were inhibited via reducing the secretion of TNF-α and MCP-1. Furthermore, the blood lipid profile and glucose level as well as adiponectin in both plasma and white adipose tissues (WAT) were preserved by L. pentosus S-PT84 through upregulation of PPAR-γ and IRS-1 expression in WAT. The above findings suggest that the metabolic homeostasis in mice treated with HFD and LPS was sustained by L. pentosus S-PT84, leading to reducing the early risk for progression into metabolic disorders.

Keywords: Lactobacillus pentosus S-PT84; gut mucosal integrity; low-grade chronic inflammation; metabolic disorders; white adipose tissue.

MeSH terms

  • Animals
  • Diet, High-Fat / adverse effects
  • Disease Models, Animal
  • Female
  • Humans
  • Insulin Receptor Substrate Proteins / genetics
  • Insulin Receptor Substrate Proteins / immunology
  • Lactobacillus pentosus / physiology*
  • Lipopolysaccharides / adverse effects
  • Metabolic Diseases / drug therapy*
  • Metabolic Diseases / etiology
  • Metabolic Diseases / immunology
  • Metabolic Diseases / microbiology
  • Mice
  • Mice, Inbred C57BL
  • Peroxisome Proliferator-Activated Receptors / genetics
  • Peroxisome Proliferator-Activated Receptors / immunology
  • Probiotics / administration & dosage*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Insulin Receptor Substrate Proteins
  • Irs1 protein, mouse
  • Lipopolysaccharides
  • Peroxisome Proliferator-Activated Receptors
  • Tumor Necrosis Factor-alpha