Akkermansia muciniphila can reduce the damage of gluco/lipotoxicity, oxidative stress and inflammation, and normalize intestine microbiota in streptozotocin-induced diabetic rats

Pathog Dis. 2018 Jun 1;76(4). doi: 10.1093/femspd/fty028.

Abstract

This study aimed to investigate how Akkermansia muciniphila can implicate type 2 diabetes mellitus and the mechanisms underlying the effects A. muciniphila on type 2 diabetes mellitus. Normal and streptozotocin-induced diabetic Sprague-Dawley rats were orally administered with A. muciniphila and solvent. After 4 weeks of treatment, diabetic rats orally administered with live or pasteurized A. muciniphila exhibited significant increase in the blood concentration of high-density lipoprotein, and decrease in the hepatic glycogen, serum plasminogen activator inhibitor-1, tumor necrosis factor-α, lipopolysaccharide, malondialdehyde and total glucagon-like peptide-1. Moreover, diabetic rats orally administered with A. muciniphila showed significantly increased species alpha diversity and gene function in gut microbes. These results indicated that A. muciniphila can improve liver function, reduce gluco/lipotoxicity, alleviate oxidative stress, suppress inflammation and normalize intestine microbiota of the host animal, thereby ameliorating type 2 diabetes mellitus. Akkermansia muciniphila might be considered as one of the ideal new probiotics used in the management of type 2 diabetes mellitus in future.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cholesterol, HDL / agonists
  • Cholesterol, HDL / immunology
  • Cholesterol, HDL / metabolism
  • Diabetes Mellitus, Experimental / chemically induced
  • Diabetes Mellitus, Experimental / diet therapy*
  • Diabetes Mellitus, Experimental / immunology
  • Diabetes Mellitus, Experimental / microbiology
  • Feces / microbiology
  • Gastrointestinal Microbiome / drug effects*
  • Gastrointestinal Microbiome / immunology
  • Gene Expression Regulation / drug effects
  • Glucagon-Like Peptide 1 / genetics
  • Glucagon-Like Peptide 1 / immunology
  • Glycogen / antagonists & inhibitors
  • Glycogen / immunology
  • Glycogen / metabolism
  • Hypoglycemic Agents / pharmacology*
  • Inflammation
  • Intestinal Mucosa / metabolism
  • Intestines / drug effects
  • Intestines / immunology
  • Lipopolysaccharides / antagonists & inhibitors
  • Lipopolysaccharides / immunology
  • Lipopolysaccharides / metabolism
  • Liver / drug effects
  • Liver / immunology
  • Liver / metabolism
  • Male
  • Malondialdehyde / antagonists & inhibitors
  • Malondialdehyde / immunology
  • Malondialdehyde / metabolism
  • Oxidative Stress / drug effects
  • Plasminogen Activator Inhibitor 1 / genetics
  • Plasminogen Activator Inhibitor 1 / immunology
  • Probiotics / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Streptozocin
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology
  • Verrucomicrobia / physiology*

Substances

  • Cholesterol, HDL
  • Hypoglycemic Agents
  • Lipopolysaccharides
  • Plasminogen Activator Inhibitor 1
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Streptozocin
  • Glucagon-Like Peptide 1
  • Glycogen