Xylobiose Prevents High-Fat Diet Induced Mice Obesity by Suppressing Mesenteric Fat Deposition and Metabolic Dysregulation

Molecules. 2018 Mar 20;23(3):705. doi: 10.3390/molecules23030705.

Abstract

Obesity is a public concern and is responsible for various metabolic diseases. Xylobiose (XB), an alternative sweetener, is a major component of xylo-oligosaccharide. The purpose of this study was to investigate the effects of XB on obesity and its associated metabolic changes in related organs. For these studies, mice received a 60% high-fat diet supplemented with 15% d-xylose, 10% XB, or 15% XB as part of the total sucrose content of the diet for ten weeks. Body weight, fat and liver weights, fasting blood glucose, and blood lipids levels were significantly reduced with XB supplementation. Levels of leptin and adipokine were also improved and lipogenic and adipogenic genes in mesenteric fat and liver were down-regulated with XB supplementation. Furthermore, pro-inflammatory cytokines, fatty acid uptake, lipolysis, and β-oxidation-related gene expression levels in mesenteric fat were down-regulated with XB supplementation. Thus, XB exhibited therapeutic potential for treating obesity which involved suppression of fat deposition and obesity-related metabolic disorders.

Keywords: adipogenesis; inflammation; lipogenesis; mesenteric adipose tissue; obesity; xylobiose.

MeSH terms

  • Adipogenesis / drug effects
  • Adipogenesis / genetics
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism*
  • Adiposity / drug effects*
  • Animals
  • Blood Glucose / metabolism
  • Body Weight / drug effects
  • Cytokines / metabolism
  • Diet, High-Fat
  • Disaccharides / pharmacology*
  • Disaccharides / therapeutic use*
  • Fatty Acids / metabolism
  • Gene Expression Regulation / drug effects
  • Inflammation Mediators / metabolism
  • Lipids / blood
  • Lipogenesis / drug effects
  • Lipogenesis / genetics
  • Lipolysis / drug effects
  • Liver / drug effects
  • Liver / metabolism
  • Mice, Inbred C57BL
  • Obesity / drug therapy*
  • Obesity / genetics
  • Obesity / metabolism*
  • Obesity / prevention & control
  • Organ Size / drug effects
  • Oxidation-Reduction

Substances

  • Blood Glucose
  • Cytokines
  • Disaccharides
  • Fatty Acids
  • Inflammation Mediators
  • Lipids
  • xylobiose