Xylobiose prevents high-fat diet induced mice obesity by suppressing mesenteric fat deposition and metabolic dysregulation

Soo Min Lim, Eunju Kim, Jae Ho Shin, Pu Reum Seok, Sangwon Jung, Sang Ho Yoo, Yuri Kim

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


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.

Original languageEnglish
Article number705
Issue number3
StatePublished - 2018

Bibliographical note

Funding Information:
Acknowledgments: This research was supported by the High Value-Added Food Technology Development Program (Project Number: 313024-03-2-HD040), Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea, and by Brain Korea 21 Plus (Project Number: 22A20130012143).

Publisher Copyright:
© 2018 by the authors.


  • Adipogenesis
  • Inflammation
  • Lipogenesis
  • Mesenteric adipose tissue
  • Obesity
  • Xylobiose


Dive into the research topics of 'Xylobiose prevents high-fat diet induced mice obesity by suppressing mesenteric fat deposition and metabolic dysregulation'. Together they form a unique fingerprint.

Cite this