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Endocrine

, Volume 49, Issue 1, pp 119–129 | Cite as

Recombinant murine fibroblast growth factor 21 ameliorates obesity-related inflammation in monosodium glutamate-induced obesity rats

  • Wen-Fei Wang
  • Si-Ming Li
  • Gui-Ping Ren
  • Wei Zheng
  • Yu-Jia Lu
  • Yin-Hang Yu
  • Wen-Juan Xu
  • Tian-He Li
  • Li-Hong Zhou
  • Yan Liu
  • De-Shan Li
Original Article

Abstract

The aim of this study is to investigate the role of FGF21 in obesity-related inflammation in livers of monosodium glutamate (MSG)-induced obesity rats. The MSG rats were injected with recombinant murine fibroblast growth factor 21(FGF21) or equal volumes of vehicle. Metabolic parameters including body weight, Lee’s index, food intake, visceral fat and liver weight, intraperitoneal glucose tolerance, glucose, and lipid levels were dynamically measured at specific time points. Liver function and routine blood test were also analyzed. Further, systemic inflammatory cytokines such as glucose transporter 1 (GLUT-1), leptin, TNF-α, and IL-6 mRNAs were determined by real-time PCR. FGF21 independently decreased body weight and whole-body fat mass without reducing food intake in the MSG rats. FGF21 reduced blood glucose level, Lee’s index, visceral fat, and liver weight, and improved glucose tolerance, lipid metabolic spectrum, and hepatic steatosis in the MSG-obesity rats. Liver function parameters including AST, ALT, ALP, TP, T.Bili, and D.Bili levels significantly reduced in the FGF21-treated obesity rats compared to the controls. Further, FGF21 ameliorated the total and differential white blood cell (WBC) count, serum C-reactive protein (CRP), IL-6, and TNF-α levels in adipose tissues of the obesity rats, suggesting inflammation amelioration in the in the obesity rats by FGF21. FGF21 improves multiple metabolic disorders and ameliorates obesity-related inflammation in the MSG-induced obesity rats.

Keywords

Obesity Monosodium glutamate Fibroblast growth factor 21 Inflammation Rat 

Notes

Acknowledgments

This study was supported by the National Natural Science Foundation of China (Nos.81172741 and 30972537).

Conflict of interest

The authors declare that there is no conflict of interest in this study.

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Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  1. 1.College of Life ScienceNortheast Agricultural UniversityHarbinChina
  2. 2.Harbin University of CommerceHarbinChina
  3. 3.College of Life SciencesUniversity of Chinese Academy of SciencesBeijingChina
  4. 4.Department of Endocrinology, The First Affiliated HospitalHarbin Medical UniversityHarbinChina
  5. 5.Department of Biostatistics, School of Public HealthHarbin Medical UniversityHarbinChina

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