Treatment with FGFR2-IIIc monoclonal antibody suppresses weight gain and adiposity in KKAy mice

K. Nonogaki, T. Kaji, T. Yamazaki, Mari Murakami, L. R. Dechristopher, J. Uribarri, K. L. Tucker

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

Expression of β-Kotho, fibroblast growth factor receptor (FGFR)-1c and 2c, which bind FGF21, is decreased in the white adipose tissue of obese mice. The aim of the present study was to determine the role of FGFR2c in the development of obesity and diabetes in KKA y mice. Treatment with mouse monoclonal FGFR2-IIIc antibody (0.5 mg kg -1) significantly suppressed body weight gain and epididymal white adipose tissue weight in individually housed KKA y mice while having no effect on daily food intake. In addition, treatment with FGFR2-IIIc antibody significantly increased plasma-free fatty acid levels while having no effect on blood glucose or plasma FGF21 levels. Moreover, treatment with FGFR2-IIIc antibody had no significant effect on the expression of uncoupling protein-1, uncoupling protein-2 or peroxisome proliferator-activated receptor-γ coactivator 1α in the epididymal white adipose tissue. The treatment with FGFR2-IIIc antibody had no significant effects on daily food intake and body weight gain in individually housed KK mice. These findings suggest that FGFR2-IIIc upregulates the adiposity induced by social isolation in KKA y mice, and that decreased expression and/or function of FGFR2c might be a compensatory response to enhanced adiposity. Inhibition of FGFR2-IIIc function might be a novel therapeutic approach for obesity.

Original languageEnglish
Article numbere233
JournalNutrition and Diabetes
Volume6
Issue number11
DOIs
Publication statusPublished - 2016 Nov 28

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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