Journal of Obesity & Metabolic Syndrome



Korean J Obes 2007; 16(2): 39-49

Published online June 1, 2007

Copyright © Korean Society for the Study of Obesity.

The Relation between Inhibition of Adipocyte Differentiation by Activation of Wnt Signaling and Impaired Glucose Metabolism in Human

Ho Han, Hee Sue Kim**, Sung Joon Kwon*, Chul Geun Kim***, Woong Hwan Choi

Department of Internal Medicine, Department of General Surgery College of Medicine*, Hanyang University; Hanyang Hospital Boen North Chungcheong Province**; and The Department of Life Science and the Research Institute of Natural Sciences College of Natural Science***, Hanyang University


Objectives: The differentiation of preadipocyte to mature adipocyte includes activation of adipogenic gene expression and induction of insulin sensitivity. Wnt signaling, primarily mediated by Wnt10b in human, functions as a promoter of preadiocyte growth and proliferation, although it also functions as a potent inhibitor of adipogenesis. Therefore, this study was undertaken to determine the effect of Wnt signaling on the degree of adipocyte differentiation and glucose metabolism.
Methods: Adipose tissue was obtained during surgery from omental fat deposits in twenty one patients who underwent elective abdominal surgery at Hanyang University Hospital. All patients were divided into NGT patients (n = 12) and patients with impaired glucose metabolism (n = 9) based on the level of the fasting plasma glucose. Tissue expression level of transcription factors for adipocyte differentiation, early and late adipocyte-specific genes, and genes for Wnt signaling and CyclinD1 were investigated in NGT patients and patients with impaired glucose metabolism through real-time quantitative PCR analysis.
Results: To control for the effect of visceral adiposity on the development of impaired glucose metabolism, all patients were subdivided into low and high visceral adiposity according to the median value of V/S ratio (0.85). Among adipocyte-specific genes, expression of genes for insulin sensitivity, such as adiponectin and GLUT4 was reduced in patients with impaired glucose metabolism than NGT patients. Gene expression of Wnt10b and CyclinD1 was significantly higher in patients with impaired glucose metabolism than NGT counterparts.
Conclusions: The major role of Wnt/β-catenin signaling in human adipose tissue seems to selectively inhibit genes for insulin sensitivity such as adiponectin and GLUT4, which require C/EBPα as wells as PPARγ.

Keywords: Wnt signaling, Adipocyte differentiation, Insulin sensitivity, Cyclin D1

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