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KMID : 0388120070160020039
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Journal of Korean Society for the Study of Obesity
2007 Volume.16 No. 2 p.39 ~ p.49
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The Relation between Inhibition of Adipocyte Differentiation by Activation of Wnt Signaling and Impaired Glucose Metabolism in Human
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Han Ho
Kim Chul-Geun
Kwon Sung-Joon
Choi Woong-Hwan
Kim Hee-Sue
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Abstract
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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.
Conclusion: The major role of Wnt/beta-catenin signaling in human adipose tissue seems to selectively inhibit genes for insulin sensitivity such as adiponectin and GLUT4, which require C/EBPalpha as wells as PPARgamma.
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KEYWORD
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Wnt signaling, Adipocyte differentiation, Insulin sensitivity, Cyclin D1
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