Fad24 Causes Hyperplasia in Adipose Tissue and Improves Glucose Metabolism

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  • Johmura Yoshikazu
    Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Watanabe Kayoko
    Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Kishimoto Keishi
    Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Ueda Takashi
    Department of Neurobiology and Anatomy, Graduate School of Medical Sciences, Nagoya City University
  • Shimada Shoichi
    Department of Neurobiology and Anatomy, Graduate School of Medical Sciences, Nagoya City University
  • Osada Shigehiro
    Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Nishizuka Makoto
    Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Imagawa Masayoshi
    Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University

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説明

We have previously reported that a novel gene, factor for adipocyte differentiation (fad) 24, promotes adipogenesis in vitro. To examine the role of fad24 in adipogenesis in vivo and the development of obesity, transgenic mice overexpressing fad24 were generated using mouse fad24 cDNA under the control of a chicken β-actin promoter and cytomegalovirus enhancer. The comparison of the ability of fibroblasts from fad24 transgenic embryos to differentiate into adipocytes with that of fibroblasts from wild-type embryos revealed that fad24 overexpression promotes adipogenesis in embryonic fibroblasts. The weight and histology of white adipose tissues, and serum adipocytokine levels were compared between fad24 transgenic mice and wild-type mice, and we found that fad24 overexpression increased the number of smaller adipocytes, caused hyperplasia rather than hypertrophy in white adipose tissue and increased the serum adiponectin level in mice fed both normal chow and a high-fat diet. Glucose and insulin tolerance tests indicated that the activity for glucose metabolism is improved in fad24 transgenic mice fed normal chow in comparison with that in wild-type mice. Our findings suggest that fad24 is a positive regulator of adipogenesis in vivo. Moreover, the increase in the number of smaller adipocytes caused by the overexpression of fad24 appears to enhance glucose metabolic activity, perhaps by increasing the serum adiponectin level.

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