Polymethoxyflavonoids from Kaempferia parviflora Induce Adipogenesis on 3T3-L1 Preadipocytes by Regulating Transcription Factors at an Early Stage of Differentiation

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  • Horikawa Takumi
    Graduate School of Natural Science and Technology, Kanazawa University Department of Pharmacognosy and Phytochemistry, Meiji Pharmaceutical University
  • Shimada Tsutomu
    Research Institute of Pharmaceutical Sciences, Musashino University
  • Okabe Yui
    Department of Pharmacognosy and Phytochemistry, Meiji Pharmaceutical University
  • Kinoshita Kaoru
    Department of Pharmacognosy and Phytochemistry, Meiji Pharmaceutical University
  • Koyama Kiyotaka
    Department of Pharmacognosy and Phytochemistry, Meiji Pharmaceutical University
  • Miyamoto Ken-ichi
    Graduate School of Natural Science and Technology, Kanazawa University
  • Ichinose Koji
    Research Institute of Pharmaceutical Sciences, Musashino University
  • Takahashi Kunio
    Department of Pharmacognosy and Phytochemistry, Meiji Pharmaceutical University
  • Aburada Masaki
    Research Institute of Pharmaceutical Sciences, Musashino University

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  • Polymethoxyflavonoids from <i>Kaempferia parviflora</i> Induce Adipogenesis on 3T3-L1 Preadipocytes by Regulating Transcription Factors at an Early Stage of Differentiation

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We previously reported that Kaempferia parviflora WALL. ex BAKER (KP) and its ethyl acetate extract (KPE) improve various metabolic disorders in obesity-model mice. However the mechanism is not certain, and, in this study, in order to elucidate the mechanism of the suppressive effect of KP on fat accumulation, we focused on adipocytes, which are closely linked to metabolic diseases. The finding was that KPE and its components, 3,5,7,4′-tetramethoxyflavone and 3,5,7,3′,4′-pentamethoxyflavone, strongly induced differentiation of 3T3-L1 preadipocytes to adipocytes. The above two polymethoxyflavonoids (PMFs) also induced adiponectin mRNA levels, and release of adiponectin into the medium. In addition, these PMFs enhanced the expression of peroxisome proliferator-activated receptor γ (PPARγ), but did not show PPARγ ligand activity. We then investigated the expression of the differentiation-regulator located upstream of PPARγ. Expression of CCAAT/enhancer-binding protein (C/EBP) β and -δ mRNA, a transcriptional regulator of PPARγ, was induced, and expression of GATA-2 mRNA, a down-regulator of adipogenesis, was suppressed by these PMFs. These functions of the KP PMFs that enhance adipogenesis and secretion of adiponectin are, to some extent at least, involved in the mechanisms of anti-metabolic disorders effects.

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