A proline-type fullerene derivative inhibits adipogenesis by preventing PPARγ activation

Megumi Funakoshi-Tago, Takahiro Hattori, Fumihito Ueda, Kenji Tago, Tomoyuki Ohe, Tadahiko Mashino, Hiroomi Tamura

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


Obesity and its associated metabolic diseases represent some of the most rapidly expanding health issues worldwide, and, thus, the development of a novel chemical compound to suppress adipogenesis is strongly expected. We herein investigated the effects of water-soluble fullerene derivatives: a bis-malonic acid derivative and three types of proline-type fullerene derivatives, on adipogenesis using NIH-3T3 cells overexpressing PPARγ. One of the proline-type fullerene derivatives (P3) harboring three carboxy groups significantly inhibited lipid accumulation and the expression of adipocyte-specific genes, such as aP2, induced by the PPARγ agonist rosiglitazone. On the other hand, the bis-malonic acid derivative (M) and the 2 other proline-type fullerene derivatives (P1, P2), which have two carboxy groups, had no effect on PPARγ-mediated lipid accumulation or the expression of aP2. P3 fullerene also inhibited lipid accumulation induced by the combined stimulation with 3-isobutyl-1-methylxanthine (IBMX), dexamethasone, and insulin in 3T3-L1 preadipocytes. During the differentiation of 3T3-L1 cells into adipocytes, P3 fullerene did not affect the expression of C/EBPδ, C/EBPβ, or PPARγ, but markedly inhibited that of aP2 mRNA. These results suggest that P3 fullerene exhibits anti-obesity activity by preventing the activation of PPARγ.

Original languageEnglish
Pages (from-to)259-265
Number of pages7
JournalBiochemistry and Biophysics Reports
Publication statusPublished - 2016 Mar 1


  • Adipogenesis
  • Fullerene
  • Obesity
  • PPARγ

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry


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