論文

査読有り 筆頭著者 責任著者 国際誌
2020年8月

Expression of clock gene Dbp in omental and mesenteric adipose tissue in patients with type 2 diabetes.

BMJ open diabetes research & care
  • Kentaro Ushijima
  • Chisato Suzuki
  • Hiroko Kitamura
  • Ken Shimada
  • Hirotoshi Kawata
  • Akira Tanaka
  • Hisanaga Horie
  • Yoshinori Hosoya
  • Yasushi Imai
  • Chikamasa Yamashita
  • Akio Fujimura
  • 全て表示

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記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1136/bmjdrc-2020-001465

INTRODUCTION: We previously reported in ob/ob mice, one of animal models of human type 2 diabetes mellitus (DM2), that (i) acetylation of histone H3 lysine 9 (H3K9) at the promoter region of clock gene Dbp and DBP mRNA expression are reduced in epididymal adipose tissue, (ii) binding of DBP to the promoter region of peroxisome proliferator-activated receptor (Ppar)-γ and mRNA expression of PPAR-γ1sv were decreased in preadipocytes and (iii) adiponectin secretion was decreased, leading to the impaired insulin sensitivity. RESEARCH DESIGN AND METHODS: The present study was undertaken to evaluate whether such the changes in visceral adipose tissue were detected in patients with DM2. We obtained omental and mesenteric adipose tissue during surgery of lymph node dissection for gastric and colorectal cancers, and investigated these variables in adipose tissue (omental from gastric cancer; 13 non-DM, 12 DM2: mesenteric from colorectal cancer; 12 non-DM, 11 DM2). RESULTS: Acetylation of histone H3K9 at the promoter region of Dbp and DBP mRNA expression in omental, but not in mesenteric adipose tissue were significantly lower in DM2 than in patients without DM. PPAR-γ mRNA expression in omental adipose tissue was also lower in patients with DM2, but not in mesenteric adipose tissue. CONCLUSIONS: The changes in DBP-PPAR-γ axis observed in mice with diabetes were also detected in patients with DM2. Because adiponectin secretion is reported to be enhanced through the PPAR-γ-related mechanism, this study supports the hypothesis that omental adipose tissue is involved in the mechanism of DM2.

リンク情報
DOI
https://doi.org/10.1136/bmjdrc-2020-001465
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32816832
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7437886
共同研究・競争的資金等の研究課題
中枢-末梢組織連関の破綻が引き起す末梢時計障害の機序解明
ID情報
  • DOI : 10.1136/bmjdrc-2020-001465
  • PubMed ID : 32816832
  • PubMed Central 記事ID : PMC7437886

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