論文

査読有り
2015年12月

The Dipeptidyl Peptidase-4 Inhibitor Teneligliptin Attenuates Hepatic Lipogenesis via AMPK Activation in Non-Alcoholic Fatty Liver Disease Model Mice

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
  • Takayasu Ideta
  • ,
  • Yohei Shirakami
  • ,
  • Tsuneyuki Miyazaki
  • ,
  • Takahiro Kochi
  • ,
  • Hiroyasu Sakai
  • ,
  • Hisataka Moriwaki
  • ,
  • Masahito Shimizu

16
12
開始ページ
29207
終了ページ
29218
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3390/ijms161226156
出版者・発行元
MDPI AG

Non-alcoholic fatty liver disease (NAFLD), which is strongly associated with metabolic syndrome, is increasingly a major cause of hepatic disorder. Dipeptidyl peptidase (DPP)-4 inhibitors, anti-diabetic agents, are expected to be effective for the treatment of NAFLD. In the present study, we established a novel NAFLD model mouse using monosodium glutamate (MSG) and a high-fat diet (HFD) and investigated the effects of a DPP-4 inhibitor, teneligliptin, on the progression of NAFLD. Male MSG/HFD-treated mice were divided into two groups, one of which received teneligliptin in drinking water. Administration of MSG and HFD caused mice to develop severe fatty changes in the liver, but teneligliptin treatment improved hepatic steatosis and inflammation, as evaluated by the NAFLD activity score. Serum alanine aminotransferase and intrahepatic triglyceride levels were significantly decreased in teneligliptin-treated mice (p < 0.05). Hepatic mRNA levels of the genes involved in de novo lipogenesis were significantly downregulated by teneligliptin (p < 0.05). Moreover, teneligliptin increased hepatic expression levels of phosphorylated AMP-activated protein kinase (AMPK) protein. These findings suggest that teneligliptin attenuates lipogenesis in the liver by activating AMPK and downregulating the expression of genes involved in lipogenesis. DPP-4 inhibitors may be effective for the treatment of NAFLD and may be able to prevent its progression to non-alcoholic steatohepatitis.

リンク情報
DOI
https://doi.org/10.3390/ijms161226156
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26670228
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000367535600077&DestApp=WOS_CPL
ID情報
  • DOI : 10.3390/ijms161226156
  • ISSN : 1422-0067
  • PubMed ID : 26670228
  • Web of Science ID : WOS:000367535600077

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