Liraglutide Activates AMPK Signaling and Partially Restores Normal Circadian Rhythm and Insulin Secretion in Pancreatic Islets in Diabetic Mice

• Wang Kexin

  Department of General Surgery, Qilu Hospital of Shandong University

• Sun Yu

  Department of Endocrinology, Qilu Hospital of Shandong University

• Lin Peng

  Department of Endocrinology, Qilu Hospital of Shandong University

• Song Jun

  Department of Endocrinology, Qilu Hospital of Shandong University

• Zhao Ruxing

  Department of Endocrinology, Qilu Hospital of Shandong University

• Li Wenjuan

  Department of Endocrinology, Qilu Hospital of Shandong University

• Hou Xinguo

  Department of Endocrinology, Qilu Hospital of Shandong University

• Wang Chuan

  Department of Endocrinology, Qilu Hospital of Shandong University

• Wang Lingshu

  Department of Endocrinology, Qilu Hospital of Shandong University

• Zhu Ping

  Department of Ophthalmology, College of Medicine, University of Florida

• Chen Li

  Department of Endocrinology, Qilu Hospital of Shandong University Institute of Endocrinology and Metabolism, Shandong University

抄録

β-Cell insufficiency plays an important role in the development of diabetes. Environmental factors, including lifestyle, play a critical role in β-cell dysfunction. Modern lifestyles affect the inherent circadian clock in central and peripheral organs. Recent studies have demonstrated that the normal intrinsic circadian clock in islets was essential for the viability of β cells and their insulin secretory function. Overall, however, the data are inconclusive. Our study demonstrated that the disrupted circadian rhythm of islets in streptozotocin induced type1 diabetic mice may be associated with impaired β-cell function and glucose intolerance. Liraglutide, a glucagon-like peptide-1 (GLP-1) analogue, could partially restore the normal circadian rhythm and activate the 5′ AMP-activated protein kinase (AMPK) signaling pathway. Our study provided evidence demonstrating that Liraglutide might restore β-cell function and protect against the development of diabetes in a mouse model by attenuating the disruption of the intrinsic circadian rhythm in islets and by activating AMPK signaling.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 38 (8), 1142-1149, 2015

  公益社団法人 日本薬学会

キーワード

• β-cell function
• glucagon-like peptide-1 (GLP-1)
• circadian clock
• 5′ AMP-activated protein kinase (AMPK)

詳細情報

• CRID: 1390282679608663680
• NII論文ID: 130005090636
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b15-00024
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 026617100
• PubMed: 26040899
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I026617100
• Web Site: https://www.jstage.jst.go.jp/article/bpb/38/8/38_b15-00024/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2016128312
• 本文言語コード: en
• データソース種別:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可