Puerarin Protects Pancreatic β-Cells in Obese Diabetic Mice via Activation of GLP-1R Signaling

Mol Endocrinol. 2016 Mar;30(3):361-71. doi: 10.1210/me.2015-1213. Epub 2016 Jan 20.

Abstract

Diabetes is characterized by a loss and dysfunction of the β-cell. Glucagon-like peptide 1 receptor (GLP-1R) signaling plays an important role in β-cell survival and function. It is meaningful to identify promising agents from natural products which might activate GLP-1R signaling. In this study, puerarin, a diet isoflavone, was evaluated its beneficial effects on β-cell survival and GLP-1R pathway. We showed that puerarin reduced the body weight gain, normalized blood glucose, and improved glucose tolerance in high-fat diet-induced and db/db diabetic mice. Most importantly, increased β-cell mass and β-cell proliferation but decreased β-cell apoptosis were observed in puerarin-treated diabetic mice as examined by immunostaining of mice pancreatic sections. The protective effect of puerarin on β-cell survival was confirmed in isolated mouse islets treated with high glucose. Further mechanism studies showed that the circulating level of GLP-1 in mice was unaffected by puerarin. However, puerarin enhanced GLP-1R signaling by up-regulating expressions of GLP-1R and pancreatic and duodenal homeobox 1, which subsequently led to protein kinase B (Akt) activation but forkhead box O1 inactivation, and promoted β-cell survival. The protective effect of puerarin was remarkably suppressed by Exendin(9-39), an antagonist of GLP-1R. Our study demonstrated puerarin improved glucose homeostasis in obese diabetic mice and identified a novel role of puerarin in protecting β-cell survival by mechanisms involving activation of GLP-1R signaling and downstream targets.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Survival / drug effects
  • Cytoprotection / drug effects*
  • Diabetes Mellitus, Experimental / pathology*
  • Diet, High-Fat
  • Glucagon-Like Peptide 1 / metabolism
  • Glucagon-Like Peptide-1 Receptor / metabolism
  • Glucose / metabolism
  • Hyperglycemia / complications
  • Insulin-Secreting Cells / metabolism*
  • Insulin-Secreting Cells / pathology*
  • Isoflavones / chemistry
  • Isoflavones / pharmacology*
  • Lipid Metabolism / drug effects
  • Mice, Inbred C57BL
  • Mice, Obese
  • Signal Transduction / drug effects*
  • Up-Regulation / drug effects

Substances

  • Glucagon-Like Peptide-1 Receptor
  • Isoflavones
  • Glucagon-Like Peptide 1
  • Glucose
  • puerarin

Grants and funding

This work was supported by the European Foundation for the Study of Diabetes (EFSD), the Chinese Diabetes Society (CDS), and the Lilly Programme for Collaborative Research between China and Europe, Natural Science Foundation of China Grants 81102488 and 81370924, the Natural Science Foundation of Jiangsu Province Grant BK2011865, the Foundation for High-Level Talent in Six Areas of Jiangsu Province Grant 2015-YY010, and the Foundation of Jiangsu Province Administration of Traditional Chinese Medicine Grant LZ13066.