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Fucoidan ameliorates pancreatic β‐cell death and impaired insulin synthesis in streptozotocin‐treated β cells and mice via a Sirt‐1‐dependent manner
Author(s) -
Yu WenChun,
Chen YenLin,
Hwang PaiAn,
Chen TsoHsiao,
Chou TzChong
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700136
Subject(s) - streptozotocin , endocrinology , medicine , apoptosis , insulin , pancreas , ampk , chemistry , diabetes mellitus , biochemistry , protein kinase a , enzyme
Scope Several beneficial biological functions of fucoidan (FO) isolated from brown algae have been demonstrated. The purpose of this study was to investigate whether FO derived from Sargassum hemiphyllum ameliorates pancreatic β‐cell damage and impaired insulin synthesis under diabetic condition. Methods and results The effects of FO were studied in streptozotocin (STZ)‐treated pancreatic β‐cell line, NIT‐1cells, and mice. The cell apoptosis, protein analyses, histological examination, and pancreatic function assays were performed. The increased pancreatic β‐cell apoptosis and decreased insulin secretion observed in STZ‐treated NIT‐1 cells and mice were greatly attenuated by FO. Moreover, FO has an ability to enhance glucagon‐like peptide‐1 receptor (GLP‐1R) and sirtuin 1 (Sirt‐1) activity through activation of AMPK/GAPDH/PDX‐1 cascade in STZ‐treated β cells. However, the effects of FO were significantly reversed by EX527, a specific Sirt‐1 inhibitor. Similarly, the hyperglycemia, lower expression of Sirt‐1, PDX‐1, and GLP‐1R in the pancreas of diabetic mice were markedly improved after FO administration. Conclusion We demonstrated that FO exhibits an anti‐diabetic effect mainly through attenuation of β‐cell death, thereby elevating insulin synthesis by upregulating PDX‐1 and GLP1‐R via a Sirt‐1‐dependent manner. Therefore, FO‐containing food or supplements may have a therapeutic effect for diabetes by preventing β‐cell damage and dysfunction.