title: Tyrosol, an olive oil polyphenol, inhibits ER stress-induced apoptosis in pancreatic β-cell through JNK signaling.
abstract: Dysfunction of pancreatic β-cell is a major determinant for the development of type 2 diabetes. Because of the stimulated insulin secretion in metabolic syndrome, endoplasmic reticulum (ER) stress plays a central mediator for β-cell failure. In this study, we investigated whether an antioxidant phenolic compound, tyrosol protects against β-cell dysfunction associated with ER stress. To address this issue, we exposed pancreatic β cells, NIT-1 to tunicamycin with tyrosol. We found tyrosol diminished tunicamycin-induced cell death in a dose-dependent manner. We also detected tyrosol decreased the expressions of apoptosis-related markers. Exposure to tunicamycin evoked UPR response and co-treatment of tyrosol led to reduction of ER stress. These effects of tyrosol were mediated by the phosphorylation of JNK. Moreover, we confirmed supplement of tyrosol ameliorated β-cell loss induced by high fat feeding. Taken together, our study provides a molecular basis for signaling transduction of protective effect of tyrosol against ER stress-induced β-cell death. Therefore, we suggest tyrosol could be a potential therapeutic candidate for amelioration of type 2 diabetes.
authors.affiliation: Research Group of Metabolic Mechanism, Korea Food Research Institute, Seongnam 13539, South Korea.
authors.forename: Hyunjung
authors.initials: H
authors.lastname: Lee
authors.affiliation: Research Group of Metabolic Mechanism, Korea Food Research Institute, Seongnam 13539, South Korea.
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Im
authors.affiliation: Research Group of Metabolic Mechanism, Korea Food Research Institute, Seongnam 13539, South Korea; Division of Food Biotechnology, University of Science & Technology, Daejeon 34113, South Korea.
authors.forename: Chang Hwa
authors.initials: CH
authors.lastname: Jung
authors.affiliation: Research Group of Metabolic Mechanism, Korea Food Research Institute, Seongnam 13539, South Korea.
authors.forename: Young Jin
authors.initials: YJ
authors.lastname: Jang
authors.affiliation: Research Group of Metabolic Mechanism, Korea Food Research Institute, Seongnam 13539, South Korea; Division of Food Biotechnology, University of Science & Technology, Daejeon 34113, South Korea.
authors.forename: Tae Youl
authors.initials: TY
authors.lastname: Ha
authors.affiliation: Research Group of Metabolic Mechanism, Korea Food Research Institute, Seongnam 13539, South Korea; Division of Food Biotechnology, University of Science & Technology, Daejeon 34113, South Korea. Electronic address: jyan@kfri.re.kr.
authors.forename: Jiyun
authors.initials: J
authors.lastname: Ahn
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects / Q000502:physiology*; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000378:metabolism*; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D010626:Phenylethyl Alcohol / Q000008:administration & dosage / Q000031:analogs & derivatives*; D010936:Plant Extracts / Q000008:administration & dosage*; D059808:Polyphenols / Q000008:administration & dosage*
chemical_list: C000601880:Bonolive; D010936:Plant Extracts; D059808:Polyphenols; C011867:4-hydroxyphenylethanol; D010626:Phenylethyl Alcohol
keywords: Apoptosis; ER stress; NIT-1; Tyrosol; β-Cell failure