https://scholars.lib.ntu.edu.tw/handle/123456789/376790
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | SHING-HWA LIU | en |
dc.creator | Liu, S.H. and Huang, Y.W. and Wu, C.T. and Chiu, C.Y. and Chiang, M.T. | - |
dc.date.accessioned | 2018-09-10T09:41:51Z | - |
dc.date.available | 2018-09-10T09:41:51Z | - |
dc.date.issued | 2013 | - |
dc.identifier.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-84878230199&partnerID=MN8TOARS | - |
dc.identifier.uri | http://scholars.lib.ntu.edu.tw/handle/123456789/376790 | - |
dc.description.abstract | Chitosan is widely employed as a dietary supplement. Several studies have shown that chitosan possesses an antidiabetic effect. An important intestinal incretin hormone, glucagon-like peptide-1 (GLP-1), is also known to contribute to the amelioration of diabetes. This study investigated whether chitosan possesses an ability in GLP-1 synthesis and secretion in human intestinal cells. Low molecular weight chitosan (LMWC) significantly increases GLP-1 secretion in human intestinal endocrine cells (NCI-H716) in a dose-dependent manner. LMWC could also dose-dependently increase the mRNA expression of proglucagon, a GLP-1 precursor, but did not affect prohormone convertase 3 (PC 3) mRNA expression. LMWC effectively increased the phosphorylation of mitogen-activated protein kinases (MAPK)-p38 and c-Jun N-terminal kinases (JNK), but not extracellular-signal-regulated kinases (ERK). An inhibitor of p38, but not JNK and ERK, significantly reversed the LMWC-increased proglucagon expression. Taken together, LMWC accelerates proglucagon expression and GLP-1 secretion through a p38/MAPK-dependent signaling pathway. These findings suggest that LMWC may provide a strategy for diabetes therapy. ? 2013 American Chemical Society. | - |
dc.language | en | en |
dc.relation.ispartof | Journal of Agricultural and Food Chemistry | en_US |
dc.source | AH | - |
dc.subject | chitosan; glucagon-like peptide-1; intestine; p38 MAPK; proglucagon | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | C-jun N-terminal kinase; Extracellular signal-regulated kinase; Glucagon-like peptide-1; intestine; Low molecular weight chitosans; Mitogen activated protein kinase; P38 MAPK; proglucagon; Enzyme activity; Molecular weight; Peptides; Physiology; Chitosan; chitosan; glucagon like peptide 1; messenger RNA; mitogen activated protein kinase p38; proglucagon; stress activated protein kinase; article; cell line; chemistry; dose response; drug effect; enteroendocrine cell; gene expression; genetics; human; metabolism; molecular weight; phosphorylation; physiology; secretion (process); signal transduction; Cell Line; Chitosan; Dose-Response Relationship, Drug; Enteroendocrine Cells; Gene Expression; Glucagon-Like Peptide 1; Humans; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; Molecular Weight; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Proglucagon; RNA, Messenger | - |
dc.title | Low molecular weight chitosan accelerates glucagon-like peptide-1 secretion in human intestinal endocrine cells via a p38-dependent pathway | - |
dc.type | journal article | en |
dc.identifier.doi | 10.1021/jf305410k | - |
dc.relation.pages | 4855-4861 | - |
dc.relation.journalvolume | 61 | - |
dc.relation.journalissue | 20 | - |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
crisitem.author.dept | Toxicology | - |
crisitem.author.orcid | 0000-0002-9976-1197 | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 毒理學研究所 |
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