Curcumin stimulates glucagon-like peptide-1 secretion in GLUTag cells via Ca²⁺/calmodulin-dependent kinase II activation

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• 作者：Masahito Takikawa ; Yuta Kurimoto ; Takanori Tsuda ; ^{tsudat@isc.chubu.ac.jp}
• 关键词：2-APB ; 2-aminoethyl diphenylborinate ; BMC ; bisdemethoxycurcumin ; CaMKII ; Ca2+/calmodulin-dependent kinaseII ; DMC ; demethoxycurcumin ; DPP-4 ; dipeptidyl peptidase IV ; ERK ; extracellular signal-regulated kinase ; Fos ; forskolin ; GLP-1 ; glucagon-like peptide-1
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2013
• 出版时间：31 May, 2013
• 年：2013
• 卷：435
• 期：2
• 页码：165-170
• 全文大小：878 K

文摘

Glucagon-like peptide-1 (GLP-1) is a hormone secreted from enteroendocrine L-cells. Enhancing GLP-1 action is an important target for prevention and treatment of type 2 diabetes. Several approaches (GLP-1 analogs, dipeptidyl peptidase IV inhibitors) are being used to develop therapeutic agents using GLP-1 action for the treatment of diabetes. However, an alternative approach is to increase endogenous GLP-1 secretion through modulation of the secretory mechanism in intestinal L cells by pharmaceutical agents or dietary ingredients. In the present study, we demonstrate that curcumin, a yellow pigment isolated from the rhizomes of Curcuma longa L, significantly increases GLP-1 secretion in GLUTag cells, and we clarified the structure-activity relationship using curcumin derivatives. Also, concerning the secretory mechanism, the significant increase in GLP-1 secretion by curcumin involved the Ca²⁺-Ca²⁺/calmodulin-dependent kinase II pathway, and was independent of extracellular signal-regulated kinase, PKC, and the cAMP/PKA-related pathway. These findings provide a molecular mechanism for GLP-1 secretion mediated by foods or drugs, and demonstrate a novel biological function of curcumin in regards to GLP-1 secretion.