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https://doi.org/10.1172/JCI22681
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論文情報
タイトル
Adipocytes from Munc18c-null mice show increased sensitivity to insulin-stimulated GLUT4 externalization
著者
Kanda, Hajime
Kanda, Hajime
Tamori, Yoshikazu
Tamori, Yoshikazu
Shinoda, Hiroaki
Shinoda, Hiroaki
Yoshikawa, Mari
Yoshikawa, Mari
Sakaue, Motoyoshi
Sakaue, Motoyoshi
Udagawa, Jun
Udagawa, Jun
Otani, Hiroki
Otani, Hiroki
Tashiro, Fumi
Tashiro, Fumi
Miyazaki, Jun-ichi
Miyazaki, Jun-ichi
Kasuga, Masato
Kasuga, Masato
抄録
Insulin-stimulated glucose uptake in adipocytes is mediated by translocation of vesicles containing the glucose transporter GLUT4 from intracellular storage sites to the cell periphery and the subsequent fusion of these vesicles with the plasma membrane, resulting in the externalization of GLUT4. Fusion of the GLUT4-containing vesicles with the plasma membrane is mediated by a soluble N-ethylmaleimide–sensitive factor attachment protein receptor (SNARE) complex consisting of vesicle-associated membrane protein 2 (VAMP2), 23-kDa synaptosomal-associated protein (SNAP23), and syntaxin4. We have now generated mouse embryos deficient in the syntaxin4 binding protein Munc18c and show that the insulin-induced appearance of GLUT4 at the cell surface is enhanced in adipocytes derived from these Munc18c−/− mice compared with that in Munc18c+/+ cells. Wortmannin, an inhibitor of PI3K, inhibited insulin-stimulated GLUT4 externalization, without affecting GLUT4 translocation to the cell periphery, in Munc18c+/+ adipocytes, but it did not affect GLUT4 externalization in Munc18c−/− cells. Phosphatidylinositol 3-phosphate, which induced GLUT4 translocation to the cell periphery without externalization in Munc18c+/+ cells, elicited GLUT4 externalization in Munc18c−/− cells. These findings demonstrate that Munc18c inhibits insulin-stimulated externalization of GLUT4 in a wortmannin-sensitive manner, and they suggest that disruption of the interaction between syntaxin4 and Munc18c in adipocytes might result in enhancement of insulin-stimulated GLUT4 externalization.
公開者
American Society for Clinical Investigation
掲載誌名
Journal of Clinical Investigation
巻
115
号
2
開始ページ
291
終了ページ
301
刊行年月
2005-02
ISSN
00219738
NCID
AA00695520
DOI
info:doi/10.1172/JCI22681
URL
http://hdl.handle.net/11094/23118
権利情報
Copyright © 2005 American Society for Clinical Investigation
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英語
カテゴリ
学術雑誌論文 Journal Article
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著者版フラグ
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学術雑誌論文
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text
DCTERMS.bibliographicCitation
Journal of Clinical Investigation.115(2) P.291-P.301
DC.title
Adipocytes from Munc18c-null mice show increased sensitivity to insulin-stimulated GLUT4 externalization
DC.creator
Kanda, Hajime
Tamori, Yoshikazu
Shinoda, Hiroaki
Yoshikawa, Mari
Sakaue, Motoyoshi
Udagawa, Jun
Otani, Hiroki
Tashiro, Fumi
Miyazaki, Jun-ichi
Kasuga, Masato
DC.publisher
American Society for Clinical Investigation
DC.language" scheme="DCTERMS.RFC1766
英語
DCTERMS.issued" scheme="DCTERMS.W3CDTF
2005-02
DC.identifier
info:doi/10.1172/JCI22681
DC.identifier" scheme="DCTERMS.URI
http://hdl.handle.net/11094/23118
DCTERMS.abstract
Insulin-stimulated glucose uptake in adipocytes is mediated by translocation of vesicles containing the glucose transporter GLUT4 from intracellular storage sites to the cell periphery and the subsequent fusion of these vesicles with the plasma membrane, resulting in the externalization of GLUT4. Fusion of the GLUT4-containing vesicles with the plasma membrane is mediated by a soluble N-ethylmaleimide–sensitive factor attachment protein receptor (SNARE) complex consisting of vesicle-associated membrane protein 2 (VAMP2), 23-kDa synaptosomal-associated protein (SNAP23), and syntaxin4. We have now generated mouse embryos deficient in the syntaxin4 binding protein Munc18c and show that the insulin-induced appearance of GLUT4 at the cell surface is enhanced in adipocytes derived from these Munc18c−/− mice compared with that in Munc18c+/+ cells. Wortmannin, an inhibitor of PI3K, inhibited insulin-stimulated GLUT4 externalization, without affecting GLUT4 translocation to the cell periphery, in Munc18c+/+ adipocytes, but it did not affect GLUT4 externalization in Munc18c−/− cells. Phosphatidylinositol 3-phosphate, which induced GLUT4 translocation to the cell periphery without externalization in Munc18c+/+ cells, elicited GLUT4 externalization in Munc18c−/− cells. These findings demonstrate that Munc18c inhibits insulin-stimulated externalization of GLUT4 in a wortmannin-sensitive manner, and they suggest that disruption of the interaction between syntaxin4 and Munc18c in adipocytes might result in enhancement of insulin-stimulated GLUT4 externalization.
DC.rights
Copyright © 2005 American Society for Clinical Investigation
citation_title
Adipocytes from Munc18c-null mice show increased sensitivity to insulin-stimulated GLUT4 externalization
citation_author
Kanda, Hajime
Tamori, Yoshikazu
Shinoda, Hiroaki
Yoshikawa, Mari
Sakaue, Motoyoshi
Udagawa, Jun
Otani, Hiroki
Tashiro, Fumi
Miyazaki, Jun-ichi
Kasuga, Masato
citation_publisher
American Society for Clinical Investigation
citation_language
英語
citation_date
2005-02
citation_journal_title
Journal of Clinical Investigation
citation_volume
115
citation_issue
2
citation_firstpage
291
citation_lastpage
301
citation_issn
00219738
citation_doi
info:doi/10.1172/JCI22681
citation_public_url
http://hdl.handle.net/11094/23118