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Title: Berberine-induced activation of 5'-adenosine monophosphate-activated protein kinase and glucose transport in rat skeletal muscles.
Authors: Ma, Xiao
Egawa, Tatsuro  kyouindb  KAKEN_id
Kimura, Hajime
Karaike, Kouhei
Masuda, Shinya
Iwanaka, Nobumasa
Hayashi, Tatsuya  kyouindb  KAKEN_id
Author's alias: 林, 達也
Issue Date: Nov-2010
Publisher: Elsevier Inc.
Journal title: Metabolism: clinical and experimental
Volume: 59
Issue: 11
Start page: 1619
End page: 1627
Abstract: Berberine (BBR) is the main alkaloid of Coptis chinensis, which has been used as a folk medicine to treat diabetes mellitus in Asian countries. We explored the possibility that 5'-adenosine monophosphate-activated protein kinase (AMPK) is involved in metabolic enhancement by BBR in skeletal muscle, the important tissue for glucose metabolism. Isolated rat epitrochlearis and soleus muscles were incubated in a buffer containing BBR, and activation of AMPK and related events were examined. In response to BBR treatment, the Thr(172) phosphorylation of the catalytic α-subunit of AMPK, an essential step for full kinase activation, increased in a dose- and time-dependent manner. Ser(79) phosphorylation of acetyl-coenzyme A carboxylase, an intracellular substrate of AMPK, increased correspondingly. Analysis of isoform-specific AMPK activity revealed that BBR activated both the α1 and α2 isoforms of the catalytic subunit. This increase in enzyme activity was associated with an increased rate of 3-O-methyl-d-glucose transport in the absence of insulin and with phosphorylation of AS160, a signaling intermediary leading to glucose transporter 4 translocation. The intracellular energy status estimated from the phosphocreatine concentration was decreased by BBR. These results suggest that BBR acutely stimulates both AMPKα1 and AMPKα2 and insulin-independent glucose transport in skeletal muscle with a reduction of the intracellular energy status.
Rights: © 2010 Elsevier Inc.
This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
DOI(Published Version): 10.1016/j.metabol.2010.03.009
PubMed ID: 20423742
Appears in Collections:Journal Articles

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