Effects of Icariin on insulin resistance via the activation of AMPK pathway in C2C12 mouse muscle cells.

Han, Y ; Jung, HW ; et al.

In: European journal of pharmacology, Jg. 758 (2015-07-05), S. 60

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Insulin resistance in skeletal muscle is a major risk factor for the development of type 2 diabetes (T2D). In this study, we investigated the effect of icariin on insulin resistance in C2C12 mouse skeletal muscle cells. C2C12 myoblasts were differentiated into myotubes for five days, then treated with icariin (50 and 100µM) or metformin (1mM) in the presence of 100nM insulin for 24h. Adiponectin production was measured in culture media by ELISA, and AMP-activated protein kinase (AMPK)/insulin signaling pathway activation was assessed by the western blot analysis. Icariin significantly increased adiponectin production in C2C12 myotubes. Moreover, icariin markedly promoted the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC). Icariin up-regulated the expression of phosphatidylinositol 3-kinase (PI3K) and the phosphorylation of insulin receptor substrate-1 (IRS-1) in C2C12 myotubes. These results suggest that icariin has therapeutic potential for the treatment of T2D via the regulation of insulin resistance in skeletal muscle.

Titel:	Effects of Icariin on insulin resistance via the activation of AMPK pathway in C2C12 mouse muscle cells.
Autor/in / Beteiligte Person:	Han, Y ; Jung, HW ; Park, YK
Link:	Zum Volltext
Zeitschrift:	European journal of pharmacology, Jg. 758 (2015-07-05), S. 60
Veröffentlichung:	2005- : Amsterdam : Elsevier Science ; <i>Original Publication</i>: Amsterdam, North Holland Pub. Co., 2015
Medientyp:	academicJournal
ISSN:	1879-0712 (electronic)
DOI:	10.1016/j.ejphar.2015.03.059
Schlagwort:	Acetyl-CoA Carboxylase metabolism Animals Cell Survival drug effects Cells, Cultured Insulin pharmacology Insulin Receptor Substrate Proteins metabolism Metformin pharmacology Mice Muscle Fibers, Skeletal cytology Muscle Fibers, Skeletal metabolism Phosphatidylinositol 3-Kinase biosynthesis Phosphorylation drug effects AMP-Activated Protein Kinases metabolism Adiponectin metabolism Flavonoids pharmacology Insulin Resistance Muscle Fibers, Skeletal drug effects Signal Transduction drug effects
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [Eur J Pharmacol] 2015 Jul 05; Vol. 758, pp. 60-3. <i>Date of Electronic Publication: </i>2015 Mar 31. MeSH Terms: Insulin Resistance* ; AMP-Activated Protein Kinases / metabolism ; Adiponectin / metabolism ; Flavonoids / pharmacology ; Muscle Fibers, Skeletal / drug effects ; Signal Transduction / *drug effects ; Acetyl-CoA Carboxylase / metabolism ; Animals ; Cell Survival / drug effects ; Cells, Cultured ; Insulin / pharmacology ; Insulin Receptor Substrate Proteins / metabolism ; Metformin / pharmacology ; Mice ; Muscle Fibers, Skeletal / cytology ; Muscle Fibers, Skeletal / metabolism ; Phosphatidylinositol 3-Kinase / biosynthesis ; Phosphorylation / drug effects Contributed Indexing: Keywords: AMPK pathway; C2C12 cells; Icariin; Insulin resistance; Skeletal muscle; Type 2 diabetes Substance Nomenclature: 0 (Adiponectin) ; 0 (Flavonoids) ; 0 (Insulin) ; 0 (Insulin Receptor Substrate Proteins) ; 9100L32L2N (Metformin) ; EC 2.7.1.137 (Phosphatidylinositol 3-Kinase) ; EC 2.7.11.31 (AMP-Activated Protein Kinases) ; EC 6.4.1.2 (Acetyl-CoA Carboxylase) ; VNM47R2QSQ (icariin) Entry Date(s): Date Created: 20150404 Date Completed: 20160426 Latest Revision: 20171116 Update Code: 20231215

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