https://scholars.lib.ntu.edu.tw/handle/123456789/454731
標題: | Suppression of free fatty acid-induced insulin resistance by phytopolyphenols in C2C12 mouse skeletal muscle cells | 作者: | Deng Y.-T. Chang T.-W. MING-SHYUE LEE Lin J.-K. |
關鍵字: | insulin resistance; phytopolyphenols; skeletal muscle cells; type 2 diabetes | 公開日期: | 2012 | 卷: | 60 | 期: | 4 | 起(迄)頁: | 1059-1066 | 來源出版物: | Journal of Agricultural and Food Chemistry | 摘要: | It was reported that increased plasma levels of free fatty acids (FFAs) are associated with profound insulin resistance in skeletal muscle and may also play a critical role in the insulin resistance of obesity and type 2 diabetes mellitus. Skeletal muscle is the major site for insulin-stimulated glucose uptake and is involved in energy regulation and homeostasis. In this study, we used 12-O-tetradecanoylphorbol 13-acetate (TPA), a protein kinase C (PKC) activator, and palmitate to induce insulin resistance in C2C12 mouse skeletal muscle cells. Our data show that epigallocatechin gallate (EGCG) and curcumin treatment reduce insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation, and curcumin is more potent to increase Akt phosphorylation in TPA induction. Moreover, we found that after 5 h of palmitate incubation, epicatechin gallate (ECG) can suppress IRS-1 Ser307 phosphorylation and significantly promote Akt, ERK1/2, p38 MAPK, and AMP-activated protein kinase activation. With a longer incubation with palmitate, IRS-1 exhibited a dramatic depletion, and treatment with EGCG, ECG, and curcumin could reverse IRS-1 expression, Akt phosphorylation, and MAPK signaling cascade activation and improve glucose uptake in C2C12 skeletal muscle cells, especially ECG and curcumin. In addition, treatment with these polyphenols can suppress acetyl-CoA carboxylase activation, but only EGCG could inhibit lipid accumulation in the intracellular site. These findings may suggest that curcumin shows the best capacity to improve FFA-induced insulin resistance than the other two, and ECG was more effective than EGCG in attenuating insulin resistance. ? 2011 American Chemical Society. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84863062486&doi=10.1021%2fjf204496f&partnerID=40&md5=b8d4f2a57decff74f924e31e6d9792d2 https://scholars.lib.ntu.edu.tw/handle/123456789/454731 |
ISSN: | 0021-8561 | DOI: | 10.1021/jf204496f | SDG/關鍵字: | Acetyl-CoA carboxylase; Akt phosphorylation; AMP-activated protein kinase; Curcumin; Energy regulation; Epicatechin; Epigallocatechin gallate; Free fatty acid; Gallate; Glucose uptake; Insulin receptor substrate-1; Insulin resistance; Insulin-stimulated glucose; MAPK signaling; P38 MAPK; phytopolyphenols; Plasma levels; Polyphenols; Protein kinase C; Skeletal muscle; Skeletal muscle cells; Type 2 diabetes mellitus; Type-2 diabetes; Chemical activation; Electrocardiography; Energy policy; Enzyme activity; Fatty acids; Glucose; Insulin; Mammals; Muscle; Phenols; Phosphorylation; Cells; catechin; curcumin; drug derivative; epigallocatechin gallate; fatty acid; insulin receptor substrate; palmitic acid; phorbol 13 acetate 12 myristate; polyphenol; protein kinase C; serine; animal; article; cell line; drug effect; enzyme activation; insulin resistance; metabolism; mouse; phosphorylation; signal transduction; skeletal muscle; Animals; Catechin; Cell Line; Curcumin; Enzyme Activation; Fatty Acids, Nonesterified; Insulin Receptor Substrate Proteins; Insulin Resistance; Mice; Muscle, Skeletal; Palmitic Acid; Phosphorylation; Polyphenols; Protein Kinase C; Serine; Signal Transduction; Tetradecanoylphorbol Acetate |
顯示於: | 生物化學暨分子生物學科研究所 |
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