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The Phosphorylation of IRS1 S307 and Akt S473 Molecules in Insulin‐Resistant C2C12 Cells Induced with Palmitate Is Influenced by Epigallocatechin Gallate from Green Tea
Author(s) -
Bakhtiyari Salar,
Zaherara Motahareh,
Haghani Karimeh,
Khatami Mehrdad,
Rashidinejad Ali
Publication year - 2019
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1002/lipd.12133
Subject(s) - protein kinase b , chemistry , rosiglitazone , phosphorylation , c2c12 , irs1 , insulin , medicine , myogenesis , biochemistry , endocrinology , microbiology and biotechnology , biology , insulin receptor , in vitro , insulin resistance , receptor
Abstract In the current investigation, the effect of epigallocatechin gallate (EGCG) on the phosphorylation of IRS1 S307 and Akt S473 molecules in insulin‐resistant C2C12 muscle cells induced with palmitate was studied and compared with the effect of the antidiabetic drug, rosiglitazone. C2C12 myoblasts were cultured in Dulbecco's modified Eagle's medium and differentiated into myotubes using horse serum and the creatine kinase test was used to confirm their differentiation. The treatment of C2C12 myotubes was carried out with palmitate, where albumin was used as the conjugator. The Western blot technique was used to check the useful phosphorylation of IRS1 S307 and Akt S473 in C2C12 myotubes, in the presence or absence of palmitate. There was a significant ( p < 0.00) and linear increase in the activity of creatine kinase over time (0 to 96 h after differentiation) with everyday myoblast formation. While neither EGCG nor rosiglitazone showed a significant ( p > 0.05) effect on palmitate content during 96 h of incubation of IRS1 S307 , EGCG alone or combined with rosiglitazone increased the phosphorylation of Akt S473 , leading to the increase of glucose uptake into C2C12 cells. Thus, it can be concluded that EGCG alone or in combination with rosiglitazone may show some therapeutic effects for the prevention or treatment of Type 2 diabetes owing to its substantial effect on increasing the phosphorylation of Akt S473 and the subsequent glucose uptake into the cells.