PGBR extract ameliorates TNF‐α induced insulin resistance in hepatocytes

The Kaohsiung Journal of Medical Sciences - Tập 34 - Trang 14-21 - 2018
Fu-Chih Chen1, Kuo-Ping Shen2, Jin-Bor Chen3, Hui-Li Lin4, Chi-Long Hao5, Hsueh-Wei Yen6, Shyh-Yu Shaw1,7
1Department of Chemistry, National Cheng Kung University, Tainan, Taiwan
2Department of Nursing, MeiHo University, Pingtung, Taiwan
3Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan
4Department of Food Science and Nutrition, Meiho University, Pingtung, Taiwan
5Division of Cardiology, Department of Internal Medicine, Pingtung Christian Hospital, Pingtung, Taiwan
6Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
7Institute of Biotechnology, National Cheng Kung University, Tainan, Taiwan

Tóm tắt

AbstractPre‐germinated brown rice (PGBR) could ameliorate metabolic syndrome, however, not much research estimates the effect of PGBR extract on insulin resistance. The aim of this study is to examine the effects of PGBR extract in TNF‐α induced insulin resistance. HepG2 cells, hepatocytes, were cultured in DMEM medium and added with 5 μM insulin or with insulin and 30 ng/ml TNF‐α or with insulin, TNF‐α and PGBR extract (50, 100, 300 μg/ml). The glucose levels of the medium were decreased by insulin, demonstrating insulin promoted glucose uptake into cell. However, TNF‐α inhibited glucose uptake into cells treated with insulin. Moreover, insulin increased the protein expressions of AMP‐activated protein kinase (AMPK), insulin receptor substrate‐1 (IRS‐1), phosphatidylinositol‐3‐kinase‐α (PI3K‐α), serine/threonine kinase PI3K‐linked protein kinase B (Akt/PKB), glucose transporter‐2 (GLUT‐2), glucokinase (GCK), peroxisome proliferator activated receptor‐α (PPAR‐α) and PPAR‐γ. TNF‐α activated p65 and MAPKs (JNK1/2 and ERK1/2) which worsened the expressions of AMPK, IRS‐1, PI3K‐α, Akt/PKB, GLUT‐2, GCK, glycogen synthase kinase‐3 (GSK‐3), PPAR‐α and PPAR‐γ. Once this relationship was established, we added PGBR extract to cell with insulin and TNF‐α. We found glucose levels of medium were lowered and that the protein expressions of AMPK, IRS‐1, PI3K‐α, Akt/PKB, GLUT‐2, GCK, GSK‐3, PPAR‐α, PPAR‐γ and p65, JNK1/2 were also recovered. In conclusion, this study found that TNF‐α inhibited insulin stimulated glucose uptake and aggravated related proteins expressions, suggesting that it might cause insulin resistance. PGBR extract was found to ameliorate this TNF‐α induced insulin resistance, suggesting that it might be used in the future to help control insulin resistance.

Tài liệu tham khảo

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Thông tin xuất bản

The Kaohsiung Journal of Medical Sciences

Tập 34

14-21

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