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Iranian Journal of Diabetes and Obesity، جلد ۱۲، شماره ۴، صفحات ۲۳۳-۲۴۰

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عنوان انگلیسی Metformin and Pioglitazone Reduce Gene Expression of Inflammatory Factors in Insulin Resistant and Hypertrophied Adipocytes
چکیده انگلیسی مقاله  Objective: In obesity, chronic low grade inflammation, created by induction of pro-inflammatory markers, causes adipocyte dysfunction in adipose tissue. Adipocytes dysfunction is associated with various diseases including insulin resistance and obesity. In obesity, inflammatory factors such as osteopontin (OPN), angiopoietin-like protein 2 (Angptl2) and transforming growth factor-β (TGF-β) are induced in adipose tissue. Metformin and pioglitazone that are used to modulate inflammation, but the relevant mechanism is poorly understood. This study aimed to investigate the effect of metformin and pioglitazone as anti-diabetic drugs, on gene expression of osteopontin, Angptl2 and TGF-β as inflammatory factors in insulin resistance and hypertrophied adipocyte in 3T3-L1 cell line model in vitro. Materials and Methods: In this experimental research, we differentiated3T3-L1 preadipocytes to adipocytes. The adipocytes treated in insulin resistance and hypertrophied conditions with metformin and pioglitazone and assayed gene expression of OPN, Angptl2 and TGF-β by Real-Time PCR. Data was analyzed by SPSS statistic software. Results: The results showed that expression of OPN, Angptl2, and TGF-β were increased significantly over 2-fold (P-value< 0.05) in insulin resistance and hypertrophied adipocytes compared to normal adipocytes. Pre- and co-treatment with metformin and pioglitazone led to reduced expression of Angptl2 and TGF-β. Only metformin significantly reduced the expression of Angptl2, TGF-β and OPN in hypertrophied adipocyte. Conclusion: These results support the proposal that metformin and pioglitazone reduce gene expression of inflammatory factors in insulin resistant and hypertrophied adipocytes.
کلیدواژه‌های انگلیسی مقاله Angptl2, metformin, Osteopontin, Pioglitazone, TGF-β

نویسندگان مقاله | Zahra Malekpour-Dehkordi
Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran


| Javad Mohiti-Ardekani
Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran


| Yousof Naghiaee
Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran


| Shahram Teimourian
Department of Genetics, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran


| Mahdie Hemati
Department of Clinical Biochemistry, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran


| Mitra Nourbakhsh
Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran



نشانی اینترنتی http://ijdo.ssu.ac.ir/browse.php?a_code=A-10-30-297&slc_lang=en&sid=1
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