Amelioration of obesity-associated inflammation and insulin resistance in c57bl/6 mice via macrophage polarization by fish oil supplementation

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• 作者：Samina Bashir ; Yadhu Sharma ; Asif Elahi ; Farah Khan ; ^{farahkhan3@gmail.com" class="auth_mail" title="E-mail the corresponding author} ; ^{fkhan@jamiahamdard.ac.in" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Immunomodulation ; Inflammation ; Macrophage polarization ; NF-κB/p65 ; Obesity
• 刊名：Journal of Nutritional Biochemistry
• 出版年：2016
• 出版时间：July 2016
• 年：2016
• 卷：33
• 期：Complete
• 页码：82-90
• 全文大小：1931 K

文摘

Enormous phenotypic plasticity makes macrophages the target cells in obesity-associated inflammatory diseases. Thus, nutritional components that polarize macrophages toward antiinflammatory phenotype can partially reverse inflammatory diseases like insulin resistance. In the present study, macrophage-polarizing and insulin-sensitizing properties of fish oil (FO) were evaluated in obese insulin-resistant c57bl/6 mice fed high-fat diet (HFD-IR) after oral supplementation with FO (4, 8 or 16 mg/kg body weight) and compared to lean and HFD-IR mice. FO-supplemented HFD-IR mice exhibited reduced adiposity index, serum cholesterol and triglycerides and increased insulin sensitization and showed improved adipose tissue physiology under light and transmission electron microscopy. NF-κB/P65 expression showed a downward shift on FO supplementation. The surface marker of M1 macrophages (CD-86) and the TLR-4 expression reduced with the increased supplementation of FO. Expression of arginase 1, an important marker of M2 macrophages, increased in a dose-dependent manner in response to FO dosage, which was observed at protein level by the western blotting and at mRNA level by real-time PCR. The cytokine profile of adipose tissue macrophages showed a steep shift toward antiinflammatory ones (IL-4 and IL-10) from the inflammatory TNF-α, IFN-γ, IL-2 and IL-1β. Thus, macrophage polarization seems to be the plausible mechanism via which FO alleviates obesity-induced inflammation and insulin resistance.