Effect of high fat diet (HFD)-induced obesity on gene expression of adipose tissue macrophage markers in male rats with different ages: Role of AMPK/SIRT1 pathway.

Hebatallah Mohammed Aboudeya, A. Abdou, Maha Mostafa Attia, Noura A. Matar
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Abstract

Obesity and aging are associated with adipose tissue (AT) inflammation and a higher risk of chronic diseases. However, the underlying mechanism remains largely unknown. Here, we investigated the effect of HFD-induced obesity on gene expressions of ATM polarization markers and inflammatory cytokines in male rats with different ages and the possible role of AMPK/SIRT1 pathway in mediating this effect. Sixty male wistar rats were divided into young, adult and old-age groups. Rats of each group were either fed standard diet or HFD. The present results revealed that HFD feeding in all age groups resulted in increased body weight, lipids, visceral adiposity and induced hyperglycemia and insulin resistance compared to controls. Findings revealed significant higher AT IL-6 levels and lower IL-10 levels with significant upregulation of CD11c and CD206 mRNA expressions in all age groups. The histological findings showed increased inflammation and presence of crown like structures in adult and old HFD groups. Moreover, the HFD-induced obesity in groups resulted in significant reduction in p-AMPK levels and SIRT1 expression in AT as compared to controls. AMPK and SIRT1 was positively correlated with IL-10 and CD206 and negatively correlated with TG, HOMA-IR, IL-6 and CD11c in obese groups of different ages. In conclusion, HFD-induced obesity in all ages leads to ATMs polarization and increased inflammatory response that may contribute to metabolic dysfunction. In addition, AMPK/SIRT1 pathway is suggested to be a mediator of ATMs polarization. Thus, targeting this pathway may be promising for treating obesity and aging-related diseases.
高脂饮食(HFD)诱导的肥胖对不同年龄雄性大鼠脂肪组织巨噬细胞标志物基因表达的影响:AMPK/SIRT1通路的作用
肥胖和衰老与脂肪组织(AT)炎症和较高的慢性疾病风险有关。然而,其背后的机制在很大程度上仍然未知。在此,我们研究了 HFD 诱导的肥胖对不同年龄雄性大鼠 ATM 极化标志物和炎症细胞因子基因表达的影响,以及 AMPK/SIRT1 通路在介导这种影响中可能发挥的作用。60 只雄性 Wistar 大鼠被分为青年组、成年组和老年组。各组大鼠均摄入标准饮食或高氟日粮。本研究结果显示,与对照组相比,各年龄组喂食高纤维食物会导致体重、血脂、内脏脂肪增加,并诱发高血糖和胰岛素抵抗。研究结果显示,所有年龄组的AT IL-6水平明显升高,IL-10水平降低,CD11c和CD206 mRNA表达明显上调。组织学研究结果表明,成人组和老年 HFD 组的炎症和冠状结构增加。此外,与对照组相比,HFD 诱导的肥胖导致 AT 中 p-AMPK 水平和 SIRT1 表达显著降低。在不同年龄的肥胖组中,AMPK 和 SIRT1 与 IL-10 和 CD206 呈正相关,与 TG、HOMA-IR、IL-6 和 CD11c 呈负相关。总之,HFD 诱导的各年龄段肥胖都会导致 ATMs 极化和炎症反应增加,从而可能导致代谢功能障碍。此外,AMPK/SIRT1 通路被认为是 ATMs 极化的介质。因此,靶向这一途径可能有望治疗肥胖和衰老相关疾病。
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