干扰素受体α/β/γ消融在AG129小鼠屈曲模型中西方饮食诱导的肥胖和胰岛素抵抗中的作用

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Interferon and Cytokine Research Pub Date : 2023-07-01 DOI:10.1089/jir.2023.0047
Emylle Costa-Bartuli, Adrielle Tenório Rodrigues, Sofia Andrade Ribeiro Bastos, Nathan Kistenmacker, Leticia Crepaldi, Christina Maeda Takiya, Patricia Zancan, Fabio Mendonça Gomes, Mauro Sola-Penna
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引用次数: 0

摘要

饮食引起的肥胖引发循环促炎细胞因子和急性期蛋白的升高,包括干扰素(ifn)。ifn强烈促进与肥胖相关并发症相关的低度炎症,如非酒精性脂肪性肝病和糖尿病。在本研究中,AG129小鼠模型(IFN α/β/γ受体双敲除株)喂食高脂高糖(HFHS)饮食(西方饮食)20周,旨在了解IFN受体消融对饮食性肥胖、胰岛素抵抗和非酒精性脂肪性肝病的影响。小鼠对HFHS饮食有反应,在食用HFHS饮食20周后变得肥胖,同时白色脂肪组织增加2倍。此外,动物出现葡萄糖和胰岛素耐受不良,以及胰岛素信号介质如胰岛素受体底物1 (IRS1)、蛋白激酶B (AKT)和S6核糖体蛋白的失调。肝脏间质细胞增多,脂质积累,纤维化标志物(转化生长因子β 1 [Tgfb1]、角蛋白18 [Krt18]、Vimentin [Vim])增强,IFN受体下游蛋白(toll样受体[TLR] 4、活化B细胞核因子kappa-轻链增强子[NFκB]、cAMP反应元件结合蛋白[CREB])表达降低。因此,IFN受体消融促进了对NFκB和CREB通路的影响,但对饮食诱导的肥胖小鼠的全身稳态没有积极影响。因此,我们得出结论,IFN受体信号不是促进饮食引起的肥胖并发症所必需的,因此不能与非感染性条件下的代谢性疾病相关。
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The Role of Interferon Receptors α/β/γ Ablation During Western Diet-Induced Obesity and Insulin Resistance in the Inflectional Model AG129 Mice Strain.

Diet-induced obesity triggers elevation of circulating pro-inflammatory cytokines and acute-phase proteins, including interferons (IFNs). IFNs strongly contribute to low-grade inflammation associated with obesity-related complications, such as nonalcoholic fat liver disease and diabetes. In this study, AG129 mice model (double-knockout strain for IFN α/β/γ receptors) was fed with a high-fat high-sucrose (HFHS) diet (Western diet) for 20 weeks aiming to understand the impact of IFN receptor ablation on diet-induced obesity, insulin resistance, and nonalcoholic fat liver disease. Mice were responsive to the diet, becoming obese after 20 weeks of HFHS diet which was accompanied by 2-fold increase of white adipose tissues. Moreover, animals developed glucose and insulin intolerance, as well as dysregulation of insulin signaling mediators such as Insulin Receptor Substrate 1 (IRS1), protein kinase B (AKT), and S6 ribosomal protein. Liver increased interstitial cells, and lipid accumulation was also found, presenting augmented fibrotic markers (transforming growth factor beta 1 [Tgfb1], Keratin 18 [Krt18], Vimentin [Vim]), yet lower expression on IFN receptor downstream proteins (Toll-like receptor [TLR] 4, nuclear factor kappa-light-chain-enhancer of activated B cells [NFκB], and cAMP response element-binding protein [CREB]). Thus, IFN receptor ablation promoted effects on NFκB and CREB pathways, with no positive effects on systemic homeostasis in diet-induced obese mice. Therefore, we conclude that IFN receptor signaling is not essential for promoting the complications of diet-induced obesity and thus cannot be correlated with metabolic diseases in a noninfectious condition.

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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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