Diet-induced adiposity alters the serum profile of inflammation in C57BL/6N mice as measured by antibody array.

Diet-induced adiposity alters the serum profile of inflammation in C57BL/6N mice as measured by antibody array.
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DOI:
10.1111/j.1463-1326.2008.00974.x
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发表时间:
2009-04
期刊:
Diabetes, obesity & metabolism
影响因子:
--
通讯作者:
Hursting SD
Hursting SD
中科院分区:
其他
文献类型:
--
作者:
Fenton JI;Nuñez NP;Yakar S;Perkins SN;Hord NG;Hursting SD

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病态肥胖被认为是一种全身性炎症状态。本项目的目的是表征脂肪因子、细胞因子和趋化因子蛋白在对照、瘦和肥胖小鼠血清中的特征。我们假设趋化因子和细胞因子被热量限制和饮食引起的肥胖所改变,作为身体成分变化的功能。6周龄雌性C57BL/6N小鼠(每组12只)随机分为3组:对照组(自由饲喂);瘦(30%卡路里限制方案相对于对照组)和饮食引起的肥胖(DIO;高卡路里饮食,随意喂养)。在整个研究过程中,对体重、身体成分和食物摄入量进行了监测。饲喂10周后,采集血液样本,采用抗体阵列法测定血清脂肪因子/细胞因子/趋化因子。与对照组相比,瘦小鼠表现出胰岛素样生长因子(IGF)结合蛋白-3、-5和-6和脂联素浓度增加,IGF-1浓度降低。这些小鼠也显示出白细胞介素(IL)-10、IL-12 p40/p70、eotaxin、单核细胞化学引诱蛋白-5和SDF-1浓度的增加。与对照组相比,DIO小鼠的瘦素、IL-6和脂多糖诱导的趋化因子增加,所有趋化因子/细胞因子浓度降低。因此,这些数据表明,DIO可能导致炎症状态,其特征是向T辅助淋巴细胞1型倾斜反应性转变。脂肪因子、细胞因子和趋化因子蛋白在对照组、瘦小鼠和DIO小鼠中的差异可能对免疫反应性和疾病风险有影响。
Morbid obesity is considered a systemic inflammatory state. The objective of this project was to characterize the adipokine, cytokine and chemokine protein profile in serum from control, lean and obese mice. We hypothesized that chemokines and cytokines are altered by caloric restriction and diet-induced obesity as a function of changes in body composition. Six-week-old female C57BL/6N mice (n = 12 per group) were randomized to one of three diets: control (fed ad libitum); lean (30% calorie-restricted regimen relative to control) and diet-induced obese (DIO; high calorie diet, fed ad libitum). Body weight, body composition and food intake were monitored throughout the study. After 10 weeks on the diets, blood samples were collected, and adipokine/cytokine/chemokine serum profiles were measured by antibody array. Lean mice, relative to the control group, displayed increased concentrations of insulin-like growth factor (IGF) binding protein-3, -5 and -6 and adiponectin and decreased IGF-1. These mice also showed increased concentrations of interleukin (IL)-10, IL-12 p40/p70, eotaxin, monocyte chemoattractant protein-5 and SDF-1. In contrast, DIO mice displayed increased leptin, IL-6 and LPS-induced chemokine and decreased concentrations of all chemokines/cytokines measured relative to control mice. As such, these data indicate that DIO may lead to an inflammatory state characterized as a shift towards a T helper lymphocyte type 1–skewed responsiveness. The demonstration of differential adipokine, cytokine and chemokine protein profile in control, lean and DIO mice may have implications for immune responsiveness and risk of disease.