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饮食诱导的肥胖会改变 C57BL/6N 小鼠的血清炎症谱,通过抗体阵列进行测量。

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

机构信息

Department of Food Science and Human Nutrition, Michigan State University, East Lansing, MI 48824, USA.

出版信息

Diabetes Obes Metab. 2009 Apr;11(4):343-54. doi: 10.1111/j.1463-1326.2008.00974.x.

Abstract

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.

摘要

病态肥胖被认为是一种全身炎症状态。本项目的目的是描述对照、瘦和肥胖小鼠血清中的脂肪因子、细胞因子和趋化因子蛋白谱。我们假设趋化因子和细胞因子会随着热量限制和饮食诱导的肥胖而改变,这是身体成分变化的一个功能。将 6 周龄雌性 C57BL/6N 小鼠(每组 12 只)随机分为三组饮食:对照(自由进食);瘦(相对于对照减少 30%热量限制方案)和饮食诱导肥胖(DIO;高热量饮食,自由进食)。在整个研究过程中监测体重、身体成分和食物摄入量。在饮食 10 周后,采集血样,并通过抗体阵列测量脂肪因子/细胞因子/趋化因子血清谱。与对照组相比,瘦鼠显示胰岛素样生长因子(IGF)结合蛋白-3、-5 和 -6 以及脂联素的浓度增加,而 IGF-1 的浓度降低。这些老鼠还显示出白介素(IL)-10、IL-12 p40/p70、嗜酸性粒细胞趋化因子、单核细胞趋化蛋白-5 和 SDF-1 的浓度增加。相比之下,DIO 小鼠显示出瘦素、IL-6 和 LPS 诱导的趋化因子浓度增加,而与对照组相比,所有测量的趋化因子/细胞因子的浓度降低。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 型倾斜的反应性转变。对照、瘦和 DIO 小鼠中不同的脂肪因子、细胞因子和趋化因子蛋白谱的显示可能对免疫反应性和疾病风险有影响。

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