淋巴细胞壁和系统性Tissue-Associated炎症在肥胖Zucker老鼠

在人类中,淋巴功能障碍和肥胖似乎互惠关系,淋巴水肿可导致脂肪沉积,和肥胖会损害淋巴功能。老鼠的最近的研究表明,肥胖诱导的高脂肪的饮食会损害淋巴引流的尾巴和后肢。淋巴管也可以成为过度渗透,泄漏淋巴在db / db的老鼠都肥胖和糖尿病。这些研究表明淋巴功能障碍与肥胖有关,但是,病理生理机制仍然未知。本研究的目的是调查的程度肥胖引起的炎症和重塑收集大鼠肠系膜淋巴管的墙。ZUCKER-Leprafa(肥胖)和ZUCKER - Leprafa / +(精益)雄性或雌性老鼠,美国实验生物学学会联合会声明符合原则的使用动物研究和教育,被用于这项研究。年龄组包括8、12和26 - 32周内。被动墙力学测量使用收集淋巴管孤立和安装到resistance-matched玻璃微量吸液管,在37°C白蛋白生理盐溶液(APSS没有Ca2 +)浴,从1 - 5厘米水腔的压力了。肠系膜拱廊与脂肪组织和收集淋巴管被解剖,固定在4%多聚甲醛、加工和嵌入在石蜡切片和疣状抗体rat-specific CD68(巨噬细胞标记)和caveolin-1(脂肪细胞标记)的量化冠状结构(cls)。血清和peri-lymphatic脂肪组织(平台)也被收集和分析炎症标记物的使用67只老鼠——RayBiotech生物标志物检测服务。 Average lymphatic wall thickness, wall:lumin ratio (X100) and medial cross sectional area were significantly greater in obese versus lean male rats at all ages. Many CLSs were observed surrounding mesenteric collecting lymphatics isolated from obese male 12 and 26-32 wk rats. Additionally, CLSs significantly increased with age. In an analyses of serum biomarkers obtained from 12 wk old lean and obese, male and female rats, we observed that many of the markers in PLAT (IL-6, IL-13, adiponectin) and in serum (GM-CSF, IL-4, Gas1) were differentially regulated by obesity and sex. The data support the ideas that obesity can permit changes to passive wall mechanics that can lead to a structural remodeling of lymphatic collecting vessels and that obesity is associated with both systemic and tissue-associated inflammation (PLAT) in both male and female Zucker rats.