Similar degrees of obesity induced by diet or aging cause strikingly different immunologic and metabolic outcomes

由饮食或衰老引起的相似程度的肥胖会导致截然不同的免疫和代谢结果。

阅读:1

Abstract

In obesity, adipose tissue (AT) and liver are infiltrated with Th-1 polarized immune cells, which are proposed to play an important role in the pathogenesis of the metabolic abnormalities of obesity. Aging is also associated with increased adiposity, but the effects of this increase on inflammation and associated metabolic dysfunction are poorly understood. To address this issue, we assessed insulin resistance (IR) andATand liver immunophenotype in aged, lean (AL) and aged, obese (AO) mice, all of whom were maintained on a standard chow diet (11% fat diet) throughout their lives. For comparison, these variables were also assessed in young, lean (YL) and young diet-induced obese mice (41% fat diet,YO). Despite similar body weight and fat accumulation,YOmice were substantially moreIRand had greater liver steatosis compared toAOmice.YOalso had elevated infiltration of macrophages/dendritic cells inATand liver, but these increases were absent inAO Furthermore, liver immune cells ofYOwere more Th-1 polarized thenAO Notably, aging was associated with accumulation of T cells, but this occurred independent of obesity. Together, the data suggest that reduced inflammation inAOunderlies the improved insulin sensitivity and lowered steatosis compared toYO.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。