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肥胖、缺乏身体活动及体重波动对慢性炎症的影响。

Influence of obesity, physical inactivity, and weight cycling on chronic inflammation.

作者信息

Strohacker K, McFarlin Brian K

机构信息

Laboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, Texas 77204-6015, USA.

出版信息

Front Biosci (Elite Ed). 2010 Jan 1;2(1):98-104. doi: 10.2741/e70.

Abstract

Obesity prevalence continues to rise due to excessive caloric intake and sedentary behavior. Weight loss can be achieved through diet and/or exercise, but maintenance of a reduced weight is rare and relapse is prevalent. Repeated periods of weight loss and regain have been termed "weight cycling." It has been speculated that weight cycling may further increase the elevated disease risk common with weight gain, obesity, and physical inactivity. Alterations in adipose tissue with weight cycling may create a more hypoxic environment; hypoxic adipose tissue secretes leptin, a stimulus for macrophage activation and accumulation within adipose tissue. Hypoxic adipocytes and macrophages release pro-inflammatory cytokines into circulation. Elevated body weight and adiposity are linked to cardiovascular disease and type 2 diabetes via an inflammatory mechanism. Thus, it is reasonable to speculate that weight cycling causes a more profound change in chronic inflammation than sustained weight gain. The purpose of this review is to explore inflammatory consequences associated with weight cycling as they are related to sustained weight gain, obesity, physical inactivity as well as relative disease risk.

摘要

由于热量摄入过多和久坐不动的行为,肥胖患病率持续上升。体重减轻可以通过饮食和/或运动来实现,但维持减轻后的体重很少见,复发很普遍。反复的体重减轻和恢复期被称为“体重循环”。据推测,体重循环可能会进一步增加与体重增加、肥胖和缺乏身体活动相关的疾病风险升高。体重循环导致的脂肪组织变化可能会创造一个更缺氧的环境;缺氧的脂肪组织会分泌瘦素,这是一种刺激巨噬细胞在脂肪组织内激活和积累的物质。缺氧的脂肪细胞和巨噬细胞会将促炎细胞因子释放到循环中。体重增加和肥胖通过炎症机制与心血管疾病和2型糖尿病相关联。因此,有理由推测,与持续体重增加相比,体重循环会导致慢性炎症发生更深刻的变化。本综述的目的是探讨与体重循环相关的炎症后果,因为它们与持续体重增加、肥胖、缺乏身体活动以及相对疾病风险有关。

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