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衰老是与脂肪组织中的缺氧和氧化应激有关的:对脂肪功能的影响。

Aging is associated with hypoxia and oxidative stress in adipose tissue: implications for adipose function.

机构信息

Pennington Biomedical Research Center/LSU System, Baton Rouge, LA 70808, USA.

出版信息

Am J Physiol Endocrinol Metab. 2011 Oct;301(4):E599-607. doi: 10.1152/ajpendo.00059.2011. Epub 2011 May 17.

Abstract

As a part of aging there are known to be numerous alterations which occur in multiple tissues of the body, and the focus of this study was to determine the extent to which oxidative stress and hypoxia occur during adipose tissue aging. In our studies we demonstrate for the first time that aging is associated with both hypoxia (38% reduction in oxygen levels, Po(2) 21.7 mmHg) and increases reactive oxygen species in visceral fat depots of aging male C57Bl/6 mice. Interestingly, aging visceral fat depots were observed to have significantly less change in the expression of genes involved in redox regulation compared with aging subcutaneous fat tissue. Exposure of 3T3-L1 adipocytes to the levels of hypoxia observed in aging adipose tissue was sufficient to alter multiple aspects of adipose biology inducing increased levels of in insulin-stimulated glucose uptake and decreased lipid content. Taken together, these data demonstrate that hypoxia and increased levels of reactive oxygen species occur in aging adipose tissue, highlighting the potential for these two stressors as potential modulators of adipose dysfunction during aging.

摘要

随着年龄的增长,身体的多个组织中会发生许多变化,本研究的重点是确定脂肪组织衰老过程中氧化应激和缺氧的程度。在我们的研究中,我们首次证明衰老与缺氧(氧气水平降低 38%,Po(2) 21.7mmHg)和内脏脂肪组织中活性氧物种的增加有关衰老雄性 C57Bl/6 小鼠。有趣的是,与衰老的皮下脂肪组织相比,衰老的内脏脂肪组织中与氧化还原调节相关的基因表达变化明显较小。将 3T3-L1 脂肪细胞暴露于衰老脂肪组织中观察到的缺氧水平足以改变脂肪生物学的多个方面,诱导胰岛素刺激的葡萄糖摄取增加和脂质含量减少。总之,这些数据表明,缺氧和活性氧水平的增加发生在衰老的脂肪组织中,突出了这两个应激源作为衰老过程中脂肪功能障碍潜在调节剂的潜力。

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