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CD8+ effector T cells contribute to macrophage recruitment and adipose tissue inflammation in obesity.CD8 + 效应T细胞在肥胖症中促进巨噬细胞募集和脂肪组织炎症。
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Normalization of obesity-associated insulin resistance through immunotherapy.通过免疫疗法使肥胖相关的胰岛素抵抗正常化。
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Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters.瘦而非肥胖的个体中,脂肪富含一群独特的调节性T细胞,这些细胞会影响代谢参数。
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Genetic deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice.肥大细胞的基因缺陷和药物稳定作用可减轻小鼠饮食诱导的肥胖和糖尿病。
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The role of LMNA in adipose: a novel mouse model of lipodystrophy based on the Dunnigan-type familial partial lipodystrophy mutation.LMNA在脂肪组织中的作用:基于邓尼根式家族性部分脂肪营养不良突变的新型脂肪营养不良小鼠模型。
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Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency.p16Ink4a和p19Arf在BubR1功能不足引起的衰老和老化过程中的相反作用。
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Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy.高效抗逆转录病毒治疗相关脂肪营养不良患者的脂肪组织炎症与肝脏脂肪
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脂肪细胞祖细胞的衰老与区域差异——综述

Aging and regional differences in fat cell progenitors - a mini-review.

机构信息

Department of Biomedical and Surgical Sciences, Division of Geriatrics, University of Verona, Verona, Italy.

出版信息

Gerontology. 2011;57(1):66-75. doi: 10.1159/000279755. Epub 2010 Jan 29.

DOI:10.1159/000279755
PMID:20110661
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3031153/
Abstract

Fat mass and fat tissue distribution change dramatically throughout life. In old age, fat becomes dysfunctional and is redistributed from subcutaneous to intra-abdominal visceral depots as well as other ectopic sites, including bone marrow, muscle and the liver. These changes are associated with increased risk of metabolic syndrome. Fat tissue is a nutrient storage, endocrine and immune organ that undergoes renewal throughout the lifespan. Preadipocytes, which account for 15-50% of cells in fat tissue, give rise to new fat cells. With aging, declines in preadipocyte proliferation and differentiation likely contribute to increased systemic exposure to lipotoxic free fatty acids. Age-related fat tissue inflammation is related to changes that occur in preadipocytes and macrophages in a fat depot-dependent manner. Fat tissue inflammation frequently leads to further reduction in adipogenesis with aging, more lipotoxicity and activation of cellular stress pathways that, in turn, exacerbate inflammatory responses of preadipocytes and immune cells, establishing self-perpetuating cycles that lead to systemic dysfunction. In this review, we will consider how inherent, age-related, depot-dependent alterations in preadipocyte function contribute to age-related fat tissue redistribution and metabolic dysfunction.

摘要

脂肪组织和脂肪组织分布在整个生命周期中发生显著变化。在老年时,脂肪变得功能失调,并从皮下重新分布到腹部内脏脂肪库以及其他异位部位,包括骨髓、肌肉和肝脏。这些变化与代谢综合征的风险增加有关。脂肪组织是一种营养储存、内分泌和免疫器官,在整个生命周期中不断更新。前脂肪细胞占脂肪组织中细胞的 15-50%,产生新的脂肪细胞。随着年龄的增长,前脂肪细胞的增殖和分化能力下降,可能导致全身暴露于脂毒性游离脂肪酸的增加。与年龄相关的脂肪组织炎症与脂肪库中前脂肪细胞和巨噬细胞的变化有关。脂肪组织炎症常导致随着年龄的增长脂肪生成进一步减少、脂毒性增加以及细胞应激途径的激活,进而加剧前脂肪细胞和免疫细胞的炎症反应,形成自我维持的循环,导致全身功能障碍。在这篇综述中,我们将考虑前脂肪细胞功能的固有、与年龄相关、与脂肪库相关的改变如何导致与年龄相关的脂肪组织再分布和代谢功能障碍。