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首页> 外文期刊>Journal of Lipid Research >Insulin sensitive and resistant obesity in humans: AMPK activity, oxidative stress, and depot-specific changes in gene expression in adipose tissue
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Insulin sensitive and resistant obesity in humans: AMPK activity, oxidative stress, and depot-specific changes in gene expression in adipose tissue

机译：人体对胰岛素敏感和抗药性肥胖：脂肪组织中AMPK活性，氧化应激和基因表达的储库特异性变化

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We previously reported that adenosine monophosphate-activated protein kinase (AMPK) activity is lower in adipose tissue of morbidly obese individuals who are insulin resistant than in comparably obese people who are insulin sensitive. However, the number of patients and parameters studied were small. Here, we compared abdominal subcutaneous, epiploic, and omental fat from 16 morbidly obese individuals classified as insulin sensitive or insulin resistant based on the homeostatic model assessment of insulin resistance. We confirmed that AMPK activity is diminished in the insulin resistant group. A custom PCR array revealed increases in mRNA levels of a wide variety of genes associated with inflammation and decreases in PGC-1α and Nampt in omental fat of the insulin resistant group. In contrast, subcutaneous abdominal fat of the same patients showed increases in PTP-1b, VEGFa, IFNγ, PAI-1, and NOS-2 not observed in omental fat. Only angiotensinogen and CD4+ mRNA levels were increased in both depots. Surprisingly, TNFα was only increased in epiploic fat, which otherwise showed very few changes. Protein carbonyl levels, a measure of oxidative stress, were increased in all depots. Thus, adipose tissues of markedly obese insulin resistant individuals uniformly show decreased AMPK activity and increased oxidative stress compared with insulin sensitive patients. However, most changes in gene expression appear to be depot-specific.
机译：我们以前曾报道过，在患有胰岛素抵抗的病态肥胖个体的脂肪组织中，腺苷单磷酸激活蛋白激酶（AMPK）的活性要比在对胰岛素敏感的肥胖者中的脂肪组织低。但是，研究的患者人数和参数很少。在这里，我们根据对胰岛素抵抗的稳态模型评估，比较了来自16个病态肥胖个体的腹部皮下脂肪，上腹部脂肪和网膜脂肪，它们被归类为胰岛素敏感性或胰岛素抵抗。我们证实，胰岛素抵抗组的AMPK活性降低。定制的PCR阵列揭示了与炎症相关的多种基因的mRNA水平增加，胰岛素抵抗组网膜脂肪中的PGC-1α和Nampt降低。相反，同一患者的腹部皮下脂肪在网膜脂肪中未观察到PTP-1b，VEGFa，IFNγ，PAI-1和NOS-2的增加。在两个仓库中仅血管紧张素原和CD4 + mRNA水平增加。令人惊讶的是，TNFα仅在表观脂肪中增加，否则几乎没有变化。在所有仓库中，蛋白质羰基水平（一种衡量氧化应激的水平）均增加了。因此，与胰岛素敏感性患者相比，明显肥胖的胰岛素抵抗者的脂肪组织均匀地显示出AMPK活性降低和氧化应激增加。但是，基因表达的大多数变化似乎都是针对仓库的。

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