Adipose tissue dysfunction in nascent metabolic syndrome.

Adipose tissue dysfunction in nascent metabolic syndrome.
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DOI:
10.1155/2013/393192
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发表时间:
2013
期刊:
影响因子:
3.3
通讯作者:
Jialal I
Jialal I
中科院分区:
其他
文献类型:
--
作者:
Bremer AA;Jialal I

文献摘要

被引文献

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代谢综合征(MetS)增加了2型糖尿病(T2 DM)和心血管疾病(CVD)的风险。此外,对未并发T2 DM和/或CVD的新生MetS中脂肪组织生物学的研究很少。最近,我们发现脂肪组织失调和异常脂肪因子分泌导致了该综合征的低度慢性促炎状态和胰岛素抵抗。具体地说,我们已经作出了新的观察,皮下脂肪组织(SAT)与新生MetS的受试者增加了巨噬细胞招募与基数冠状结构。我们还表明,患有新生MetS的受试者增加了SAT分泌的脂肪因子(IL-1、IL-6、IL-8、瘦素、RBP-4、CRP、SAA、派-1、MCP-1和趋化因子)和血浆脂肪因子(IL-1、IL-6、瘦素、RBP-4、CRP、SAA和趋化因子)的水平,以及血浆脂联素和血浆和SAT网膜素-1的水平降低。大多数这些异常在纠正肥胖增加后仍然存在。因此,我们的数据以及其他研究者的数据突出了皮下脂肪组织功能障碍在MetS受试者中的重要性及其对促炎状态和胰岛素抵抗的贡献。这种脂肪因子谱可能有助于增加胰岛素抵抗和低度炎症,促进T2 DM和CVD的风险增加。
The metabolic syndrome (MetS) confers an increased risk for both type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Moreover, studies on adipose tissue biology in nascent MetS uncomplicated by T2DM and/or CVD are scanty. Recently, we demonstrated that adipose tissue dysregulation and aberrant adipokine secretion contribute towards the syndrome's low-grade chronic proinflammatory state and insulin resistance. Specifically, we have made the novel observation that subcutaneous adipose tissue (SAT) in subjects with nascent MetS has increased macrophage recruitment with cardinal crown-like structures. We have also shown that subjects with nascent MetS have increased the levels of SAT-secreted adipokines (IL-1, IL-6, IL-8, leptin, RBP-4, CRP, SAA, PAI-1, MCP-1, and chemerin) and plasma adipokines (IL-1, IL-6, leptin, RBP-4, CRP, SAA, and chemerin), as well as decreased levels of plasma adiponectin and both plasma and SAT omentin-1. The majority of these abnormalities persisted following correction for increased adiposity. Our data, as well as data from other investigators, thus, highlight the importance of subcutaneous adipose tissue dysfunction in subjects with MetS and its contribution to the proinflammatory state and insulin resistance. This adipokine profile may contribute to increased insulin resistance and low-grade inflammation, promoting the increased risk of T2DM and CVD.