'Metabolically healthy obesity': origins and implications.
'Metabolically healthy obesity': origins and implications.
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DOI：
10.1016/j.mam.2012.10.004
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发表时间：
2013-02
影响因子：
10.6
通讯作者：
Obin, Martin S.
中科院分区：
文献类型：
--
作者：
Denis, Gerald V.;Obin, Martin S.
当人类吃得多而运动得少时，他们往往会变得肥胖和不健康。将肥胖与2型糖尿病和心血管疾病等严重疾病联系起来的分子途径已经成为深入科学研究的主题，因为全球肥胖症的爆炸性流行对数亿人的健康构成了严重的新威胁。然而，肥胖并不总是命中注定的。有两个重要的临床人群对理解这一难题背后的机制很有价值：一是那些表现出代谢功能障碍、糖尿病和心血管疾病风险升高的人，尽管体型偏瘦；二是那些尽管明显肥胖，但相对免受这些危险的人。对第二组“新陈代谢健康的肥胖者”的研究尤其揭示了一些问题，因为这些人表现出特定的、可识别的、解剖学的、细胞的和分子的特征，这些特征使他们与我们这些健康状况下降、体重增加的人区别开来。在这里，我们研究了其中的一些特征，包括一些提供机制信息的小鼠模型，并提出了进一步研究的假设，包括免疫系统的基因和途径可能提供新的诊断或治疗靶点的可能性。
When humans eat more and exercise less, they tend to become obese and unhealthy. The molecular pathways that link obesity to serious diseases like Type 2 diabetes and cardiovascular disease have become a subject of intensive scientific investigation because the exploding prevalence of obesity worldwide represents a grave new threat to the health of hundreds of millions of people. However, obesity is not always destiny. Two important clinical populations have been valuable to understand the mechanisms behind this conundrum: individuals who exhibit metabolic dysfunction, diabetes and elevated cardiovascular disease risk despite a lean body type, and individuals who are relatively protected from these dangers despite significant obesity. Study of this second group of ‘metabolically healthy obese’ people in particular has been revealing because such individuals exhibit specific, identifiable, anatomic, cellular and molecular features that set them apart from the rest of us who suffer declining health with increasing weight. Here, we examine some of these features, including some mouse models that are informative of mechanism, and suggest hypotheses for further study, including the possibility that genes and pathways of the immune system might offer new diagnostic or therapeutic targets.
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