Weight loss regulates inflammation-related genes in white adipose tissue of obese subjects

Weight loss regulates inflammation-related genes in white adipose tissue of obese subjects
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DOI:
10.1096/fj.04-2204com
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发表时间:
2004-11-01
期刊:
影响因子:
4.8
通讯作者:
Langin, D
Langin, D
中科院分区:
生物学2区
文献类型:
--
作者:
Clément, K;Viguerie, N;Langin, D

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脂肪组织会产生炎症和免疫分子,这些分子被怀疑与肥胖相关并发症有关。人类对这些分子的表达模式和营养调控了解甚少。我们利用cDNA微阵列和逆转录定量PCR分析了29名肥胖受试者在极低热量饮食(VLCD)期间皮下白色脂肪组织的基因表达谱。将其表达模式与17名非肥胖受试者进行了比较。我们确定了受调控的基因是在脂肪细胞还是基质血管成分细胞中表达。基因表达谱分析确定了100种与炎症相关的转录本,肥胖个体在进行28天的VLCD(而非2天的VLCD)时这些转录本受到调控。聚类分析表明,肥胖受试者在进行28天VLCD后的基因表达模式比VLCD前更接近消瘦受试者的基因表达谱。减肥通过减少促炎因子和增加抗炎分子来改善肥胖受试者的炎症状况。这些基因主要在脂肪组织的基质血管成分中表达,该成分含有大量巨噬细胞。减肥对肥胖相关并发症的有益作用可能与脂肪组织炎症状况的改变有关。
Adipose tissue produces inflammation and immunity molecules suspected to be involved in obesity-related complications. The pattern of expression and the nutritional regulation of these molecules in humans are poorly understood. We analyzed the gene expression profiles of subcutaneous white adipose tissue from 29 obese subjects during very low calorie diet (VLCD) using cDNA microarray and reverse transcription quantitative PCR. The patterns of expression were compared with that of 17 non-obese subjects. We determined whether the regulated genes were expressed in adipocytes or stromavascular fraction cells. Gene expression profiling identified 100 inflammation-related transcripts that are regulated in obese individuals when eating a 28 day VLCD but not a 2 day VLCD. Cluster analysis showed that the pattern of gene expression in obese subjects after 28 day VLCD was closer to the profile of lean subjects than to the pattern of obese subjects before VLCD. Weight loss improves the inflammatory profile of obese subjects through a decrease of proinflammatory factors and an increase of anti-inflammatory molecules. The genes are expressed mostly in the stromavascular fraction of adipose tissue, which is shown to contain numerous macrophages. The beneficial effect of weight loss on obesity-related complications may be associated with the modification of the inflammatory profile in adipose tissue.