High-fat diet triggers inflammation-induced cleavage of SIRT1 in adipose tissue to promote metabolic dysfunction.
High-fat diet triggers inflammation-induced cleavage of SIRT1 in adipose tissue to promote metabolic dysfunction.
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DOI：
10.1016/j.cmet.2012.07.003
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发表时间：
2012-08-08
期刊：
影响因子：
29
通讯作者：
Guarente L
中科院分区：
文献类型：
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作者：
Chalkiadaki A;Guarente L
脂肪组织在储存过量营养和防止其他器官异位脂肪堆积方面发挥着重要作用。肥胖导致脂肪细胞储存过多的脂肪，导致应激信号的产生和代谢功能的紊乱。SIRT1是许多代谢组织中营养物质可利用性的重要调节传感器。在此，我们报道了SIRT1在脂肪组织中的功能，在正常饮食条件下防止炎症和肥胖，并防止在饮食应激和衰老下进展为代谢功能障碍。基因消融脂肪组织中的SIRT1导致了基因表达的变化，这种变化与高脂饮食诱导的变化高度重叠，表明饮食应激信号抑制了SIRT1的活性。事实上，我们发现，高脂饮食通过炎症激活的caspase-1诱导脂肪组织中SIRT1蛋白的裂解，在饮食应激和代谢功能障碍的易感性之间提供了联系。
Adipose tissue plays an important role in storing excess nutrients and preventing ectopic lipid accumulation in other organs. Obesity leads to excess lipid storage in adipocytes, resulting in the generation of stress signals and the derangement of metabolic functions. SIRT1 is an important regulatory sensor of nutrient availability in many metabolic tissues. Here we report that SIRT1 functions in adipose tissue to protect from inflammation and obesity under normal feeding conditions, and to forestall the progression to metabolic dysfunction under dietary stress and aging. Genetic ablation of SIRT1 in adipose tissue leads to gene expression changes that highly overlap with changes induced by high-fat diet in wild-type mice, suggesting that dietary stress signals inhibit the activity of SIRT1. Indeed, we show that high-fat diet induces the cleavage of SIRT1 protein in adipose tissue by the inflammation-activated caspase-1, providing a link between dietary stress and predisposition to metabolic dysfunction.
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影响因子：
64.8
作者：
Guarente, Leonard
通讯作者：
Guarente, Leonard
影响因子：
7.7
作者：
Gillum MP;Kotas ME;Erion DM;Kursawe R;Chatterjee P;Nead KT;Muise ES;Hsiao JJ;Frederick DW;Yonemitsu S;Banks AS;Qiang L;Bhanot S;Olefsky JM;Sears DD;Caprio S;Shulman GI
通讯作者：
Shulman GI
DOI：
10.1073/pnas.2536828100
发表时间：
2003-12-23
影响因子：
11.1
作者：
He, WM;Barak, Y;Evans, RM
通讯作者：
Evans, RM
影响因子：
29
作者：
Banks AS;Kon N;Knight C;Matsumoto M;Gutiérrez-Juárez R;Rossetti L;Gu W;Accili D
通讯作者：
Accili D
影响因子：
82.9
作者：
通讯作者：
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