Intersection of the unfolded protein response and hepatic lipid metabolism.
Intersection of the unfolded protein response and hepatic lipid metabolism.
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DOI：
10.1007/s00018-009-0049-8
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发表时间：
2009-09
影响因子：
8
通讯作者：
Glimcher, Laurie H.
中科院分区：
文献类型：
--
作者：
Lee, Ann-Hwee;Glimcher, Laurie H.
肝脏通过控制脂质的合成、氧化、运输和排泄，在全身脂质代谢中起核心作用。未折叠蛋白反应（UPR）被认为是内质网应激激活的信号转导系统。最近的研究表明，UPR在肝脏脂质代谢中起着关键作用。UPR的IRE 1/XBP 1分支被高膳食碳水化合物激活，并控制参与脂肪酸和胆固醇生物合成的基因的表达。PERK介导的eIF 2 α磷酸化也是脂肪生成基因表达和肝脂肪变性发展所必需的，可能通过激活C/EBP和PPARγ转录因子。进一步的研究，以确定的分子途径，导致激活的UPR的营养线索在肝脏中，和他们的贡献，人类代谢紊乱，如肝脂肪变性，动脉粥样硬化和2型糖尿病，与脂质稳态失调，是必要的。
The liver plays a central role in whole-body lipid metabolism by governing the synthesis, oxidization, transport and excretion of lipids. The unfolded protein response (UPR) was identified as a signal transduction system that is activated by ER stress. Recent studies revealed a critical role of the UPR in hepatic lipid metabolism. The IRE1/XBP1 branch of the UPR is activated by high dietary carbohydrates and controls the expression of genes involved in fatty acid and cholesterol biosynthesis. PERK mediated eIF2α phosphorylation is also required for the expression of lipogenic genes and the development of hepatic steatosis, likely by activating C/EBP and PPARγ transcription factors. Further studies to define the molecular pathways that lead to the activation of the UPR by nutritional cues in the liver, and their contribution to human metabolic disorders such as hepatic steatosis, atherosclerosis and type 2 diabetes that are associated with dysregulation of lipid homeostasis, are warranted.
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影响因子：
4.8
作者：
BACHHAWAT, N;OUYANG, QA;HENRY, SA
通讯作者：
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影响因子：
5
作者：
Ciccaglione, A. R.;Marcantonio, C.;Rapicetta, M.
通讯作者：
Rapicetta, M.
影响因子：
1.5
作者：
Adachi, Yusuke;Yamamoto, Keisuke;Mori, Kazutoshi
通讯作者：
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影响因子：
4.8
作者：
Cnop, Miriam;Ladriere, Laurence;Eizirik, Decio L.
通讯作者：
Eizirik, Decio L.
DOI：
10.1097/01.alc.0000169265.36440.ee
发表时间：
2005-06-01
影响因子：
3.2
作者：
Blasco, C;Caballería, J;Rodés, J
通讯作者：
Rodés, J