TXNIP in Metabolic Regulation: Physiological Role and Therapeutic Outlook.
TXNIP in Metabolic Regulation: Physiological Role and Therapeutic Outlook.
复制标题
DOI：
10.2174/1389450118666170130145514
复制
发表时间：
2017
影响因子：
3.2
通讯作者：
Mohammad S
中科院分区：
文献类型：
--
作者：
Alhawiti NM;Al Mahri S;Aziz MA;Malik SS;Mohammad S
硫氧还蛋白相互作用蛋白（TXNIP）也称为硫氧还蛋白结合蛋白-2（thioredoxinbindingprotein-2），是一种广泛表达的蛋白质，其与硫氧还蛋白（TXN）相互作用并负调控其表达和功能。在过去的几年中，TXNIP由于其影响能量代谢的几个方面的广泛功能而引起了相当大的关注。TXNIP通过多效性作用（包括调节β细胞功能、肝葡萄糖产生、外周葡萄糖摄取、脂肪生成和底物利用）作为葡萄糖和脂质代谢的重要调节剂。在动物模型中，TXNIP的过表达已显示诱导胰腺β细胞的凋亡，降低外周组织如骨骼肌和脂肪中的胰岛素敏感性，并降低能量消耗。相反，TXNIP缺乏的动物被保护免于饮食诱导的胰岛素抵抗和2型糖尿病。因此，靶向TXNIP被认为提供了新的治疗机会，TXNIP抑制剂有可能成为治疗糖尿病的强大治疗工具。在这里，我们总结了我们对TXNIP生物学的理解的现状，强调了它在代谢调节中的作用，并提出了一些关键问题，这些问题可能有助于未来的研究将TXNIP作为治疗靶点。
Thioredoxin-interacting protein (TXNIP) also known as thioredoxin binding protein-2 is a ubiquitously expressed protein that interacts and negatively regulates expression and function of Thioredoxin (TXN). Over the last few years, TXNIP has attracted considerable attention due to its wide-ranging functions impacting several aspects of energy metabolism. TXNIP acts as an important regulator of glucose and lipid metabolism through pleiotropic actions including regulation of β-cell function, hepatic glucose production, peripheral glucose uptake, adipogenesis, and substrate utilization. Overexpression of TXNIP in animal models has been shown to induce apoptosis of pancreatic β-cells, reduce insulin sensitivity in peripheral tissues like skeletal muscle and adipose, and decrease energy expenditure. On the contrary, TXNIP deficient animals are protected from diet induced insulin resistance and type 2 diabetes. Consequently, targeting TXNIP is thought to offer novel therapeutic opportunity and TXNIP inhibitors have the potential to become a powerful therapeutic tool for the treatment of diabetes mellitus. Here we summarize the current state of our understanding of TXNIP biology, highlight its role in metabolic regulation and raise critical questions that could help future research to exploit TXNIP as a therapeutic target.
登录
查看更多内容
影响因子：
4.2
作者：
Donnelly, KL;Margosian, MR;Parks, EJ
通讯作者：
Parks, EJ
DOI：
10.1093/gerona/glv071
发表时间：
2016-06-01
影响因子：
5.1
作者：
Bedarida, Tatiana;Baron, Stephanie;Nivet-Antoine, Valerie
通讯作者：
Nivet-Antoine, Valerie
影响因子：
4.3
作者：
Fang, Shaohong;Jin, Yuhong;Zhou, Hongbo
通讯作者：
Zhou, Hongbo
影响因子：
5.3
作者：
Ferreira, Noely E.;Omae, Samantha;Pereira, Alexandre C.
通讯作者：
Pereira, Alexandre C.
影响因子：
3.6
作者：
Cha-Molstad, Hyunjoo;Xu, Guanlan;Shalev, Anath
通讯作者：
Shalev, Anath