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血管紧张素转换酶抑制剂可增加肥胖大鼠肝脏和肌肉中胰岛素诱导的pp185磷酸化。

Angiotensin-converting enzyme inhibitor increases insulin-induced pp185 phosphorylation in liver and muscle of obese rats.

作者信息

Carvalho D S, Villaça V, Brenelli S L, Carvalho C R, Saad M J

机构信息

Departamento de Clínica Médica, FCM, UNICAMP, Campinas, SP, Brasil.

出版信息

Biochem Mol Biol Int. 1998 Oct;46(2):259-66. doi: 10.1080/15216549800203772.

Abstract

The clinical use of angiotensin-converting enzyme (ACE) inhibitors has been associated with increased insulin sensitivity. However, the molecular mechanism is unknown. The authors examined the early steps in insulin action, i.e., the phosphorylation status of the insulin receptor and of the pp185 in liver and muscle of obese rats treated acutely with captopril, using immunoblotting with antiphosphotyrosine antibodies. Following treatment with captopril there was an improvement in insulin-induced insulin receptor and pp185 phosphorylation in the liver and muscle of obese rats. This finding contribute to an explanation of the mechanism by which ACE inhibitors appear to improve insulin sensitivity.

摘要

血管紧张素转换酶(ACE)抑制剂的临床应用与胰岛素敏感性增加有关。然而,其分子机制尚不清楚。作者使用抗磷酸酪氨酸抗体进行免疫印迹,研究了急性给予卡托普利的肥胖大鼠肝脏和肌肉中胰岛素作用的早期步骤,即胰岛素受体和pp185的磷酸化状态。给予卡托普利治疗后,肥胖大鼠肝脏和肌肉中胰岛素诱导的胰岛素受体和pp185磷酸化得到改善。这一发现有助于解释ACE抑制剂似乎改善胰岛素敏感性的机制。

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