Accompanied with profound efficacy, atypical antipsychotics (AAPs) contribute to metabolic adverse effects with few effective strategies to attenuate. Serotonin 5-HT2C receptor (HTR2C) plays a critical role in hyperphagia and weight gain induced by AAPs, and expression of phosphatase tensin homolog (PTEN) in the hypothalamus also affects feeding behavior and weight change. Moreover, PTEN has a physical crosstalk between PTEN and a region in the third intracellular loop (3L4F) of the HTR2C. Tat-3L4F has the property to disrupt crosstalk between PTEN and HTR2C. This is the first study to our knowledge to investigate the effect of Tat-3L4F on olanzapine-induced metabolic abnormalities and PTEN/ phosphatidylinositol 3-kinase/protein kinase B expression in the hypothalamus in rats.

中文翻译：

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一种新型合成干扰肽 Tat-3L4F 通过破坏大鼠血清素受体 2C 与蛋白质磷酸酶和张力蛋白同源物之间的串扰来减弱奥氮平诱导的体重增加。

伴随着深远的疗效，非典型抗精神病药 (AAPs) 会导致代谢不良反应，但几乎没有有效的减轻策略。5-羟色胺 5-HT2C 受体 (HTR2C) 在 AAP 诱导的食欲过盛和体重增加中起关键作用，下丘脑中磷酸酶张力蛋白同源物 (PTEN) 的表达也会影响进食行为和体重变化。此外，PTEN 在 PTEN 和 HTR2C 的第三个细胞内环 (3L4F) 中的区域之间存在物理串扰。Tat-3L4F 具有破坏 PTEN 和 HTR2C 之间串扰的特性。据我们所知，这是第一项研究 Tat-3L4F 对奥氮平诱导的大鼠下丘脑代谢异常和 PTEN/磷脂酰肌醇 3-激酶/蛋白激酶 B 表达的影响的研究。