芋螺是海的天敵。他們通過注入獵物包含了不同物質的雞尾酒來捕獲魚。蝸牛的毒液,所謂conopeptides是單一的組分,具有非凡的藥理特性和開發潛力。
一個代表例子就是作為止痛藥處方的芋螺毒素Ziconotid(Prialt)。芋螺毒素是第一個含有海洋生物物質的藥物之一。在與來自加拿大和美國,在呂貝克大學研究團隊和哥廷根大學的科學家合作研究的錐形蝸牛芋葉蟬的毒液。他們能夠表現出一定的肽(Conkunitzin-S1),能改變胰島素的胰腺細胞釋放。他們的研究結果發表在EMBO Molecular Medicine雜誌上。
葡萄糖是我們營養的一部分。當它進入消化系統,胰腺細胞釋放胰島素。糖化學分解到血液中。在2型糖尿病患者,這種機制被打亂,他們從患血糖水平過高或高血糖。新發現的物質,芋螺毒素S1期Conkunitzin,綁定到一個特定的鉀離子通道在胰腺細胞,並導致暫時的胰島素釋放增加,但只有當血糖水平提高的時候
大鼠口服葡萄糖耐受性測試之後,科學家們發現,Conkunitzin-S1不會導致低血糖。換句話說,一些傳統的2型糖尿病藥物的典型副作用不會發生。 Terlau說:我們研究工作在於發現管理肽口服的方式。(生物谷:Bioon.com)
Block of Kv1.7 potassium currents increases glucose-stimulated insulin secretion
Rocio K. Finol-Urdaneta, Maria S. Remedi, Walter Raasch, Stefan Becker, Robert B. Clark, Nina Strüver, Evgeny Pavlov, Colin G. Nichols, Robert J. French,*, Heinrich Terlau*
Glucose-stimulated insulin secretion (GSIS) relies on repetitive, electrical spiking activity of the beta cell membrane. Cyclic activation of voltage-gated potassium channels (Kv) generates an outward, 『delayed rectifier』 potassium current, which drives the repolarizing phase of each spike and modulates insulin release. Although several Kv channels are expressed in pancreatic islets, their individual contributions to GSIS remain incompletely understood. We take advantage of a naturally occurring cone-snail peptide toxin, Conkunitzin-S1 (Conk-S1), which selectively blocks Kv1.7 channels to provide an intrinsically limited, finely graded control of total beta cell delayed rectifier current and hence of GSIS. Conk-S1 increases GSIS in isolated rat islets, likely by reducing Kv1.7-mediated delayed rectifier currents in beta cells, which yields increases in action potential firing and cytoplasmic free calcium. In rats, Conk-S1 increases glucose-dependent insulin secretion without decreasing basal glucose. Thus, we conclude that Kv1.7 contributes to the membrane-repolarizing current of beta cells during GSIS and that block of this specific component of beta cell Kv current offers a potential strategy for enhancing GSIS with minimal risk of hypoglycaemia during metabolic disorders such as Type 2 diabetes.