The voltage-gated potassium channel Kv1.3 regulates energy homeostasis and body weight
The voltage-gated potassium channel Kv1.3 regulates energy homeostasis and body weight
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DOI：
10.1093/hmg/ddg049
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发表时间：
2003-03-01
影响因子：
3.5
通讯作者：
Desir, GV
中科院分区：
文献类型：
--
作者：
Xu, JC;Koni, PA;Desir, GV
电压门控钾通道调节细胞膜电位并控制多种细胞过程。Kv1.3通道在多种组织中表达，被认为参与细胞体积调节、细胞凋亡、T细胞活化和肾溶质稳态。对基因靶向产生的Kv1.3缺陷小鼠（Kv1.3(-/-)）的检查揭示了Kv1.3在体重调节中的作用，这是以前未被认识到的。事实上，Kv1.3（-/-）小鼠的体重明显低于对照组。此外，基因敲除小鼠不受饮食引起的肥胖的影响，在高脂肪饮食中，它们的体重增加明显少于对照组。虽然Kv1.3（-/-）和对照组之间的食物摄取量没有显著差异，但通过间接量热法在休息时测量的基础代谢率在敲除动物中显着更高。这些数据表明，Kv1.3通道可能参与调节体重的途径，通道抑制可增加基础代谢率。
Voltage-gated potassium (Kv) channels regulate cell membrane potential and control a variety of cellular processes. Kv1.3 channels are expressed in several tissues and believed to participate in cell volume regulation, apoptosis, T cell activation and renal solute homeostasis. Examination of Kv1.3-deficient mice (Kv1.3(-/-)), generated by gene targeting, revealed a previously unrecognized role for Kv1.3 in body weight regulation. Indeed, Kv1.3(-/-) mice weigh significantly less than control littermates. Moreover, knockout mice are protected from diet-induced obesity and gain significantly less weight than littermate controls when placed on a high-fat diet. While food intake did not differ significantly between Kv1.3(-/-) and controls, basal metabolic rate, measured at rest by indirect calorimetry, was significantly higher in knockout animals. These data indicate that Kv1.3 channels may participate in the pathways that regulate body weight and that channel inhibition increases basal metabolic rate.