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首页> 外文期刊>American Journal of Physiology >Volume-sensitive outwardly rectifying chloride channel in white adipocytes from normal and diabetic mice.
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Volume-sensitive outwardly rectifying chloride channel in white adipocytes from normal and diabetic mice.

机译：正常和糖尿病小鼠的白色脂肪细胞中的体积敏感的向外整流氯通道。

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The volume-sensitive outwardly rectifying (VSOR) chloride channel is ubiquitously expressed and involved in cell volume regulation after osmotic swelling, called regulatory volume decrease (RVD), in various cell types. In adipocytes, the expression of the VSOR channel has not been explored to date. Here, by employing the whole-cell patch-clamp technique, we examined whether or not the VSOR channel is expressed in white adipocytes freshly isolated from epididymal fat pads of normal (C57BL/6 or KK) and diabetic (KKA(y)) mice. Whole cell voltage-clamp recordings revealed that Cl(-) currents were gradually activated upon cell swelling induced by application of a hypotonic solution, both in normal and diabetic adipocytes. Although both the mean cell size (or cell capacitance) and the current magnitude in KKA(y) adipocytes were larger than those in C57BL/6 cells, the current density was significantly lower in KKA(y) adipocytes (23.32 +/- 1.94 pA in C57BL/6 adipocytes vs. 13.04 +/- 2.41 pA in KKA(y) adipocytes at +100 mV). Similarly, the current density in diabetic KKA(y) adipocytes was lower than that in adipocytes from KK mice (a parental strain of KKA(y) mice), which do not present diabetes until an older age. The current was inhibited by Cl(-) channel blockers, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and glibenclamide, or hypertonic solution, and showed outward rectification and inactivation kinetics at large positive potentials. These electrophysiological and pharmacological properties are consistent with those of the VSOR channel in other cell types. Moreover, adipocytes showed RVD, which was inhibited by NPPB. In KKA(y) adipocytes, RVD was significantly slower (tau; 8.42 min in C57BL/6 adipocytes vs. 11.97 min in KKA(y) adipocytes) and incomplete during the recording period (25 min). It is concluded that the VSOR channel is functionally expressed and involved in volume regulation in white adipocytes. RVD is largely impaired in adipocytes from diabetic mice, presumably as a consequence of the lower density of the functional VSOR channel in the plasma membrane.
机译：在各种细胞类型中，渗透性溶胀后，体积敏感的向外整流（VSOR）氯化物通道被普遍表达并参与细胞体积调节，称为调节体积减少（RVD）。在脂肪细胞中，迄今为止尚未探索VSOR通道的表达。在这里，通过采用全细胞膜片钳技术，我们检查了VSOR通道是否在从正常小鼠（C57BL / 6或KK）和糖尿病小鼠（KKA（y））的附睾脂肪垫新鲜分离的白色脂肪细胞中表达。全细胞电压钳记录显示，在正常和糖尿病脂肪细胞中，通过应用低渗溶液诱导的细胞肿胀，会逐渐激活Cl（-）电流。尽管KKA（y）脂肪细胞的平均细胞大小（或细胞电容）和电流大小均大于C57BL / 6细胞，但KKA（y）脂肪细胞的电流密度显着较低（23.32 +/- 1.94 pA在C57BL / 6脂肪细胞中的血红蛋白含量与在+100 mV的KKA（y）脂肪细胞中的13.04 +/- 2.41 pA相比）。同样，糖尿病KKA（y）脂肪细胞中的电流密度低于来自KK小鼠（KKA（y）小鼠的亲本品系）的脂肪细胞，后者直到年纪大了才出现糖尿病。该电流被Cl（-）通道阻滞剂，5-硝基-2-（3-苯基丙基氨基）苯甲酸（NPPB）和格列本脲或高渗溶液抑制，并在大正电势下表现出向外的整流和失活动力学。这些电生理学和药理学特性与其他细胞类型中VSOR通道的电生理学和药理学特性一致。此外，脂肪细胞显示RVD，其被NPPB抑制。在KKA（y）脂肪细胞中，RVD明显较慢（tau;在C57BL / 6脂肪细胞中为8.42分钟，而在KKA（y）脂肪细胞中为11.97分钟），并且在记录期间（25分钟）不完全。结论是VSOR通道在白色脂肪细胞中功能性表达并参与体积调节。 RVD在糖尿病小鼠的脂肪细胞中大大受损，大概是由于质膜中功能性VSOR通道密度较低的结果。

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