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Ion channels and second messengers involved in transduction and modulation of sweet taste in mouse taste cells

机译：离子通道和第二信使参与小鼠味觉细胞中甜味的转导和调节

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Leptin, a hormone released from the adipose tissue, inhibits food intake and increases energy expenditure. We have found a novel function of leptin as a modulator of sweet taste sensitivity in mice. In lean normal mice, the gustatory nerve responses to sweet stimuli were selectively suppressed depending on plasma leptin level after an intraperitoneal injection of recombinant leptin. Patch-clamp studies using isolated taste cells of lean mice showed that extracellular leptin enhanced K+ currents of sweet-responsive taste cells, which led to membrane hyperpolarization and a reduction of sweetener-induced depolarization. Reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization analyses demonstrated specific expression of mRNA of the long-form functional leptin receptor (Ob-Rb) in taste tissue and cells of lean mice. The genetically diabetic db/db mice, which have defects in Ob-Rb, demonstrated neither a suppression of gustatory neural responses to sweeteners nor an increment of whole-cell K+ conductance of taste cells even with high doses of leptin. These results suggest that Ob-Rb is specifically expressed in sweet-responsive taste cells of lean mice and that leptin suppresses sweetener-induced depolarization via activation of K+ channels, leading to a decrease in impulses of sweet-best fibers. The enhanced sweet responses of db/db mice may result from the lack of inhibitory modulation by leptin. [References: 36]
机译：瘦素是一种从脂肪组织释放的激素，会抑制食物摄入并增加能量消耗。我们已经发现瘦蛋白作为小鼠甜味敏感性调节剂的新功能。在瘦的正常小鼠中，根据腹膜内注射重组瘦素后的血浆瘦素水平，选择性地抑制了味觉神经对甜味刺激的反应。使用瘦小鼠的分离的味觉细胞进行的膜片钳研究表明，细胞外瘦素增强了甜味反应性味觉细胞的K +电流，这导致膜超极化并减少了甜味剂引起的去极化。逆转录聚合酶链反应（RT-PCR）和原位杂交分析表明，长形功能瘦素受体（Ob-Rb）mRNA在瘦肉小鼠的味觉组织和细胞中特异性表达。在Ob-Rb中有缺陷的遗传性糖尿病db / db小鼠，即使使用高剂量的瘦素，也未显示出对甜味剂的味觉神经反应的抑制，也不显示味觉细胞的全细胞K +电导增加。这些结果表明，Ob-Rb在瘦小鼠的甜味反应性味觉细胞中特异性表达，并且瘦素通过激活K +通道抑制甜味剂诱导的去极化，从而导致甜味最佳纤维冲动的减少。 db / db小鼠甜味反应增强可能归因于瘦素缺乏抑制性调节作用。 [参考：36]

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