Leptin, a hormone rleased from the adiose 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 selectivity suppressed depending on plasma leptin level after an intraperitoneal injectin of recobinant leptin. Patch-clamp studies using isolated taste cells of lean mice showed that extracellular leptin enhnced K~+ currents of sweet-responsive taste cells, which led to membrane hyperpolarization 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 geneticaly diabetic db/db mice, which have defects in Ob-Rb, demonstrated neither a suppresion 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 reult from the lack of inhibitory modulation by leptin.
展开▼
机译：瘦素是一种从脂肪组织中释放出来的激素，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，根据腹膜内注射瘦素后血浆瘦素水平，选择性刺激抑制了味觉神经对甜味刺激的反应。使用瘦小鼠的分离出的味觉细胞进行的膜片钳研究表明，胞外瘦素增强了甜味反应性味觉细胞的K〜+电流，这导致了膜超极化链反应（RT-PCR），并且原位杂交分析表明该蛋白的mRNA特异性表达瘦小鼠的味觉组织和细胞中的长型功能性瘦素受体（Ob-Rb）。具有Ob-Rb缺陷的遗传性糖尿病db / db小鼠，即使使用高剂量的瘦素，也未显示味觉神经对甜味剂的反应性增强，也未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。
展开▼
