Nutritional Physiology & Toxicology Team, INSERM UMR 1231, Faculté des Sciences de la Vie, Université de Bourgogne-Franche Comté (UBFC), 6 Boulevard Gabriel, 21000 Dijon, France.
Nutrients. 2021 Dec 31;14(1):197. doi: 10.3390/nu14010197.
Leptin, an anorectic hormone, regulates food intake, energy expenditure and body weight. We assessed the implication of tongue leptin in the modulation of oro-sensory detection of dietary fatty acids in mice. The RT-PCR analysis showed that mRNA encoding leptin and leptin receptor (Ob-Rb) was expressed in mice taste bud cells (TBC). Confocal microscopic studies showed that the lipid sensor CD36 was co-expressed with leptin in mice TBC. Silencing of leptin or Ob-Rb mRNA in tongue papillae upregulated preference for a long-chain fatty acid (LCFA), i.e., linoleic acid (LA), in a two-bottle paradigm in mice. Furthermore, tongue leptin application decreased the preference for the LCFA. These results suggest that tongue leptin exerts an inhibitory action on fatty acid preference. In isolated mice TBC, leptin decreased LCFA-induced increases in free intracellular calcium concentrations, [Ca]i. Leptin and LCFA induced the phosphorylation of ERK1/2 and STAT-3 and there were no additive or opposite effects of the two agents on the degree of phosphorylation. However, leptin, but not the LCFA, induced phosphoinositide-3-kinase (PI-3-K)-dependent Akt phosphorylation in TBC. Furthermore, leptin induced hyperpolarization, whereas LCFA induced depolarization in TBC. Our study demonstrates that tongue leptin exerts an inhibitory action on oro-sensory detection of a dietary fatty acid by interfering with Ca signaling and membrane potential in mice TBC.
瘦素是一种厌食激素，可调节食物摄入、能量消耗和体重。我们评估了舌瘦素在调节小鼠对膳食脂肪酸的口腔感觉检测中的作用。RT-PCR 分析显示，编码瘦素和瘦素受体（Ob-Rb）的 mRNA 在小鼠味觉细胞（TBC）中表达。共聚焦显微镜研究显示，脂质传感器 CD36 与小鼠 TBC 中的瘦素共表达。舌乳头上的瘦素或 Ob-Rb mRNA 沉默上调了小鼠对长链脂肪酸（LCFA），即亚油酸（LA）的偏好，在双瓶实验中。此外，舌瘦素的应用降低了对 LCFA 的偏好。这些结果表明舌瘦素对脂肪酸偏好施加抑制作用。在分离的小鼠 TBC 中，瘦素降低了 LCFA 诱导的细胞内游离钙浓度 ([Ca]i) 的增加。瘦素和 LCFA 诱导 ERK1/2 和 STAT-3 的磷酸化，并且两种药物对磷酸化程度没有相加或相反的作用。然而，瘦素而非 LCFA 诱导 TBC 中磷酸肌醇-3-激酶 (PI-3-K) 依赖性 Akt 磷酸化。此外，瘦素引起 TBC 的超极化，而 LCFA 引起 TBC 的去极化。我们的研究表明，舌瘦素通过干扰小鼠 TBC 中的钙信号和膜电位对膳食脂肪酸的口腔感觉检测发挥抑制作用。
