Obesity, triggered by high-fat diet (HFD), is associated to altered gustatory perception of dietary lipids. Oleanolic acid (OLA), a triterpene, has been reported to exert anti-obesity effects in animal models. Hence, we investigated the role of OLA in the modulation of oro-sensory perception of lipids in control and HFD-induced obese mice. As expected, OLA-treated obese mice exhibited a decrease in body, liver, and visceral adipose tissue weights. OLA treatment improved glucose tolerance, insulin level, plasma lipopolysaccharide (LPS), and hepatic cholesterol and triglyceride concentrations. OLA-treated obese mice exhibited higher fat preference compared to untreated obese mice, probably due to the increase in mRNA encoding CD36, a fat taste receptor, in mouse taste bud cells (mTBC). This phenomenon was associated with fatty-acid induced increases in free intracellular calcium concentrations, [Ca²⁺]i, induced in mTBC from OLA-treated obese mice. OLA also influenced the expression of mRNA encoding pro-inflammatory cytokines (IL-1β and IL-6) and some lipogenic genes (PPARα, SREBP1, FAS, ChREBP, and G6Pase) in liver and adipose tissue. These findings reveal that OLA improves gustatory perception of lipids and exerts protective effects in obesity.

由高脂饮食（HFD）引发的肥胖与饮食脂质的味觉改变有关。据报道，齐墩果酸（OLA）是一种三萜烯，在动物模型中具有抗肥胖作用。因此，我们调查了OLA在控制和HFD诱导的肥胖小鼠中脂质对口感的调节中的作用。正如预期的那样，用OLA治疗的肥胖小鼠的身体，肝脏和内脏脂肪组织的重量均减少。OLA治疗改善了葡萄糖耐量，胰岛素水平，血浆脂多糖（LPS）以及肝胆固醇和甘油三酸酯的浓度。与未治疗的肥胖小鼠相比，OLA治疗的肥胖小鼠表现出更高的脂肪偏爱，这可能是由于小鼠味蕾细胞（mTBC）中编码CD36（一种脂肪味觉受体）的mRNA增加所致。²⁺ ] i，在OTB处理的肥胖小鼠的mTBC中诱导产生。OLA还影响肝脏和脂肪组织中编码促炎性细胞因子（IL-1β和IL-6）和某些脂肪形成基因（PPARα，SREBP1，FAS，ChREBP和G6Pase）的mRNA的表达。这些发现表明，OLA改善了人们对脂质的味觉感知，并在肥胖症中发挥了保护作用。