OEA 对食物摄入的影响独立于肠道和迷走神经节中 PPARα 的存在，而 OEA 对能量消耗的影响则需要在小鼠体内存在 PPARα。
The OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in mice.
机构信息
Laboratory of Metabolism, Department of Medicine Specialties, Faculty of Medicine, University of Geneva, Geneva, Switzerland; Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Center for Integrative Genomics, University of Lausanne, Le Génopode, 1015 Lausanne, Switzerland.
出版信息
Metabolism. 2018 Oct;87:13-17. doi: 10.1016/j.metabol.2018.06.005. Epub 2018 Jun 21.
BACKGROUND
Oleoylethanolamide (OEA) is an endocannabinoid that controls food intake, energy expenditure and locomotor activity. Its anorexigenic effect appears to be mediated by PPARα, but the tissue where the presence of this receptor is required for OEA to inhibit feeding is unknown as yet. Previous studies point to a possible role of proximal enterocytes and neurons of the nodose ganglion.
MATERIALS AND METHODS
Acute intraperitoneal OEA effects on food intake, energy expenditure, respiratory exchange ratio (RER) and locomotor activity were studied in control mice (PPARα-loxP) and intestinal (Villin-Cre;PPARα-loxP) or nodose ganglion (Phox2B-Cre;PPARα-loxP) specific PPARα knockout mice placed in calorimetric cages.
RESULTS
OEA administration to both intestinal and nodose ganglion PPARα knockout mice decreased food intake, RER (leading to increased lipid oxidation) and locomotor activity as in control mice. However, while OEA injection acutely decreased energy expenditure in controls, this effect was not observed in mice devoid of PPARα in the intestine.
CONCLUSION
These results indicate that the OEA effect on food intake is independent from the presence of PPARα in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARα in the intestine.
背景
油酰乙醇酰胺（OEA）是一种内源性大麻素，可控制食物摄入、能量消耗和运动活性。其抑制摄食的作用似乎是通过 PPARα 介导的，但目前尚不清楚该受体在哪个组织中存在，OEA 才能抑制摄食。先前的研究表明，近端肠细胞和迷走神经节神经元可能发挥作用。
材料和方法
在代谢笼中，对对照小鼠（PPARα-loxP）和肠道（Villin-Cre；PPARα-loxP）或迷走神经节（Phox2B-Cre；PPARα-loxP）特异性 PPARα 敲除小鼠进行急性腹腔内 OEA 对食物摄入、能量消耗、呼吸交换率（RER）和运动活性的影响研究。
结果
OEA 给药至肠道和迷走神经节 PPARα 敲除小鼠均如对照小鼠一样，减少了食物摄入、RER（导致脂质氧化增加）和运动活性。然而，虽然 OEA 注射可急性降低对照小鼠的能量消耗，但在肠道缺乏 PPARα 的小鼠中未观察到这种作用。
结论
这些结果表明，OEA 对食物摄入的作用独立于肠道和迷走神经节中 PPARα 的存在，而 OEA 对能量消耗的影响需要肠道中存在 PPARα。
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