Department of Neurology, University of Iowa, USA.
Eur J Pain. 2013 May;17(5):649-53. doi: 10.1002/j.1532-2149.2012.00230.x. Epub 2012 Oct 16.
Obesity is a risk factor associated with several pain syndromes. However, the mechanisms underlying the association between obesity and pain are not known. The aim of this study was to test the hypothesis that obesity enhances neuronal responses to nociceptive stimulation within the trigeminal nucleus caudalis (TNC).
Male and female C57BL/6J mice were fed a high-fat or regular diet from the time of weaning until 20 weeks of age. We then quantified neuronal activation by measuring Fos immunoreactivity within the TNC in response to a facial injection of a low dose of capsaicin (1 μg/10 μL).
We found that 0.01% capsaicin did not significantly increase Fos immunoreactivity in control mice fed a regular diet. In contrast, this low dose of capsaicin caused a 3.3-fold increase in Fos in the TNC in obese mice (p < 0.001).
These results support the hypothesis that diet-induced obesity in mice enhances nociceptive processing within the TNC. Diet-induced obesity may be a useful model for mechanistic studies. Future studies will improve our understanding of how obesity may contribute to trigeminal pain by sensitizing the trigeminal nociceptive system.
肥胖是与多种疼痛综合征相关的一个风险因素。然而，肥胖与疼痛之间的关联的机制尚不清楚。本研究旨在验证肥胖增强三叉神经尾核（TNC）内伤害性刺激的神经元反应的假说。
雄性和雌性 C57BL/6J 小鼠从断奶开始至 20 周龄时分别喂食高脂肪饮食或常规饮食。然后，我们通过测量 TNC 中 Fos 免疫反应来量化对低剂量辣椒素（1μg/10μL）的面部注射的神经元激活。
我们发现，0.01%辣椒素对喂食常规饮食的对照组小鼠的 Fos 免疫反应没有显著影响。相比之下，这种低剂量的辣椒素在肥胖小鼠的 TNC 中引起了 3.3 倍的 Fos 增加（p<0.001）。
这些结果支持肥胖症小鼠饮食诱导的肥胖增强 TNC 内伤害性加工的假说。饮食诱导的肥胖症可能是一种用于机制研究的有用模型。未来的研究将通过敏化三叉神经伤害性系统来提高我们对肥胖如何可能导致三叉神经痛的理解。
