日本科学家在最新一期《欧洲心脏病学杂志》上报告说，他们发现肥胖导致交感神经活动增强，这是肥胖者患上高血压的主要原因之一。
日本东北大学教授片桐秀树率领的研究小组首先选定血压正常的瘦弱实验鼠，然后通过特殊方法使实验鼠增肥，特别是让其肝脏区域脂肪增加。在变胖后，多数实验鼠患上高血压。
接下来，科学家们切断了实验鼠体内连接肝脏和脊髓的交感神经。手术后，即使实验鼠进一步增肥，其血压仍会保持在一定水平，不再继续上升。
然后，科学家们选取一批原本就肥胖并患有高血压的实验鼠，对它们进行了类似的神经切断手术。术后，这些肥胖实验鼠的血压也稳定在一定水平。
日本科学家对实验结果分析说，当过量脂肪积累在肝脏区域的时候，肝脏会发出信号，要求提高交感神经活跃程度，以便刺激代谢，控制体重不再过快增长。而交感神经活跃，极易诱发高血压。在切断神经后，由于肝脏无法再发出增进代谢的要求，血压升高的诱因也就消失了。
生物探索推荐英文论文摘要：
Hepatic peroxisome proliferator-activated receptor-γ–fat-specific protein 27 pathway contributes to obesity-related hypertension via afferent vagal signals
Abstract
Aims Obesity is commonly associated with hypertension. Increased sympathetic tonus in obese subjects contributes to the underlying mechanism. However, the precise mechanisms whereby obesity induces this sympathetic activation remain unclear. Hepatic peroxisome proliferator-activated receptor (PPAR)-γ2 expression, which is reportedly upregulated during obesity development, affects sympathetic activation via hepatic vagal afferents. Herein, we report involvement of this neuronal relay in obesity-related hypertension.
Methods and results Peroxisome proliferator-activated receptor-γ and a direct PPARγ target, fat-specific protein 27 (Fsp27), were adenovirally overexpressed or knocked down in the liver, in combination with surgical dissection or pharmacological deafferentation of the hepatic vagus. Adenoviral PPARγ2 expression in the liver raised blood pressure (BP) in wild-type but not in β1/β2/β3 adrenergic receptor-deficient mice. In addition, knockdown of endogenous PPARγ in the liver lowered BP in murine obesity models. Either surgical dissection or pharmacological deafferentation of the hepatic vagus markedly blunted BP elevation in mice with diet-induced and genetically-induced obesity. In contrast, BP was not elevated in other models of hepatic steatosis, DGAT1 and DGAT2 overexpressions, in which PPARγ is not upregulated in the liver. Thus, hepatic PPARγ upregulation associated with obesity is involved in BP elevation during obesity development. Furthermore, hepatic expression of Fsp27 raised BP and the effect was blocked by hepatic vagotomy. Hepatic Fsp27 is actually upregulated in murine obesity models and its knockdown reversed BP elevation.
Conclusion The hepatic PPARγ–Fsp27 pathway plays important roles in the development of obesity-related hypertension via afferent vagal signals from the liver.
