Simonds Stephanie E, Pryor Jack T, Cowley Michael A
aDepartment of Physiology, Monash Biomedical Discovery Institute, Monash University, Clayton, Victoria, Australia bWarwick Medical School, University of Warwick; Neurosolutions Ltd., Coventry, UK.
Curr Opin Nephrol Hypertens. 2017 Jan;26(1):20-25. doi: 10.1097/MNH.0000000000000287.
Cardiovascular diseases (CVDs) are the number one cause of death globally. The risk for the development of CVDs is significantly increased in obesity. Leptin, the product of white adipose tissue, appears to contribute to the development of CVDs in obesity. Here, we discuss the premise that leptin engages the sympathetic nervous system and contributes to elevated blood pressure (BP) developing in obesity.
The long-term regulation of BP is dependent on the activity of the autonomic nervous system and specifically the sympathetic nervous system. Sympathetic nerve activity is significantly increased in obese rodents and humans. Leptin increases sympathetic nerve activity in rodents and humans; however, leptin only consistently increases BP chronically in rodents. The ability of leptin to increase BP in rodents is via both hypothalamic and extrahypothalamic regions. In leptin-deficient and leptin receptor-deficient humans, leptin appears to be the key reason for decreased systolic BP. However, in other research conducted in humans, chronic administration of leptin does not elevate BP.
Further research into the role of leptin in the development of CVDs, especially in humans, needs to be conducted.
心血管疾病(CVDs)是全球首要死因。肥胖会显著增加患心血管疾病的风险。瘦素是白色脂肪组织的产物,似乎在肥胖相关心血管疾病的发生中起作用。在此,我们讨论瘦素作用于交感神经系统并导致肥胖人群血压(BP)升高这一假设。
血压的长期调节依赖于自主神经系统尤其是交感神经系统的活动。肥胖啮齿动物和人类的交感神经活动显著增加。瘦素可增加啮齿动物和人类的交感神经活动;然而,瘦素仅能持续使啮齿动物的血压长期升高。瘦素在啮齿动物中升高血压的能力是通过下丘脑和下丘脑外区域实现的。在瘦素缺乏和瘦素受体缺乏的人类中,瘦素似乎是收缩压降低的关键原因。然而,在针对人类的其他研究中,长期给予瘦素并不会升高血压。
需要对瘦素在心血管疾病发生中的作用进行进一步研究,尤其是在人类中的研究。