Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Australia.
Pharmacol Ther. 2010 May;126(2):159-72. doi: 10.1016/j.pharmthera.2010.02.002. Epub 2010 Feb 19.
The world wide prevalence of obesity and the metabolic syndrome is escalating. Contrary to earlier experimental evidence, human obesity is characterised by sympathetic nervous activation, with the outflows to both the kidney and skeletal muscle being activated. While the mechanisms responsible for initiating the sympathetic activation remain to be unequivocally elucidated, hyperinsulinemia, obstructive sleep apnoea, increased circulating adipokines, stress and beta adrenergic receptor polymorphisms are implicated. The pattern of sympathetic activation may be the pathophysiological mechanism underpinning much obesity-related illnesses with the consequences including, amongst others, the development of hypertension, insulin resistance, diastolic dysfunction and renal impairment. While diet and exercise are the first line therapy for the treatment of obesity and the metabolic syndrome, pharmacological interventions targeting the sympathetic nervous system, either directly or indirectly are also likely to be of benefit. Importantly, the benefit may not necessarily be weight related but may be associated with a reduction in end organ damage.
肥胖症和代谢综合征在全球范围内的流行率正在不断上升。与早期的实验证据相反，人类肥胖症的特征是交感神经激活，肾脏和骨骼肌的传出均被激活。虽然引起交感神经激活的确切机制仍有待明确，但高胰岛素血症、阻塞性睡眠呼吸暂停、循环中脂肪因子增加、应激和β肾上腺素能受体多态性都与之相关。交感神经激活模式可能是肥胖相关疾病的病理生理机制基础，其后果包括高血压、胰岛素抵抗、舒张功能障碍和肾功能损害的发展等。虽然饮食和运动是肥胖症和代谢综合征的一线治疗方法，但针对交感神经系统的药物干预（直接或间接）也可能有益。重要的是，这种益处不一定与体重相关，而可能与减少终末器官损伤有关。
