Department of Human Physiology, University of Oregon, Eugene, OR 97403-1240, USA.
J Physiol. 2012 Apr 15;590(8):1787-801. doi: 10.1113/jphysiol.2011.221036. Epub 2012 Feb 20.
Excess body weight is a major risk factor for cardiovascular disease, increasing the risk of hypertension, hyperglycaemia and dyslipidaemia, recognized as the metabolic syndrome. Adipose tissue acts as an endocrine organ by producing various signalling cytokines called adipokines (including leptin, free fatty acids, tumour necrosis factor-α, interleukin-6, C-reactive protein, angiotensinogen and adiponectin). A chronic dysregulation of certain adipokines can have deleterious effects on insulin signalling. Chronic sympathetic overactivity is also known to be present in central obesity, and recent findings demonstrate the consequence of an elevated sympathetic outflow to organs such as the heart, kidneys and blood vessels. Chronic sympathetic nervous system overactivity can also contribute to a further decline of insulin sensitivity, creating a vicious cycle that may contribute to the development of the metabolic syndrome and hypertension. The cause of this overactivity is not clear, but may be driven by certain adipokines. The purpose of this review is to summarize how obesity, notably central or visceral as observed in the metabolic syndrome, leads to adipokine expression contributing to changes in insulin sensitivity and overactivity of the sympathetic nervous system.
超重是心血管疾病的一个主要危险因素，会增加高血压、高血糖和血脂异常的风险，这些被认为是代谢综合征。脂肪组织通过产生各种称为脂肪因子的信号细胞因子（包括瘦素、游离脂肪酸、肿瘤坏死因子-α、白细胞介素-6、C 反应蛋白、血管紧张素原和脂联素）起内分泌器官的作用。某些脂肪因子的慢性失调可能对胰岛素信号产生有害影响。众所周知，在中心性肥胖中存在慢性交感神经过度活跃，最近的研究结果表明，升高的交感神经输出对心脏、肾脏和血管等器官的后果。慢性交感神经系统过度活跃也可能导致胰岛素敏感性进一步下降，形成一个恶性循环，可能导致代谢综合征和高血压的发展。这种过度活跃的原因尚不清楚，但可能是由某些脂肪因子驱动的。本综述的目的是总结肥胖，尤其是代谢综合征中观察到的中心性或内脏性肥胖，如何导致脂肪因子表达，从而导致胰岛素敏感性变化和交感神经系统过度活跃。
