Lai Yun-Ru, Chen Meng Hsiang, Lin Wei Che, Chiu Wen-Chan, Cheng Ben-Chung, Chen Jung-Fu, Tsai Nai-Wen, Huang Chih-Cheng, Lu Cheng-Hsien
Department of Biological Science, National Sun Yat-Sen University, Kaohsiung, Taiwan.
Departments of Neurology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, No. 123, Ta Pei Road, Niao Sung Hsiang, Kaohsiung City, 833, Taiwan.
J Transl Med. 2020 Oct 19;18(1):396. doi: 10.1186/s12967-020-02559-7.
Evidences support the view that central obesity is an independently cardiovascular risk. It is thought that leptin contributes to autonomic dysfunction and cardiovascular risks in type 1 and type 2 diabetes mellitus (T1DM and T2DM). This raises the possibility that leptin might mediate the relationship between central obesity and the severity of cardiovascular autonomic neuropathy (CAN) in patients with well-controlled T2DM and prediabetes.
The complete cardiovascular reflex tests and biomarkers were assessed for each patient. The severity of CAN was assessed using composite autonomic scoring scale (CASS). A single-level three-variable mediation model was used to investigate the possible relationships among central obesity [as indicated by waist circumference (WC)], leptin level, and severity of CAN (as indicated by CASS value).
A total of 107 patients were included in this study: 90 with diabetes and 17 with prediabetes. The results demonstrate that increased WC is associated with increased severity of CAN (r = 0.242, P = 0.017). We further discovered that leptin level is positively correlated with WC (r = 0.504, P < 0.0001) and the CASS value (r = 0.36, P < 0.0001). Further mediation analysis shows that leptin level serves as mediators between higher WC and higher CASS.
Our results highlighted the relationship among leptin, central obesity, and severity of CAN. As the leptin level serves as mediator between central obesity and severity of CAN, a longitudinal study is needed to confirm that control of WC can decrease leptin levels and can be effective in reducing CAN progression.
有证据支持中心性肥胖是一种独立的心血管风险这一观点。人们认为瘦素在1型和2型糖尿病（T1DM和T2DM）中会导致自主神经功能障碍和心血管风险。这就增加了一种可能性，即瘦素可能介导了血糖控制良好的2型糖尿病患者和糖尿病前期患者的中心性肥胖与心血管自主神经病变（CAN）严重程度之间的关系。
对每位患者进行完整的心血管反射测试和生物标志物评估。使用综合自主神经评分量表（CASS）评估CAN的严重程度。采用单水平三变量中介模型来研究中心性肥胖[以腰围（WC）表示]、瘦素水平和CAN严重程度[以CASS值表示]之间的可能关系。
本研究共纳入107例患者：90例糖尿病患者和17例糖尿病前期患者。结果表明，WC增加与CAN严重程度增加相关（r = 0.242，P = 0.017）。我们进一步发现，瘦素水平与WC呈正相关（r = 0.504，P < 0.0001），与CASS值也呈正相关（r = 0.36，P < 0.0001）。进一步的中介分析表明，瘦素水平在较高的WC和较高的CASS之间起中介作用。
我们的结果突出了瘦素、中心性肥胖和CAN严重程度之间的关系。由于瘦素水平在中心性肥胖和CAN严重程度之间起中介作用，因此需要进行纵向研究以证实控制WC可降低瘦素水平，并能有效减少CAN的进展。
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