Center of Clinical Pharmacology, University of Siena, Siena, Italy.
Neurosci Lett. 2010 Jul 19;479(1):54-7. doi: 10.1016/j.neulet.2010.05.027. Epub 2010 May 15.
Autism is a neurodevelopmental disorder with pathogenesis not completely understood. Although a genetic origin has been recognized, it has been hypothesized a role for environmental factors, immune dysfunctions, and alterations of neurotransmitter systems. In young autistic patients we investigated plasma leptin and adiponectin levels over a year period. Thirty-five patients, mean age at the basal time 14.1+/-5.4 years, were enrolled. Controls were 35 healthy subjects, sex and age matched. Blood samples were withdrawn in the morning at the baseline and 1 year after. In patients leptin concentrations significantly increased, while adiponectin did not significantly change. Leptin values in patients were significantly higher than those found in controls at each time; adiponectin values did not differ at each time between patients and controls. Since patients were not obese, we could hypothesize that leptin might participate to clinical manifestations other than weight balance. The role of adiponectin in autism is still debatable.
自闭症是一种神经发育障碍，其发病机制尚未完全阐明。尽管已经认识到其具有遗传起源，但也有人假设环境因素、免疫功能紊乱和神经递质系统的改变也与之相关。在自闭症的年轻患者中，我们在一年的时间内研究了血浆瘦素和脂联素的水平。共纳入了 35 名患者，其基础时间的平均年龄为 14.1±5.4 岁。对照组为 35 名健康受试者，性别和年龄匹配。在基线和一年后，于早晨采集血液样本。患者的瘦素浓度显著升高，而脂联素浓度没有显著变化。在每个时间点，患者的瘦素值均显著高于对照组；在每个时间点，患者和对照组的脂联素值均无差异。由于患者不肥胖，我们可以假设瘦素可能参与了体重平衡以外的临床表现。脂联素在自闭症中的作用仍存在争议。
