Unitat de Farmacologia i Farmacognòsia, Institut de Biomedicina, Centros de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat de Barcelona, Nucli Universitari de Pedralbes, 08028 Barcelona, Spain.
J Mol Endocrinol. 2012 Oct 10;49(3):R149-56. doi: 10.1530/JME-12-0151. Print 2012 Dec.
Leptin (Lep), an adipose-derived hormone, exerts very important functions in the body mainly on energy storage and availability. The physiological effects of Lep controlling the body weight and suppressing appetite are mediated by the long form of Lep receptor in the hypothalamus. Lep receptor activates several downstream molecules involved in key pathways related to cell survival such as STAT3, PI3K, MAPK, AMPK, CDK5 and GSK3β. Collectively, these pathways act in a coordinated manner and form a network that is fully involved in Lep physiological response. Although the major interest in Lep is related to its role in the regulation of energy balance, and since resistance to Lep affects is the primary risk factor for obesity, the interest on their effects on brain cognition and neuroprotection is increasing. Thus, Lep and Lep mimetic compounds now await and deserve systematic exploration as the orchestrator of protective responses in the nervous system. Moreover, Lep might promote the activation of a cognitive process that may retard or even partially reverse selected aspects of Alzheimer's disease or ageing memory loss.
瘦素（Lep）是一种脂肪源性激素，主要在能量储存和供应方面发挥非常重要的作用。瘦素通过在下丘脑的长型瘦素受体来控制体重和抑制食欲的生理作用。瘦素受体激活了几个与细胞存活相关的关键途径中的下游分子，如 STAT3、PI3K、MAPK、AMPK、CDK5 和 GSK3β。总的来说，这些途径以协调的方式发挥作用，并形成一个网络，全面参与瘦素的生理反应。虽然人们对瘦素的主要兴趣与其在能量平衡调节中的作用有关，并且由于对瘦素的抵抗是肥胖的主要风险因素，因此人们对其在大脑认知和神经保护方面的作用的兴趣正在增加。因此，瘦素和瘦素模拟化合物现在正在等待并值得系统地探索，作为神经系统保护反应的协调者。此外，瘦素可能促进认知过程的激活，从而延缓甚至部分逆转阿尔茨海默病或衰老性记忆丧失的某些方面。
