Balthasar Nina, Coppari Roberto, McMinn Julie, Liu Shun M, Lee Charlotte E, Tang Vinsee, Kenny Christopher D, McGovern Robert A, Chua Streamson C, Elmquist Joel K, Lowell Bradford B
Department of Medicine, Division of Endocrinology, Beth Israel Deaconess Medical Center, Harvard Medical School, 99 Brookline Avenue RN, Boston, MA 02215, USA.
Neuron. 2004 Jun 24;42(6):983-91. doi: 10.1016/j.neuron.2004.06.004.
Neuroanatomical and electrophysiological studies have shown that hypothalamic POMC neurons are targets of the adipostatic hormone leptin. However, the physiological relevance of leptin signaling in these neurons has not yet been directly tested. Here, using the Cre/loxP system, we critically test the functional importance of leptin action on POMC neurons by deleting leptin receptors specifically from these cells in mice. Mice lacking leptin signaling in POMC neurons are mildly obese, hyperleptinemic, and have altered expression of hypothalamic neuropeptides. In summary, leptin receptors on POMC neurons are required but not solely responsible for leptin's regulation of body weight homeostasis.
神经解剖学和电生理学研究表明,下丘脑促黑素细胞激素(POMC)神经元是脂肪稳态激素瘦素的作用靶点。然而,瘦素信号在这些神经元中的生理相关性尚未得到直接验证。在此,我们利用Cre/loxP系统,通过特异性敲除小鼠POMC神经元中的瘦素受体,严格检验了瘦素对POMC神经元作用的功能重要性。POMC神经元中缺乏瘦素信号的小鼠轻度肥胖、高瘦素血症,且下丘脑神经肽表达发生改变。总之,POMC神经元上的瘦素受体是瘦素调节体重稳态所必需的,但并非唯一原因。