Nara-ashizawa N, Tsukada T, Maruyama K, Akiyama Y, Kajimura N, Nagasaki K, Iwanaga T, Yamaguchi K
Growth Factor Division, National Cancer Center Research Institute, Tokyo, Japan.
Metabolism. 2001 Oct;50(10):1213-9. doi: 10.1053/meta.2001.26706.
We previously reported that the human melanoma cell line, SEKI, induces severe weight loss in nude mice. In the present study, we examined the expression of weight-regulating neuropeptide mRNAs in the hypothalamus of this cancer cachectic model by using a sensitive quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method and in situ hybridization. mRNA levels of neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) in the whole hypothalamus were elevated significantly in the SEKI mice as compared with control mice. In situ hybridization showed that NPY and CRH mRNA were upregulated in the arcuate nucleus and the paraventricular nucleus, respectively. There were no significant differences in melanin-concentrating hormone (MCH), orexin (OX), and cholecystokinin mRNA levels between the SEKI and control mice. These results suggest that the NPYergic system is functioning in the rodent model of cancer cachexia; however, the role of the CRHergic system in energy homeostasis remains to be elucidated. This is the first report of the hypothalamic neuropeptide response to cachexia-inducing human cells.
我们之前报道过，人类黑色素瘤细胞系SEKI可导致裸鼠严重体重减轻。在本研究中，我们通过使用灵敏的定量逆转录聚合酶链反应（RT-PCR）方法和原位杂交技术，检测了该癌症恶病质模型下丘脑内体重调节神经肽mRNA的表达。与对照小鼠相比，SEKI小鼠整个下丘脑内神经肽Y（NPY）和促肾上腺皮质激素释放激素（CRH）的mRNA水平显著升高。原位杂交显示，NPY和CRH mRNA分别在弓状核和室旁核中上调。SEKI小鼠和对照小鼠之间，促黑素细胞激素（MCH）、食欲素（OX）和胆囊收缩素的mRNA水平没有显著差异。这些结果表明，NPY能系统在癌症恶病质的啮齿动物模型中发挥作用；然而，CRH能系统在能量稳态中的作用仍有待阐明。这是关于下丘脑神经肽对诱导恶病质的人类细胞反应的首次报道。
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