@article{oai:hirosaki.repo.nii.ac.jp:00003641,
 author = {Sakihara, Satoru and Kageyama, Kazunori and Nigawara, Takeshi and Hanada, Komaki and Suda, Toshihiro},
 issue = {Supplement},
 journal = {弘前医学},
 month = {Nov},
 note = {application/pdf, Corticotropin-releasing factor （CRF） is primary regulator of hypothalamus-pituitary-adrenal（ HPA） axis,which is activated by various types of stress. Starvation is also a potent activating factor of CRF. Because theperipheral energy store refl ects on plasma levels of leptin, secreted from adipose tissue, it is presumed that leptin maybe involved in the CRF activity during starvation. Indeed, the attenuation of CRF or HPA axis activity by leptintreatment has been demonstrated in several reports. While many studies indicate the leptins involvement in CRFactivity, its precise regulation has not been elucidated. The aim of this study is to determine the impact of leptin onthe hypothalamic CRF neuron. To exclude the other hypothalamic factors, associated with leptins central eff ect, weemployed the in vitro study using immortalized CRF expressing neuron（ IVB cell）. Since the mRNA expression of longformleptin receptor was detected clearly in IVB cell with RT-PCR, we next investigated the impact of leptin on this cell.IVB cell was treated with leptin in diff erent concentrations and periods, then, the mRNA expression and the promoteractivity of CRF were analyzed with real-time PCR and luciferase assay, respectively. In result, leptin suppressed CRFpromoter activity with dose- and time- dependent manner in IVB cell. This indicates that leptin can suppress the CRFtranscription directly in hypothalamus. Our result might explain the mechanism partially how leptin attenuate theactivation of CRF or HPA axis induced by stress or starvation., 弘前医学. 59(Suppl.), 2007, p.S193-S198},
 pages = {S193--S198},
 title = {Leptin can suppress the transcription of corticotropin-releasing factor in the immortalized hypothalamic neuron},
 volume = {59},
 year = {2007}
}