rm of thyrotopin-releasing hormone into its active form. In cell culture of neuronal cells from the hippocampus (the area of the brain where leptin acts), leptin treatment led to a significant increase in the expression of these two enzymes at both the genetic and protein level. Rats that were starved, and thus had low levels of leptin in their blood serum levels also had lower levels of these two enzymes. Consistent with the lower levels of the enzymes, these fasted rats likewise did not have a significant amount of the active (cleaved form) of thyrotopin-releasing hormone. Giving leptin directly to these rats, increased enzyme levels and, inevitably, the amount of active thyrotopin-releasing hormone. These data provide evidence for an additional key regulatory point in the control of energy balance through leptin and may suggest novel therapeutic strategies for treatment of obesity and thyroid axisrelated diseases.
TITLE: Regulation of hypothalamic prohormone convertases 1 and 2 and effects on processing of prothyrotropin-releasing hormone
AUTHOR CONTACT:
Eduardo A. Nillni Brown Medical School/Rhode Island Hospital, 55 Claverick St. Providence, RI 02903, USA.
Phone: 401-444-5733; Fax: 401-444-6964; E-mail: Eduardo_Nillni@Brown.edu
View the PDF of this article at: https://www.the-jci.org/press/21620.pdf
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Wasting Away in Muscle-ville
Loss of skeletal muscle tissue, termed cachexia, occurs in over half of cancer patients and, rather than tumor burden, is the direct cause of nearly one-third of cancer deaths. There are several regulatory proteins that are released from immune cells are known to be involved in the development of cachexia. These proteins are called cytokines and include TNF-alpha and IFN-gamma. The pr
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Contact: Laurie Goodman
press_releases@the-jci.org
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Journal of Clinical Investigation
2-Aug-2004
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