In an associated commentary, William Mitch writes that "the development of molecules capable of preventing these regulatory abnormalities holds the promise of eliminating the contribution of anorexia to the development of cachexia."

TITLE: Role of leptin and melanocortin signaling in uremia-associated cachexia

AUTHOR CONTACT:
Robert Mak
Oregon Health & Science University, Portland, OR USA
Phone: 503-494-7564; Fax: 503-494-0428; E-mail: makr@ohsu.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=22521

ACCOMPANYING COMMENTARY:

TITLE: Cachexia in chronic kidney disease: a link to defective central nervous system control of appetite

AUTHOR CONTACT:
William E. Mitch
University of Texas, Galveston, TX USA
Phone: 409-772-9891; Fax: 409-772-8762; E-mail: wmitch@utmb.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=25255

PHYSIOLOGY

Drawing blood from red cell disorders

Erythropoietic protoporphyria (EPP) and beta-thalassemia are two types of inherited red blood cell disorders. In a new study appearing in the June 1 print issue of The Journal of Clinical Investigation, Jane-Jane Chen and colleagues from MIT demonstrate a protective role of a protein called HRI, which had never previously been shown to play a role in any known human disease, in these red cell disorders. In both diseases, HRI deficiency worsens EPP and beta-thalassemia, while HRI itself decreases disease severity in mice, by reducing the amount of a protein called alpha globin, which has toxic effects.

In an accom
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Contact: Stacie Bloom
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
1-Jun-2005