TITLE: Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells
AUTHOR CONTACT:
Dennis D. Taub
National Institute on Aging, Baltimore, Maryland, USA.
Phone: 410-558-8181; Fax: 410-558-8284; Email: TaubD@prc.nia.nih.gov

View the PDF of this article at: https://www.the-jci.org/press/21134.pdf

PPAR for the Course

Diabetes is often promoted in obesity by higher concentrations of free fatty acids in the blood. Understanding how this process works currently remains very limited. Free fatty acids are generated when glycerol is broken down in the liver or in fat tissue. One gene family thought to be involved in this increasing free fatty acids is the PPAR gene family. Sander Kersten and colleagues, from Wageningen University, now begin to build our understanding of this process with a series of studies on PPAR in mice. The authors utilized array technology and as well as other mechanisms to block PPAR gene family action. In doing so, they were able to dissect specific roles for different members of the PPAR gene family in different tissues. Specifically, their data here show a direct role for PPAR_lpha in the metabolism of glycerol metabolism in the liver, while another member of the PPAR gene family, PPAR_amma_ controls glycerol metabolism in adipose tissue. These data will aid in understanding the complex interactions of genes, small molecules, and proteins that are involved in mechanisms underlying diseases such as diabetes.

TITLE: PPARalpha governs glycerol metabolism
AUTHOR CONTACT:
Sander Kersten Wageningen University, Wageningen, The Netherlands.
Phone: 31-317-48-57-87; Fax: 31-317-48-
'"/>

Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
1-Jul-2004