JCI Table of Contents, 15 A...( ter in Durham North Carolina show tha...)

ter in Durham, North Carolina, show that allergen-sensitized mice with a targeted deletion of the gene encoding beta-arrestin-2 (a G proteincoupled receptor regulator) do not accumulate lymphocytes in their airways, nor do they demonstrate other physiological and inflammatory features characteristic of asthma. Because beta-arrestin-2 regulates the development of allergic inflammation at a proximal step in the inflammatory cascade, targeting this protein may become a treatment for asthma.

TITLE: Beta-arrestin-2 regulates the development of allergic asthma

AUTHOR CONTACT:
Robert J. Lefkowitz
Duke University Medical Center, Durham, North Carolina, USA.
Phone: (919) 684-2974
Fax: (919)-684-8875
Email: lefko001@receptor-biol.duke.edu

View the PDF of this article at: https://www.the-jci.org/press/17265.pdf

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Muscling in on the specificity of anti-diabetic agents

Thiazolidinediones (TZDs) are pharmacologic agents that improve glucose balance by increasing insulin sensitivity in skeletal muscle in type 2 diabetes. The antidiabetic actions of TZDs are believed to be mediated by their interactions with the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-gamma). As PPAR-gamma is expressed primarily in fat cells, with lower levels in skeletal muscle, it has remained debatable whether the effect of TZDs on muscle is direct or indirect. Using muscle-specific PPAR-gamma--knockout mice, C. Ronald Kahn and colleagues at the Joslin Diabetes Center in Boston, Massachusetts, demonstrated that muscle PPAR-gamma is not required for a whole-animal response to TZDs. Disruption of PPAR-gamma led to increased fat mass and insulin resistance, however it did not block the beneficial effects of TZDs. The data indicate that the effects of TZDs on muscle are indirect, but tha
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
15-Aug-2003

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