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JCI online early table of contents: Jan. 10 2008
Date:1/10/2008

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In the study, activation of NOD2 by its ligand MDP was shown to protect mice from experimental colitis, a model of CD, by downregulating signaling through many different TLRs, not just TLR2. Further analysis showed that the effects of NOD2 required the downstream signaling molecule IRF4. The authors therefore suggested that MDP activation of NOD2 controls the innate immune response to commensal bacteria in the gut by negatively regulating signaling through multiple TLRs and that the absence of such regulation in individuals with CARD15 mutations leads to increased susceptibility to CD.

TITLE: Muramyl dipeptide activation of nucleotide-binding oligomerization domain 2 protects mice from experimental colitis

AUTHOR CONTACT:
Warren Strober
National Institutes of Health, Bethesda, Maryland, USA.
Phone: (301) 496-6810; Fax: (301) 402-2240; E-mail: wstrober@niaid.nih.gov.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33145


METABOLIC DISEASE: How antioxidant therapy may play a role in the treatment of type 2 diabetes

The incidence of type 2 diabetes in Western society is on the rise, due largely to an increasing prevalence of obesity. Dysfunction of skeletal muscle mitochondria, the powerhouses of a cell, is associated with type 2 diabetes; however, whether this association is causal or consequential has not been understood. A new study by Jennifer Rieusset and her colleagues at INSERM U870, France, has shed light on this question and has provided evidence that alterations in mitochondrial function are the result, and not the cause, of insulin resistance (which usually precedes full-blown clinical type 2 diabetes) in mice.

Mice fed a high-fat, high-sucrose diet (HFHSD) developed insulin resistance and type 2 diabetes. The authors found
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Contact: Karen Honey
press_releases@the-jci.org
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Journal of Clinical Investigation
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