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

that mitochondrial defects were present in diabetic, but not pre-diabetic glucose intolerant, mice. The mitochondrial disruptions were subsequently shown to be the result of the generation of reactive oxygen species (ROS), highly reactive molecules implicated in a number of cellular disruptions. Indeed, ROS production coincided with mitochondrial dysfunction, and antioxidant treatment blocked the mitochondrial alterations in muscle cells. The authors therefore concluded that treatment of diabetics with medications that either block ROS production or counteract their deleterious effects might improve the success of conventional therapies.

TITLE: Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice

AUTHOR CONTACT:
Jennifer Rieusset
INSERM U870, Facult de Mdecine Lyon Sud, Oullins, France.
Phone: 33-4-26-23-59-20; Fax: 33-4-26-23-59-16; E-mail: jennifer.rieusset@univ-lyon1.fr.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32601


NEPHROLOGY: Claudin 16 and claudin 19 synergize to select what escapes through the kidney

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a genetic disorder that can lead to kidney failure. It is characterized by calcium and magnesium loss by the kidneys, due to mutations in the genes CLN16 and CLN19, which encode the claudin family proteins claudin 16 and claudin 19, respectively. Claudins are important components of cellular tight junctions, areas where two cells meet and form a barrier that is almost impermeable to fluid. Loss of function in tight junctions is believed to be responsible for FHHNC, although the mechanisms underlying the specific roles of claudins 16 and 19 in the process have not been understood. A new study by Daniel Goodenoug
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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