JCI table of contents: April 22, 2008

AUTHOR CONTACT:
Matthias Ernst
Ludwig Institute for Cancer Research, Royal Melbourne Hospital, Melbourne, Victoria, Australia.
Phone: 61-3-9341-3155; Fax: 61-3-9341-3104; E-mail: .

Brendan J. Jenkins
Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
Phone: 61-3-9594-7218; Fax: 61-3-9594-7211; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=34944

ACCOMPANYING COMMENTARY
TITLE: What lurks beneath: IL-11, via Stat3, promotes inflammation-associated gastric tumorigenesis

AUTHOR CONTACT:
Juanita L. Merchant
University of Michigan, Ann Arbor, Michigan, USA.
Phone: (734) 647-2944; Fax: (734) 763-4686; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=35344

NEPHROLOGY: Connecting the dots between obesity and kidney disease

Individuals who are obese have a greater risk of developing kidney disease than those who are not obese. New data, generated by a team of researchers at the University of California at San Diego, La Jolla, and Jefferson Medical College, Philadelphia, have outlined a mechanism by which obesity can cause a clinical condition that is an indicator of kidney damage — albuminuria (the presence of the protein albumin in the urine). As noted by the authors and discussed in detail by Rexford Ahima, from the University of Pennsylvania School of Medicine, Philadelphia, in an accompanying commentary, the results have important implications for the diagnosis, prevention, and treatment of kidney disease.

Adiponectin is a soluble factor secreted by fat tissue, but the amount of adiponectin secreted decreases as an individual becomes more obese. In the study, it was shown that in a group of obese individuals at high risk of developing kidney disease levels of adiponectin in the bloodstream correlated inversely with albuminuria. Consistent with this data, mice lacking adiponectin exhibited increased albuminuria when compared with normal mice. In vitro studies indicated that adiponectin affected kidney cells known as podocytes, causing layers of these cells to become more permeable to albumin. Treating podocyte layers and mice lacking adiponectin with adiponectin reduced permeability to albumin and albuminuria, respectively. Further studies revealed that the effects of adiponectin on podocytes were mediated by AMPK activation and a subsequent reduction in Nox4 levels. The authors therefore suggested that targeting the adiponectin-AMPK-Nox4 pathway might protect against albuminuria and thereby early kidney disease.

TITLE: Adiponectin regulates albuminuria and podocyte function in mice

AUTHOR CONTACT:
Kumar Sharma
University of California at San Diego, La Jolla, California, USA.
Phone: (858) 822-0860; Fax: (858) 822-7483; E-mail: .