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Adipokines as a link between obesity and chronic kidney disease

Journal

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Volume 305, Issue 12, Pages F1629-F1636

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00263.2013

Keywords

adipokines; obesity; chronic kidney disease; leptin; adiponectin

Funding

  1. Australian Postgraduate Award scholarship
  2. Helen McPherson Smith Trust Grant [6662]
  3. Australian Government's Collaborative Research Networks program

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Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.

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