Open AccessObesity‐associated glomerular inflammation increases albuminuria without renal histological changes
Author(s) -
Mima Akira,
Yasuzawa Toshinori,
King George L.,
Ueshima Shigeru
Publication year - 2018
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12400
Subject(s) - albuminuria , medicine , endocrinology , inflammation , oxidative stress , kidney disease , obesity , pathological , immunohistochemistry
Obesity is one of risk factors for chronic kidney disease ( CKD ), but the precise mechanism involved is unclear. This study characterizes the effect of obesity‐induced glomerular inflammation, oxidative stress, and albuminuria in obese rats. Glomerular samples were collected from fatty ( ZF ) and lean ( ZL ) Zucker rats. After 2 months of feeding, body weight and albuminuria were significantly increased in ZF rats when compared to ZL rats. Expression of the inflammatory markers TNF ‐α and CCR 2 was significantly increased in the glomeruli of ZF rats. However, expression of IL ‐6 mRNA was not increased. Analysis of renal pathology showed no glomerular expansion. As inflammatory and oxidative stress markers are associated with NF ‐κB, we evaluated whether NF ‐κB activation was increased in the glomeruli of mice on a high‐fat diet. Immunohistochemistry showed increased NF ‐κB activation in the glomeruli when transgenic mice overexpressing an NF ‐κB‐dependent enhanced green fluorescent protein were fed with a high‐fat diet. These results suggest that obesity of only 2 months duration can cause albuminuria, due to increased inflammation or oxidative stress, but may not be long enough to develop renal pathological changes.