The distribution and appearance of anionic charge sides (ACS) in the glomer
ular basement membrane (GBM) and mesangium were studied in two different an
imal models of diabetes mellitus (DM), the obese Zucker rat as an animal mo
del of type 2 diabetes mellitus (DM) and streptozocin-induced Sprague-Dawle
y rat as tin animal model of type 1 DM.
Four obese Zucker rats (ZR) and four Sprague-Dawley rats were analyzed for
the following parameters: number of ACS per length of lamina rare externa (
LRE), (ACS/LRE); number of ACE per length of lamina rara interna (LRI) (ACS
/LRI); percent of mesangial matrix as ACS (%MMACS); percent of LRE as ACS (
%LREACS); percent of LRI as ACS (%LRIACS); length of ACS in LRI (LACSLRI);
length of ACS in LRE (LACSLRE); width of ACS in LRI (WACSLRI); width of ACS
in the LRE (WACSLRE); area of ACS in the LRI (AACSLRI); and the area of AC
S in the LRE (AACSLRE).
Statistical analyses include a one-way analysis of variance (ANOVA), Pearso
n's correlation coefficient, and stepwise multiple regression.
This study confirms that a loss of ACS occurs as proteinuria develops in a
variety of animal models. The majority of the ACS were more prominently loc
alized, and thus lost form the LRE of the GBM in DN. This study also demons
trated that defined alterations in the glomerular ACS can be identified ear
ly in the evolution of DN in both animal models, and that the similarity of
the changes in the ACS suggest that a common pathophysiologic mechanism in
duced the changes in both animal models.