FP488EFFECT OF CONVERSION FROM TACROLIMUS TO CTLA4IG IN EXPERIMENTAL MODEL OF DIABETES MELLITUS

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Kang Luo ◽  
Lim Sun Woo ◽  
Y I QUAN ◽  
Sheng Cui ◽  
Jin Shin Yoo ◽  
...  
1993 ◽  
Vol 264 (1) ◽  
pp. F100-F105 ◽  
Author(s):  
P. Churchill ◽  
M. Churchill ◽  
A. Bidani ◽  
J. Dunbar

Streptozotocin (STZ)-induced diabetes mellitus is associated with decreased renal clearances of inulin and p-aminohippurate (PAH). The present experiments were designed to determine whether STZ-induced renal hemodynamic changes are due to the drug per se, rather than to the diabetic state that it induces. Isogenic Lewis rats with native right and transplanted left kidneys were studied. In one group, kidney donors received 50 mg STZ/kg body wt on day 1 and transplantation was performed on day 4 (untreated recipients). On day 29, the inulin and PAH clearances of these nondiabetic recipients were, respectively, 0.94 +/- 0.04 and 2.58 +/- 0.11 ml.min-1 x g-1 for the transplanted left kidney (previously exposed to STZ) and 0.95 +/- 0.07 and 2.54 +/- 0.14 ml.min-1 x g-1 for the native right kidney (never exposed to STZ). In another group, recipients received STZ on day 1 and transplantation was performed on day 4 (untreated donors). On day 29, the inulin and PAH clearances of these diabetic recipients were, respectively, 0.62 +/- 0.04 and 1.46 +/- 0.11 ml.min-1 x g-1 for the transplanted left kidney (never exposed to STZ) and 0.61 +/- 0.05 and 1.42 +/- 0.08 ml.min-1 x g-1 for the native right kidney (previously exposed to STZ). We conclude that the diabetic state, rather than STZ, is responsible for the decreased renal clearances of inulin and PAH in this experimental model.


2003 ◽  
Vol 18 (spe) ◽  
pp. 60-64 ◽  
Author(s):  
Eliziane Nitz de Carvalho ◽  
Nestor Antônio Schmidt de Carvalho ◽  
Lydia Masako Ferreira

Diabetes mellitus is a potentially morbid condition with high prevalence worldwide, thus being a major medical concern. Experimental models play an important role in understanding such a disease, which is treatable only. This study describes a rat diabetes mellitus model induced by administering a reduced dose of alloxan, thus greatly reducing the animals’ death rate.


Bone ◽  
2011 ◽  
Vol 48 (6) ◽  
pp. S286
Author(s):  
V.A. Rodríguez ◽  
M.E. Peralta López ◽  
M.A. Rivoira ◽  
N.G. Tolosa de Talamoni

Author(s):  
Surboyo Meircurius Dwi Condro ◽  
Ernawati Diah Savitri ◽  
Radithia Desiana ◽  
Soebadi Bagus ◽  
Mahdani Fatma Yasmin ◽  
...  

Author(s):  
Jose A Gonzalez-Correa ◽  
Maria Dolores Rodriguez-Perez ◽  
Beatriz Villanueva-Torres ◽  
Juan A Lopez-Villodres ◽  
Leticia Vallejo-Carmona ◽  
...  

2009 ◽  
Vol 102 (9) ◽  
pp. 1246-1253 ◽  
Author(s):  
Amaya Aleixandre de Artiñano ◽  
Marta Miguel Castro

Being the metabolic syndrome a multifactorial condition, it is difficult to find adequate experimental models to study this pathology. The obese Zucker rats, which are homozygous for the fa allele, present abnormalities similar to those seen in human metabolic syndrome and are a widely extended model of insulin resistance. The usefulness of these rats as a model of non-insulin-dependent diabetes mellitus is nevertheless questionable, and they neither can be considered a clear experimental model of hypertension. Some experimental models different from the obese Zucker rats have also been used to study the metabolic syndrome. Some derive from the spontaneously hypertensive rats (SHR). In this context, the most important are the obese SHR, usually named Koletsky rats. Hyperinsulinism, associated with either normal or slightly elevated levels of blood glucose, is present in these animals, but SHR/N-corpulent rats are a more appropriated model of non-insulin-dependent diabetes mellitus. The SHR/NDmc corpulent rats, a subline of SHR/N-corpulent rats, also exhibit metabolic and histopathologic characteristics associated with human metabolic disorders. A new animal model of the metabolic syndrome, stroke-prone–SHR (SHRSP) fatty rats, was obtained by introducing a segment of the mutant leptin receptor gene from the Zucker line heterozygous for the fa gene mutation into the genetic background of the SHRSP. Very recently, it has been developed as a non-obese rat model with hypertension, fatty liver and characteristics of the metabolic syndrome by transgenic overexpression of a sterol-regulatory element-binding protein in the SHR rats. The Wistar Ottawa Karlsburg W rats are also a new strain that develops a nearly complete metabolic syndrome. Moreover, a new experimental model of low-capacity runner rats has also been developed with elevated blood pressure levels together with the other hallmarks of the metabolic syndrome.


2000 ◽  
Vol 18 ◽  
pp. S144
Author(s):  
R. García-Robles ◽  
F. Villalba-Díaz ◽  
O. González-Albarrán ◽  
S. Calvo ◽  
O. Gómez ◽  
...  

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