scholarly journals Effect of canagliflozin or metformin on metabolic disorders in obese diabetic rats

2015 ◽  
Vol 9 (46) ◽  
pp. 1071-1079 ◽  
Author(s):  
S Marie Mohamed Assem ◽  
Mohamed Said Arafa Nadia ◽  
Abdullah Mubarak Alazimi Sara
2001 ◽  
Vol 120 (5) ◽  
pp. A674-A674 ◽  
Author(s):  
A FUNAKOSHI ◽  
M ICHIKAWA ◽  
Y SATO ◽  
S KANAI ◽  
M OHTA ◽  
...  

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Noriko Ichinoseki‐Sekine ◽  
Takamasa Tsuzuki ◽  
Matthew J. Hinkley ◽  
Toshinori Yoshihara ◽  
Hiroyuki Kobayashi ◽  
...  

2008 ◽  
Vol 294 (5) ◽  
pp. F1136-F1145 ◽  
Author(s):  
Katherine J. Kelly ◽  
Pengfei Wu ◽  
Carolyn E. Patterson ◽  
Constance Temm ◽  
Jesus H. Dominguez

The early nephropathy in obese, diabetic, dyslipidemic (ZS) rats is characterized by tubular lipid accumulation and pervasive inflammation, two critically interrelated events. We now tested the hypothesis that proximal tubules from ZS obese diabetic rats in vivo, and proximal tubule cells (NRK52E) exposed to oxidized LDL (oxLDL) in vitro, change their normally quiescent epithelial phenotype into a proinflammatory phenotype. Urine of obese diabetic rats contained more lipid peroxides, and LOX-1, a membrane receptor that internalizes oxidized lipids, was mobilized to luminal sites. Levels of ICAM-1 and focal adhesion kinase, which participate in leukocyte migration and epithelial dedifferentiation, respectively, were also upregulated in tubules. NRK52E cells exposed to oxLDL showed similar modifications, plus suppression of anti-inflammatory transcription factor peroxisome proliferator-activated receptor-δ. In addition, oxLDL impaired epithelial barrier function. These alterations were prevented by an anti-LOX-1 antibody. The data support the concept that tubular LOX-1 activation driven by lipid oxidants in the preurine fluid is critical in the inflammatory changes. We suggest that luminal lipid oxidants and abnormal tubular permeability may be partly responsible for the renal tubulointerstitial injury of obesity, diabetes, and dyslipidemia.


2019 ◽  
Vol 6 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Yuka Kohda ◽  
Junpei Ueda ◽  
Rie Azuma ◽  
Yuuka Nakatani ◽  
Hiroto Murase ◽  
...  

2012 ◽  
Vol 1444 ◽  
pp. 11-19 ◽  
Author(s):  
Wen-shan Lv ◽  
Jun-ping Wen ◽  
Li Li ◽  
Rui-xia Sun ◽  
Jing Wang ◽  
...  

2009 ◽  
Vol 297 (4) ◽  
pp. F923-F931 ◽  
Author(s):  
K. J. Kelly ◽  
James L. Burford ◽  
Jesus H. Dominguez

Diabetes is a major epidemic, and diabetic nephropathy is the most common cause of end-stage renal disease. Two critical components of diabetic nephropathy are persistent inflammation and chronic renal ischemia from widespread vasculopathy. Moreover, acute ischemic renal injury is common in diabetes, potentially causing chronic kidney disease or end-stage renal disease. Accordingly, we tested the hypothesis that acute renal ischemia accelerates nephropathy in diabetes by activating proinflammatory pathways. Lean and obese-diabetic ZS rats (F1 hybrids of spontaneously hypertensive heart failure and Zucker fatty diabetic rats) were subjected to bilateral renal ischemia or sham surgery before the onset of proteinuria. The postischemic state in rats with obesity-diabetes was characterized by progressive chronic renal failure, increased proteinuria, and renal expression of proinflammatory mediators. Leukocyte number in obese-diabetic rat kidney was markedly increased for months after ischemia. Intrarenal blood flow velocity was decreased after ischemia in lean control and obese-diabetic rats, although it recovered in lean rats. At 2 mo after ischemia, blood flow velocity decreased further in sham-surgery and postischemia obese-diabetic rats, so that RBC flow velocity was only 39% of control in the obese-diabetic rats after ischemia. In addition, microvascular density remained depressed at 2 mo in kidneys of obese-diabetic rats after ischemia. Abnormal microvascular permeability and increases in interstitial fibrosis and apoptotic renal cell death were also more pronounced after ischemia in obese-diabetic rats. These data support the hypothesis that acute renal ischemia in obesity-diabetes severely aggravates chronic inflammation and vasculopathy, creating a self-perpetuating postischemia inflammatory syndrome, which accelerates renal failure.


Author(s):  
Maryem Ben Salem ◽  
Rihab Ben Abdallah Kolsi ◽  
Raouia Dhouibi ◽  
Kamilia Ksouda ◽  
Slim Charfi ◽  
...  

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