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2017 ; 8
(33
): 54821-54837
Nephropedia Template TP
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DPP-4 enzyme deficiency protects kidney from acute ischemia-reperfusion injury:
role for remote intermittent bowel ischemia-reperfusion preconditioning
#MMPMID28903385
Chen YT
; Wallace CG
; Yang CC
; Chen CH
; Chen KH
; Sung PH
; Chen YL
; Chai HT
; Chung SY
; Chua S
; Lee FY
; Ko SF
; Lee MS
; Yip HK
Oncotarget
2017[Aug]; 8
(33
): 54821-54837
PMID28903385
show ga
We analyzed the effects of acute ischemia-reperfusion (KIR) injury on the status
of kidney function and architecture in dipeptidyl peptidase4-difficient (DPP4(D))
rats and the effect of remote small bowel ischemia-reperfusion (BIR)
preconditioning. DPP4-deficient (DPP4(D)) and normal Fischer344 (F344) rats were
divided into 6 groups: (1) sham-F344, (2) sham-DPP4(D), (3) KIR-F344 (4)
KIR-DPP4(D), (5) DPP4(D)-KIR-extendin-9-39 and (6) BIR-KIR-F344. Blood creatinine
and urea nitrogen levels and the urinary protein-to-creatinine ratio was higher
in KIR-F344 rats than BIR-KIR-F344 or KIR-DPP4(D) rats 72 h after acute KIR.
Conversely, the circulating glucagon-like peptide 1 (GLP-1) levels were higher in
BIR-KIR-F344 and KIR-DPP4(D) than KIR-F344 rats after acute KIR. KIR-F344 rats
showed greater inflammation, oxidative stress, apoptosis, DNA damage and kidney
injury than other rat groups. Damage to the kidney architecture in KIR-F344 rats
was greater than in BIR-KIR-F344 or KIR-DPP4(D) rats. Expression of antioxidant
proteins and GLP-1 receptor was higher in kidneys from KIR-DPP4(D) and
BIR-KIR-F344 than KIR-F344 rats, which suggests better intrinsic responses. We
therefore suggest that elevated circulating GLP-1 levels due to DPP4 deficiency
and BIR preconditioning protect kidney function and architecture during acute IR
injury.