Liraglutide Improves the Kidney Function in a Murine Model of Chronic Kidney Disease
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Liraglutide Improves the Kidney Function in a Murine Model of Chronic Kidney Disease. / Ougaard, Maria E.; Sembach, Frederikke E.; Jensen, Henrik E.; Pyke, Charles; Knudsen, Lotte B.; Kvist, Peter H.
I: Nephron, Bind 144, 2020, s. 595–606.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Liraglutide Improves the Kidney Function in a Murine Model of Chronic Kidney Disease
AU - Ougaard, Maria E.
AU - Sembach, Frederikke E.
AU - Jensen, Henrik E.
AU - Pyke, Charles
AU - Knudsen, Lotte B.
AU - Kvist, Peter H.
PY - 2020
Y1 - 2020
N2 - Background: Chronic kidney disease (CKD) is a global health burden, and the current treatment options only slow down the disease progression. GLP-1 receptor agonists (GLP-1 RA) have shown a renal protective effect in models of CKD; however, the mechanism behind the beneficial effect is not understood. In this study, we investigate the effect of the GLP-1 RA liraglutide in the nephrotoxic serum nephritis (NTN) CKD model. Moreover, we compare the gene expression pattern of liraglutide-Treated mice to the gene expression pattern of mice treated with the angiotensin converting enzyme inhibitor, enalapril. Methods: The effect of liraglutide was tested in the NTN model by evaluating the glomerular filtration rate (GFR), albuminuria, mesangial expansion, renal fibrosis, and renal inflammation. Furthermore, the regulation of selected genes involved in CKD and in glomerular, cortical tubulointerstitial, and whole kidney structures was analyzed using a gene expression array on samples following laser capture microdissection. Results: Treatment with liraglutide improved CKD hallmarks including GFR, albuminuria, mesangial expansion, renal inflammation, and renal fibrosis. The gene expression revealed that both liraglutide and enalapril reversed the regulation of several fibrosis and inflammation associated genes, which are also regulated in human CKD patients. Furthermore, liraglutide and enalapril both regulated genes in the kidney involved in blood pressure control. Conclusions: Treatment with liraglutide improved the kidney function and diminished renal lesions in NTN-induced mice. Both liraglutide and enalapril reversed the regulation of genes involved in CKD and regulated genes involved in blood pressure control.
AB - Background: Chronic kidney disease (CKD) is a global health burden, and the current treatment options only slow down the disease progression. GLP-1 receptor agonists (GLP-1 RA) have shown a renal protective effect in models of CKD; however, the mechanism behind the beneficial effect is not understood. In this study, we investigate the effect of the GLP-1 RA liraglutide in the nephrotoxic serum nephritis (NTN) CKD model. Moreover, we compare the gene expression pattern of liraglutide-Treated mice to the gene expression pattern of mice treated with the angiotensin converting enzyme inhibitor, enalapril. Methods: The effect of liraglutide was tested in the NTN model by evaluating the glomerular filtration rate (GFR), albuminuria, mesangial expansion, renal fibrosis, and renal inflammation. Furthermore, the regulation of selected genes involved in CKD and in glomerular, cortical tubulointerstitial, and whole kidney structures was analyzed using a gene expression array on samples following laser capture microdissection. Results: Treatment with liraglutide improved CKD hallmarks including GFR, albuminuria, mesangial expansion, renal inflammation, and renal fibrosis. The gene expression revealed that both liraglutide and enalapril reversed the regulation of several fibrosis and inflammation associated genes, which are also regulated in human CKD patients. Furthermore, liraglutide and enalapril both regulated genes in the kidney involved in blood pressure control. Conclusions: Treatment with liraglutide improved the kidney function and diminished renal lesions in NTN-induced mice. Both liraglutide and enalapril reversed the regulation of genes involved in CKD and regulated genes involved in blood pressure control.
U2 - 10.1159/000509418
DO - 10.1159/000509418
M3 - Journal article
C2 - 32877912
AN - SCOPUS:85091034012
VL - 144
SP - 595
EP - 606
JO - Nephron - Clinical Practice
JF - Nephron - Clinical Practice
SN - 1660-8151
ER -
ID: 249063905