Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Standard

Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice. / Bisgaard, Line S; Bosteen, Markus H; Fink, Lisbeth N; Sørensen, Charlotte M; Rosendahl, Alexander; Mogensen, Christina K; Rasmussen, Salka E; Rolin, Bidda; Nielsen, Lars Bo; Pedersen, Tanja X.

I: PLOS ONE, Bind 11, Nr. 12, e0168396, 2016.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Bisgaard, LS, Bosteen, MH, Fink, LN, Sørensen, CM, Rosendahl, A, Mogensen, CK, Rasmussen, SE, Rolin, B, Nielsen, LB & Pedersen, TX 2016, 'Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice', PLOS ONE, bind 11, nr. 12, e0168396. https://doi.org/10.1371/journal.pone.0168396

APA

Bisgaard, L. S., Bosteen, M. H., Fink, L. N., Sørensen, C. M., Rosendahl, A., Mogensen, C. K., Rasmussen, S. E., Rolin, B., Nielsen, L. B., & Pedersen, T. X. (2016). Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice. PLOS ONE, 11(12), [e0168396]. https://doi.org/10.1371/journal.pone.0168396

Vancouver

Bisgaard LS, Bosteen MH, Fink LN, Sørensen CM, Rosendahl A, Mogensen CK o.a. Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice. PLOS ONE. 2016;11(12). e0168396. https://doi.org/10.1371/journal.pone.0168396

Author

Bisgaard, Line S ; Bosteen, Markus H ; Fink, Lisbeth N ; Sørensen, Charlotte M ; Rosendahl, Alexander ; Mogensen, Christina K ; Rasmussen, Salka E ; Rolin, Bidda ; Nielsen, Lars Bo ; Pedersen, Tanja X. / Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice. I: PLOS ONE. 2016 ; Bind 11, Nr. 12.

Bibtex

@article{7f271cc3f74c4a62b0c696e5fdafea6c,
title = "Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice",
abstract = "Chronic kidney disease (CKD) leads to uremia. CKD is characterized by a gradual increase in kidney fibrosis and loss of kidney function, which is associated with a progressive increase in risk of atherosclerosis and cardiovascular death. To prevent progression of both kidney fibrosis and atherosclerosis in uremic settings, insight into new treatment options with effects on both parameters is warranted. The GLP-1 analogue liraglutide improves glucose homeostasis, and is approved for treatment of type 2 diabetes. Animal studies suggest that GLP-1 also dampens inflammation and atherosclerosis. Our aim was to examine effects of liraglutide on kidney fibrosis and atherosclerosis in a mouse model of moderate uremia (5/6 nephrectomy (NX)). Uremic (n = 29) and sham-operated (n = 14) atherosclerosis-prone low density lipoprotein receptor knockout mice were treated with liraglutide (1000 μg/kg, s.c. once daily) or vehicle for 13 weeks. As expected, uremia increased aortic atherosclerosis. In the remnant kidneys from NX mice, flow cytometry revealed an increase in the number of monocyte-like cells (CD68+F4/80-), CD4+, and CD8+ T-cells, suggesting that moderate uremia induced kidney inflammation. Furthermore, markers of fibrosis (i.e. Col1a1 and Col3a1) were upregulated, and histological examinations showed increased glomerular diameter in NX mice. Importantly, liraglutide treatment attenuated atherosclerosis (~40%, p < 0.05) and reduced kidney inflammation in NX mice. There was no effect of liraglutide on expression of fibrosis markers and/or kidney histology. This study suggests that liraglutide has beneficial effects in a mouse model of moderate uremia by reducing atherosclerosis and attenuating kidney inflammation.",
author = "Bisgaard, {Line S} and Bosteen, {Markus H} and Fink, {Lisbeth N} and S{\o}rensen, {Charlotte M} and Alexander Rosendahl and Mogensen, {Christina K} and Rasmussen, {Salka E} and Bidda Rolin and Nielsen, {Lars Bo} and Pedersen, {Tanja X}",
year = "2016",
doi = "10.1371/journal.pone.0168396",
language = "English",
volume = "11",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "12",

}

RIS

TY - JOUR

T1 - Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice

AU - Bisgaard, Line S

AU - Bosteen, Markus H

AU - Fink, Lisbeth N

AU - Sørensen, Charlotte M

AU - Rosendahl, Alexander

AU - Mogensen, Christina K

AU - Rasmussen, Salka E

AU - Rolin, Bidda

AU - Nielsen, Lars Bo

AU - Pedersen, Tanja X

PY - 2016

Y1 - 2016

N2 - Chronic kidney disease (CKD) leads to uremia. CKD is characterized by a gradual increase in kidney fibrosis and loss of kidney function, which is associated with a progressive increase in risk of atherosclerosis and cardiovascular death. To prevent progression of both kidney fibrosis and atherosclerosis in uremic settings, insight into new treatment options with effects on both parameters is warranted. The GLP-1 analogue liraglutide improves glucose homeostasis, and is approved for treatment of type 2 diabetes. Animal studies suggest that GLP-1 also dampens inflammation and atherosclerosis. Our aim was to examine effects of liraglutide on kidney fibrosis and atherosclerosis in a mouse model of moderate uremia (5/6 nephrectomy (NX)). Uremic (n = 29) and sham-operated (n = 14) atherosclerosis-prone low density lipoprotein receptor knockout mice were treated with liraglutide (1000 μg/kg, s.c. once daily) or vehicle for 13 weeks. As expected, uremia increased aortic atherosclerosis. In the remnant kidneys from NX mice, flow cytometry revealed an increase in the number of monocyte-like cells (CD68+F4/80-), CD4+, and CD8+ T-cells, suggesting that moderate uremia induced kidney inflammation. Furthermore, markers of fibrosis (i.e. Col1a1 and Col3a1) were upregulated, and histological examinations showed increased glomerular diameter in NX mice. Importantly, liraglutide treatment attenuated atherosclerosis (~40%, p < 0.05) and reduced kidney inflammation in NX mice. There was no effect of liraglutide on expression of fibrosis markers and/or kidney histology. This study suggests that liraglutide has beneficial effects in a mouse model of moderate uremia by reducing atherosclerosis and attenuating kidney inflammation.

AB - Chronic kidney disease (CKD) leads to uremia. CKD is characterized by a gradual increase in kidney fibrosis and loss of kidney function, which is associated with a progressive increase in risk of atherosclerosis and cardiovascular death. To prevent progression of both kidney fibrosis and atherosclerosis in uremic settings, insight into new treatment options with effects on both parameters is warranted. The GLP-1 analogue liraglutide improves glucose homeostasis, and is approved for treatment of type 2 diabetes. Animal studies suggest that GLP-1 also dampens inflammation and atherosclerosis. Our aim was to examine effects of liraglutide on kidney fibrosis and atherosclerosis in a mouse model of moderate uremia (5/6 nephrectomy (NX)). Uremic (n = 29) and sham-operated (n = 14) atherosclerosis-prone low density lipoprotein receptor knockout mice were treated with liraglutide (1000 μg/kg, s.c. once daily) or vehicle for 13 weeks. As expected, uremia increased aortic atherosclerosis. In the remnant kidneys from NX mice, flow cytometry revealed an increase in the number of monocyte-like cells (CD68+F4/80-), CD4+, and CD8+ T-cells, suggesting that moderate uremia induced kidney inflammation. Furthermore, markers of fibrosis (i.e. Col1a1 and Col3a1) were upregulated, and histological examinations showed increased glomerular diameter in NX mice. Importantly, liraglutide treatment attenuated atherosclerosis (~40%, p < 0.05) and reduced kidney inflammation in NX mice. There was no effect of liraglutide on expression of fibrosis markers and/or kidney histology. This study suggests that liraglutide has beneficial effects in a mouse model of moderate uremia by reducing atherosclerosis and attenuating kidney inflammation.

U2 - 10.1371/journal.pone.0168396

DO - 10.1371/journal.pone.0168396

M3 - Journal article

C2 - 27992511

VL - 11

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 12

M1 - e0168396

ER -

ID: 170700919