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Sitagliptin Prevents Inflammation and Apoptotic Cell Death in the Kidney of Type 2 Diabetic Animals
Open accessAbstract
This study aimed to evaluate the efficacy of sitagliptin, a dipeptidyl peptidase IV (DPP-IV) inhibitor, in preventing the deleterious effects of diabetes on the kidney in an animal model of type 2 diabetes mellitus; the Zucker diabetic fatty (ZDF) rat: 20-week-old rats were treated with sitagliptin (10 mg/kg bw/day) during 6 weeks. Glycaemia and bloodHbA1clevels were monitored, as well as kidney function and lesions. Kidney mRNA and/or protein content/distribution of DPP-IV, GLP-1, GLP-1R, TNF-α, IL-1β, BAX, Bcl-2, and Bid were evaluated by RT-PCR and/or western blotting/immunohistochemistry. Sitagliptin treatment improved glycaemic control, as reflected by the significantly reduced levels of glycaemia andHbA1c(by about 22.5% and 1.2%, resp.) and ameliorated tubulointerstitial and glomerular lesions. Sitagliptin prevented the diabetes-induced increase in DPP-IV levels and the decrease in GLP-1 levels in kidney. Sitagliptin increased colocalization of GLP-1 and GLP-1R in the diabetic kidney. Sitagliptin also decreased IL-1βand TNF-αlevels, as well as, prevented the increase of BAX/Bcl-2 ratio, Bid protein levels, and TUNEL-positive cells which indicates protective effects against inflammation and proapoptotic state in the kidney of diabetic rats, respectively. In conclusion, sitagliptin might have a major role in preventing diabetic nephropathy evolution due to anti-inflammatory and antiapoptotic properties.
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“emerging data suggest that GLP-1-based therapies also showed anti-inflammatory effects on the liver, vascular system including aorta and vein endothelial cells, brain, kidney, lung, testis, and skin by reducing the production of inflammatory cytokines and infiltration of immune cells in the tissues [17, 21–25].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [25]
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“Sitagliptin (10 mg/kg/day) treatment decreased the expression of proinflammatory cytokine genes IL-1β and TNF-α in kidney of diabetic ZDF rat [25].”
From Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control (2016) · cites this paper as [25]
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BackgroundResultDiabetic Nephropathy: Mechanisms of Renal Disease Progression
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“In fact, there are reports of infiltration of mononuclear cells in the kidney of patients with DN [63], showing that interstitial inflammatory cells infiltrates are associated with progression of renal injuries in DN [64, 65].”
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“DPP-IV is widely distributed in numerous tissues and cells, and its enzymatic activity is exhibited in bothmembrane-anchored cell-surface peptidase and as a smaller soluble form in blood plasma [49].”
BackgroundKodera, R., Shikata, K., Kataoka, H. U., Takatsuka, T., Miyamoto, S., Sasaki, M., Kajitani, N., Nishishita, S., Sarai, K., Hirota, D., et al. (2011) · Diabetologia · doi:10.1007/s00125-010-2028-x · Cited by 394
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Zucker Diabetic Fatty Rat as a Model for Non-insulin-dependent Diabetes Mellitus
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“…Teixeira-Lemos,1,2 Frederico Teixeira,1 Carlos Fontes-Ribeiro,1 Flávio Reis,1 and Rosa Fernandes1,6 1 Laboratory of Pharmacology and Experimental Therapeutics, Institute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra, Azinhaga de Santa Comba,…”
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“In addition, we found reduced expression of GLP-1R in the diabetic rats, which was restored in the sitagliptin-treated rats, suggesting a role of GLP-1R signaling in the amelioration of nephropathy, according to other reports [54].”
ResultKluck, R. M., Esposti, M. D., Perkins, G. A., Renken, C. W., Kuwana, T., Bossy‐Wetzel, E., Goldberg, M. W., Allen, T., Barber, M. J., Green, D. R., et al. (1999) · The Journal of Cell Biology · doi:10.1083/jcb.147.4.809 · Cited by 327
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“In fact, there are reports of infiltration of mononuclear cells in the kidney of patients with DN [63], showing that interstitial inflammatory cells infiltrates are associated with progression of renal injuries in DN [64, 65].”
BackgroundGlucagon-like peptide-1 treatment delays the onset of diabetes in 8 week-old db/db mice
Wang, Q., & Brubaker, P. H. (2002) · Diabetologia · doi:10.1007/s00125-002-0828-3 · Cited by 316 · cited 15×
“It has been previously described that activation of incretin receptors in pancreatic𝛽-cells promotes resistance to apoptosis through the activation of several pathways leading to inhibition of caspase-3, by increasing expression of Bcl2 and decreasing expression of BAX [70, 71].”
BackgroundInfluentialAcute-Phase Markers of Inflammation and Glomerular Structure in Patients with Type 2 Diabetes
Vestra, M. D., Mussap, M., Gallina, P., Bruseghin, M., Cernigoi, A. M., Saller, A., Plebani, M., & Fioretto, P. (2005) · Journal of the American Society of Nephrology · doi:10.1681/asn.2004110961 · Cited by 299 · cited 1×
“Accumulating evidences point to a critical role of inflammation and proinflammatory cytokines in the development and progression of DN [10, 11].”
BackgroundDiabetic nephropathy is associated with low-grade inflammation in Type 1 diabetic patients
Saraheimo, M., Teppo, A.-M., Forsblom, C., Fagerudd, J., & Groop, P.-H. (2003) · Diabetologia · doi:10.1007/s00125-003-1194-5 · Cited by 255 · cited 1×
“Accumulating evidences point to a critical role of inflammation and proinflammatory cytokines in the development and progression of DN [10, 11].”
BackgroundKim, S., Winter, K. D., Nian, C., Tsuneoka, M., Koda, Y., & McIntosh, C. H. S. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m500540200 · Cited by 241
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Read, P. A., Khan, F. Z., Heck, P. M., Hoole, S. P., & Dutka, D. P. (2010) · Circulation Cardiovascular Imaging · doi:10.1161/circimaging.109.899377 · Cited by 226
The role of protein kinase C activation in diabetic nephropathy
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Dipeptidyl Peptidase IV Inhibitor Attenuates Kidney Injury in Streptozotocin-Induced Diabetic Rats
Liu, W. J., Xie, S. H., Liu, Y., Kim, W. B., Jin, H. Y., Park, S. K., Shao, Y. M., & Park, T. S. (2011) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.111.186866 · Cited by 209 · cited 1×
“However, until now, few studies have addressed the putative beneficial impact of these agents, including sitagliptin, on DN [33–35].”
BackgroundEfficacy and safety of sitagliptin monotherapy in Japanese patients with type 2 diabetes
Nonaka, K., Kakikawa, T., Sato, A., Okuyama, K., Fujimoto, G., Kato, N., Suzuki, H., Hirayama, Y., Ahmed, T., Davies, M. J., et al. (2008) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2007.08.021 · Cited by 203 · cited 2×
“Our results showed that chronic treatment with sitagliptin is able to promote a partial, but significant, decrease of glycaemia and HbA 1c and also prevented the aggravation of weight loss, characteristic of a more advanced stage of T2DM, which confirms the results obtained in studies performed in humans [24–28].”
BackgroundResultDPP-4 inhibitors in the management of type 2 diabetes: A critical review of head-to-head trials
Scheen, A. J. (2011) · Diabetes & Metabolism · doi:10.1016/j.diabet.2011.11.001 · Cited by 202 · cited 1×
“A novel class of oral antidiabetic agents, the dipeptidyl peptidase-IV (DPP-IV) inhibitors (or gliptins), such as sitagliptin, has increasingly gained emphasis in the therapeutic managing of T2DM patients by potentiating the action of incretins [20, 21].”
BackgroundMatsubara, J., Sugiyama, S., Akiyama, E., Iwashita, S., Kurokawa, H., Ohba, K., Maeda, H., Fujisue, K., Yamamoto, E., Kaikita, K., et al. (2013) · Circulation Journal · doi:10.1253/circj.cj-12-1168 · Cited by 201 · cited 1×
“Several reports have suggested that sitagliptin, a DPPIV inhibitor, confers cytoprotective effects on several tissues, such as heart, kidney, pancreas, and retina [32, 33, 35, 47, 48].”
BackgroundFerreira, L., Teixeira‐Lemos, E., Pinto, F., Parada, B., Mega, C., Vala, H., Pinto, R. M. A., Garrido, P., Sereno, J., Fernandes, R., et al. (2010) · Mediators of Inflammation · doi:10.1155/2010/592760 · Cited by 196 · cited 1×
“In conclusion, sitagliptin might be viewed as a promising preventive renoprotective therapeutic strategy against the development and/or progression of diabetic nephropathy.”
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Renin-angiotensin system activation and interstitial inflammation in human diabetic nephropathy
Mezzano, S. A., Droguett, A., Burgos, M. E., Ardiles, L. G., Flores, C., Aros, C., Caorsi, I., Vio, C. P., Ruiz‐Ortega, M., & Egido, J. (2003) · Kidney International · doi:10.1046/j.1523-1755.64.s86.12.x · Cited by 190
Pathogenic perspectives for the role of inflammation in diabetic nephropathy
Rivero, A., Fernández, C. M., Muros, M., Garcı́a, J. G., Herrera, H., & Navarro‐González, J. F. (2009) · Clinical Science · doi:10.1042/cs20080394 · Cited by 190
Activation of tubular epithelial cells in diabetic nephropathy.
Morcos, M., Sayed, A., Bierhaus, A., Yard, B., Waldherr, R., Merz, W., Kloeting, I., Schleicher, E., Mentz, S., el Baki, R. F. A., et al. (2002) · Diabetes · doi:10.2337/diabetes.51.12.3532 · Cited by 180 · cited 1×
“The proinflammatory transcription factor NF-κB was also detected mainly in tubular cells of human and rat kidney, with T2DM and overt nephropathy [67].”
BackgroundDobrian, A. D., Ma, Q., Lindsay, J. W., Leone, K. A., Ma, K., Coben, J., Galkina, E. V., & Nadler, J. L. (2011) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00463.2010 · Cited by 166 · cited 1×
“In addition, it was reported that sitagliptin decreases local inflammation in other tissues, such as the adipose tissue and pancreatic islet of obese mice [61].”
BackgroundHigh glucose promotes mesangial cell apoptosis by oxidant-dependent mechanism.
Kang, B. P. S., Frencher, S. K., Reddy, V., Kessler, A., Malhotra, A., & Meggs, L. (2003) · AJP - Renal Physiology · doi:10.1152/ajprenal.00137.2002 · Cited by 162
Mega, C., de Lemos, E. T., Vala, H., Fernandes, R., Oliveira, J., Mascarenhas-Melo, F., Teixeira, F., & Reis, F. (2011) · International Journal of Experimental Diabetes Research · doi:10.1155/2011/162092 · Cited by 161 · cited 4×
“Our group has recently shown that sitagliptin corrected the glycaemic dysmetabolism, hypertriglyceridaemia, and inflammation, reduced the severity of histopathological pancreatic lesions, and prevented kidney lesions [35, 44].”
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“In fact, it was found that GLP-1 upregulates Bcl-2 and inhibits BAX expression in cholangiocytes [72], neuronal cells [73, 74], and endothelial cells [75].”
BackgroundAugustyns, K., Bal, G., Thonus, G., Belyaev, A., Zhang, X.-M., Bollaert, W., Lambeir, A., Durinx, C., Goossens, F., & Haemers, A. (1999) · Current Medicinal Chemistry · doi:10.1002/chin.199929294 · Cited by 137
The role of reactive oxygen species in apoptosis of the diabetic kidney
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“In the present study, a proapoptotic state seems to be favored in the kidney of diabetic ZDF rats, which can lead to loss of renal cells and consequent renal function loss [15, 16].”
BackgroundTaurine Prevents Apoptosis Induced by High Ambient Glucose in Human Tubule Renal Cells
Verzola, D., Bertolotto, M. B., Villaggio, B., Ottonello, L. C., Dallegri, F., Frumento, G., Berruti, V., Gandolfo, M. T., Garibotto, G., & Deferrari, G. (2002) · Journal of Investigative Medicine · doi:10.1136/jim-50-06-04 · Cited by 116 · cited 15×
“It has been previously described that activation of incretin receptors in pancreatic𝛽-cells promotes resistance to apoptosis through the activation of several pathways leading to inhibition of caspase-3, by increasing expression of Bcl2 and decreasing expression of BAX [70, 71].”
BackgroundInfluentialApaijai, N., Pintana, H., Chattipakorn, S. C., & Chattipakorn, N. (2013) · British Journal of Pharmacology · doi:10.1111/bph.12176 · Cited by 116
Sitagliptin protects renal ischemia reperfusion induced renal damage in diabetes.
Vaghasiya, J., Sheth, N., Bhalodia, Y., & Manek, R. (2011) · Regulatory Peptides · doi:10.1016/j.regpep.2010.08.007 · Cited by 113 · cited 1×
“Several reports have suggested that sitagliptin, a DPPIV inhibitor, confers cytoprotective effects on several tissues, such as heart, kidney, pancreas, and retina [32, 33, 35, 47, 48].”
BackgroundDiabetes, Inflammation, Proinflammatory Cytokines, and Diabetic Nephropathy
Navarro‐González, J. F., & Fernández, C. M. (2006) · The Scientific World JOURNAL · doi:10.1100/tsw.2006.179 · Cited by 110
Picatoste, B., Ramírez, E., Caro‐Vadillo, A., Iborra, C., Egido, J., Tuñón, J., & Lorenzo, Ó. (2013) · PLoS ONE · doi:10.1371/journal.pone.0078330 · Cited by 103 · cited 1×
“It was recently suggested that sitagliptin, via GLP1 stabilization, is able to promote cardioprotection in a model of type 2 diabetic by reducing and limiting hyperglycemia and hyperlipidemia, as well as by promotion of survival and antihypertrophic/fibrotic effects on cultured cardiac cells, via GLP-1 and GLP-1(9-36)…”
BackgroundKodera, R., Shikata, K., Takatsuka, T., Oda, K., Miyamoto, S., Kajitani, N., Hirota, D., Ono, T., Usui, H. K., & Makino, H. (2014) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2013.12.049 · Cited by 101
The Role of Interstitial Macrophages in Nephropathy of Type 2 Diabetic db/db Mice
Ninichuk, V., Khandoga, A. G., Segerer, S., Loetscher, P., Schlapbach, A., Révész, L., Feifel, R., Khandoga, A., Krombach, F., Nelson, P. J., et al. (2007) · American Journal Of Pathology · doi:10.2353/ajpath.2007.060937 · Cited by 92 · cited 1×
“In fact, there are reports of infiltration of mononuclear cells in the kidney of patients with DN [63], showing that interstitial inflammatory cells infiltrates are associated with progression of renal injuries in DN [64, 65].”
BackgroundGonçalves, A., Leal, E. C., Paiva, A. A., Teixeira‐Lemos, E., Teixeira, F. J., Ribeiro, C., Reis, F., Ambrósio, A. F., & Fernandes, R. (2011) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2011.01548.x · Cited by 90
Self-citationMethotrexate prevents renal injury in experimental diabetic rats via anti-inflammatory actions.
Yozai, K., Shikata, K., Sasaki, M., Tone, A., Ohga, S., Usui, H., Okada, S., Wada, J., Nagase, R., Ogawa, D., et al. (2005) · Journal of the American Society of Nephrology · doi:10.1681/asn.2004111011 · Cited by 85 · cited 2×
“Previous works have shown that the decrease in inflammation promotes an amelioration of diabetic nephropathy [35–37, 60].”
BackgroundKirino, Y., Sato, Y., Kamimoto, T., Kawazoe, K., Minakuchi, K., & Nakahori, Y. (2008) · Journal of Endocrinology · doi:10.1677/joe-08-0424 · Cited by 82 · cited 1×
“Accordingly to our results, it was reported in a streptozotocin (STZ-) induced diabetic model that enhanced expression of Dpp-IV mRNA in the kidney tissue is correlated with increased circulatingDPP-IV enzyme activity, althoughDPPIV activity in the tissue was found to be significantly reduced after STZ treatment [50].”
BackgroundDipeptidyl peptidase-IV expression and activity in human glomerular endothelial cells
Pala, L., Mannucci, E., Pezzatini, A., Ciani, S., Sardi, J., Raimondi, L., Ognibene, A., Cappadona, A., Vannelli, B., & Rotella, C. M. (2003) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2003.08.111 · Cited by 76 · cited 2×
“In fact, there are also some reports suggesting that microvascular endothelial cells are the main sources of endogenous DPP-IV [53] and in vitro studies showed that both Dpp-IV mRNA expression and DPP-IV activity were enhanced by exposure of human glomerular endothelial cells to high glucose [51].”
BackgroundResultMatheeussen, V., Baerts, L., Meyer, G. D. D., Keulenaer, G. D., der Veken, P. V., Augustyns, K., Dubois, V., Scharpe, S., & Meester, I. D. (2011) · Biological chemistry · doi:10.1515/bc.2011.002 · Cited by 76 · cited 1×
“In fact, there are also some reports suggesting that microvascular endothelial cells are the main sources of endogenous DPP-IV [53] and in vitro studies showed that both Dpp-IV mRNA expression and DPP-IV activity were enhanced by exposure of human glomerular endothelial cells to high glucose [51].”
BackgroundExendin-4, a glucagon-like peptide 1 receptor agonist, protects cholangiocytes from apoptosis
Marzioni, M., Alpini, G., Saccomanno, S., Candelaresi, C., Venter, J., Rychlicki, C., Fava, G., Francis, H., Trozzi, L., & Benedetti, A. (2009) · Gut · doi:10.1136/gut.2008.150870 · Cited by 73 · cited 1×
“In fact, it was found that GLP-1 upregulates Bcl-2 and inhibits BAX expression in cholangiocytes [72], neuronal cells [73, 74], and endothelial cells [75].”
BackgroundQin, Z., Sun, Z., Huang, J., Hu, Y., Wu, Z., & Mei, B. (2008) · Neuroscience Letters · doi:10.1016/j.neulet.2008.08.047 · Cited by 66
New paradigms in cell death in human diabetic nephropathy
Sánchez-Niño, M. D., Benito‐Martín, A., & Ortíz, A. (2010) · Kidney International · doi:10.1038/ki.2010.270 · Cited by 64
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“In addition, it was shown that GLP-1 enhances Bcl-2 upregulation [76], BAD inactivation [77], and caspase3 activity reduction [78] in pancreatic β cells.”
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BackgroundPathogenesis of Diabetic Nephropathy
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Erythromycin ameliorates renal injury via anti-inflammatory effects in experimental diabetic rats
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Flagged first, then by citations
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Research works printed but not linked: 17
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Cited by
Sorted by citations
Bhatti, J. S., Sehrawat, A., Mishra, J., Sidhu, I. S., Navik, U., Khullar, N., Kumar, S., Bhatti, G. K., & Reddy, P. H. (2022) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2022.03.019 · Cited by 753
Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control
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Metadata
- Authors
- Marques, C., Mega, C., Gonçalves, A., Rodrigues-Santos, P., Teixeira-Lemos, E., Teixeira, F., Fontes-Ribeiro, C., Reis, F., & Fernandes, R.
- Affiliations
- University of Coimbra (PT)
- Centro de Estudos em Educação Tecnologia e Saúde (PT)
- Institute of Immunology, Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal
- Laboratory of Pharmacology and Experimental Therapeutics, Institute for Biomedical Imaging and Life Sciences (IBILI), Faculty of Medicine, University of Coimbra, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal
- Corresponding author
- Fernandes, Rosa
- ORCID
- Venue
- Mediators of Inflammation
- Publisher
- Wiley
- Published
- 2014
- Volume
- 2014
- Pages
- 1-15
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC4000968
- OpenAlex
- W2105771613
- Cited by
- 126
- References
- 80
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 8 · 2023: 7 · 2022: 6 · 2021: 15 · 2020: 15 · 2019: 10 · 2018: 11 · 2017: 21 · 2016: 15 · 2015: 8 · 2014: 1
- FWCI
- 12.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, cc-by)
- Funders
- Foundation for Science and Technology, Portugal (PEst-C/SAU/UI3282/2011, PEst-C/SAU/UI3282/2013, COMPETE)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Keywords
- sitagliptin, type 2 diabetes, diabetic nephropathy, DPP-4 inhibitors, glucagon-like peptide-1, GLP-1 receptor, renal inflammation, apoptosis, Bax/Bcl-2 ratio, Bid, TNF-α, IL-1β, tubulointerstitial injury, glomerular lesions, glycemic control, Zucker diabetic fatty rats
- MeSH terms
- Sitagliptin Phosphate, Animals, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Inflammation, Kidney, Pyrazines, Rats, Zucker, Triazoles, Tumor Necrosis Factor-alpha, Apoptosis, Rats, Glucagon-Like Peptide 1, Dipeptidyl-Peptidase IV Inhibitors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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