P1016EMPAGLIFLOZIN REDUCES URINARY MITOCHONDRIAL DNA IN PATIENTS WITH TYPE 2 DIABETES MELLITUS
Abstract Background and Aims Recent evidences has shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors improve cardiovascular and renal outcomes of type 2 diabetes mellitus (T2DM) patients. However, the mechanisms by which SGLT2 inhibitors improve clinical outcomes are unclear. Mitochondria...
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| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2020-06, Vol.35 (Supplement_3) |
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| creator | Lee, Haekyung Yang, Wonmi Kim, Hyoungnae Jeon, Jin Seok Noh, Hyunjin Han, Dong cheol Byun, Dong Won Kim, Hye Jeong Suh, Kyoil Park, Hyeong Kyu Kwon, Soon hyo |
| description | Abstract
Background and Aims
Recent evidences has shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors improve cardiovascular and renal outcomes of type 2 diabetes mellitus (T2DM) patients. However, the mechanisms by which SGLT2 inhibitors improve clinical outcomes are unclear. Mitochondrial dysfunction plays a principal role in the pathophysiology of T2DM and its complications. We hypothesized empagliflozin, an SGLT2 inhibitor improves mitochondrial dysfunction in T2DM patients.
Method
We prospectively recruited healthy volunteers (n = 22) and SGLT2 naïve T2DM patients (n = 21). Copy numbers of urinary and serum mitochondrial DNA (mtDNA) nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND-1) and cytochrome-c oxidase 3 (mtCOX-3) were measured using quantitative polymerase chain reaction in healthy volunteers and T2DM patients at baseline and in T2DM patients after 3 months of treatment with empagliflozin (10 mg, n = 17 or 25 mg, n = 4).
Results
Patients with T2DM were older than healthy volunteers and had higher body mass index and systolic blood pressure, but lower estimated glomerular filtration rate. Urinary mtND-1 and mtCOX-3 copy numbers were significantly higher in the T2DM group than in healthy volunteers. Urinary mtDNA copy numbers were correlated with diabetes duration (8.74 ± 7.60 years, r = 0.54, P = 0.01 for mtND-1, r = 0.50, P = 0.02 for mtCOX-3). Urinary copy numbers of mtND-1 and mtCOX-3 decreased after empagliflozin treatment. The amount of reduction of urinary mtDNA copy number did not differ according to empagliflozin dose (P = 0.897 for mtND-1, P = 0.462 for mtCOX-3).
Conclusion
In this study, we found that T2DM is associated with elevated urinary mtND-1 and mtCOX-3 copy numbers. Empagliflozin reduces the elevated urinary mtND-1 and mtCOX-3 copy numbers in patients with T2DM. Our results suggest that empagliflozin could attenuate mitochondrial damage in the kidney cells of T2DM patients. |
| doi_str_mv | 10.1093/ndt/gfaa142.P1016 |
| format | Article |
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Background and Aims
Recent evidences has shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors improve cardiovascular and renal outcomes of type 2 diabetes mellitus (T2DM) patients. However, the mechanisms by which SGLT2 inhibitors improve clinical outcomes are unclear. Mitochondrial dysfunction plays a principal role in the pathophysiology of T2DM and its complications. We hypothesized empagliflozin, an SGLT2 inhibitor improves mitochondrial dysfunction in T2DM patients.
Method
We prospectively recruited healthy volunteers (n = 22) and SGLT2 naïve T2DM patients (n = 21). Copy numbers of urinary and serum mitochondrial DNA (mtDNA) nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND-1) and cytochrome-c oxidase 3 (mtCOX-3) were measured using quantitative polymerase chain reaction in healthy volunteers and T2DM patients at baseline and in T2DM patients after 3 months of treatment with empagliflozin (10 mg, n = 17 or 25 mg, n = 4).
Results
Patients with T2DM were older than healthy volunteers and had higher body mass index and systolic blood pressure, but lower estimated glomerular filtration rate. Urinary mtND-1 and mtCOX-3 copy numbers were significantly higher in the T2DM group than in healthy volunteers. Urinary mtDNA copy numbers were correlated with diabetes duration (8.74 ± 7.60 years, r = 0.54, P = 0.01 for mtND-1, r = 0.50, P = 0.02 for mtCOX-3). Urinary copy numbers of mtND-1 and mtCOX-3 decreased after empagliflozin treatment. The amount of reduction of urinary mtDNA copy number did not differ according to empagliflozin dose (P = 0.897 for mtND-1, P = 0.462 for mtCOX-3).
Conclusion
In this study, we found that T2DM is associated with elevated urinary mtND-1 and mtCOX-3 copy numbers. Empagliflozin reduces the elevated urinary mtND-1 and mtCOX-3 copy numbers in patients with T2DM. Our results suggest that empagliflozin could attenuate mitochondrial damage in the kidney cells of T2DM patients.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfaa142.P1016</identifier><language>eng</language><publisher>Oxford University Press</publisher><ispartof>Nephrology, dialysis, transplantation, 2020-06, Vol.35 (Supplement_3)</ispartof><rights>The Author(s) 2020. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids></links><search><creatorcontrib>Lee, Haekyung</creatorcontrib><creatorcontrib>Yang, Wonmi</creatorcontrib><creatorcontrib>Kim, Hyoungnae</creatorcontrib><creatorcontrib>Jeon, Jin Seok</creatorcontrib><creatorcontrib>Noh, Hyunjin</creatorcontrib><creatorcontrib>Han, Dong cheol</creatorcontrib><creatorcontrib>Byun, Dong Won</creatorcontrib><creatorcontrib>Kim, Hye Jeong</creatorcontrib><creatorcontrib>Suh, Kyoil</creatorcontrib><creatorcontrib>Park, Hyeong Kyu</creatorcontrib><creatorcontrib>Kwon, Soon hyo</creatorcontrib><title>P1016EMPAGLIFLOZIN REDUCES URINARY MITOCHONDRIAL DNA IN PATIENTS WITH TYPE 2 DIABETES MELLITUS</title><title>Nephrology, dialysis, transplantation</title><description>Abstract
Background and Aims
Recent evidences has shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors improve cardiovascular and renal outcomes of type 2 diabetes mellitus (T2DM) patients. However, the mechanisms by which SGLT2 inhibitors improve clinical outcomes are unclear. Mitochondrial dysfunction plays a principal role in the pathophysiology of T2DM and its complications. We hypothesized empagliflozin, an SGLT2 inhibitor improves mitochondrial dysfunction in T2DM patients.
Method
We prospectively recruited healthy volunteers (n = 22) and SGLT2 naïve T2DM patients (n = 21). Copy numbers of urinary and serum mitochondrial DNA (mtDNA) nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND-1) and cytochrome-c oxidase 3 (mtCOX-3) were measured using quantitative polymerase chain reaction in healthy volunteers and T2DM patients at baseline and in T2DM patients after 3 months of treatment with empagliflozin (10 mg, n = 17 or 25 mg, n = 4).
Results
Patients with T2DM were older than healthy volunteers and had higher body mass index and systolic blood pressure, but lower estimated glomerular filtration rate. Urinary mtND-1 and mtCOX-3 copy numbers were significantly higher in the T2DM group than in healthy volunteers. Urinary mtDNA copy numbers were correlated with diabetes duration (8.74 ± 7.60 years, r = 0.54, P = 0.01 for mtND-1, r = 0.50, P = 0.02 for mtCOX-3). Urinary copy numbers of mtND-1 and mtCOX-3 decreased after empagliflozin treatment. The amount of reduction of urinary mtDNA copy number did not differ according to empagliflozin dose (P = 0.897 for mtND-1, P = 0.462 for mtCOX-3).
Conclusion
In this study, we found that T2DM is associated with elevated urinary mtND-1 and mtCOX-3 copy numbers. Empagliflozin reduces the elevated urinary mtND-1 and mtCOX-3 copy numbers in patients with T2DM. Our results suggest that empagliflozin could attenuate mitochondrial damage in the kidney cells of T2DM patients.</description><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNqNkEtOwzAQQC0EEqVwAHY-AGk9TpzP0iRua8lNosQVKgsi4zgIBLRKYMHtCW0PwGoW895I8xC6BTIDkvjzz_Zr_tIZAwGdlUAgPEMTCELiUT9m52gyMuARRpJLdDUMb4SQhEbRBD0dYLEu-VLJhSoeZY4rkW1SUeNNJXNebfFa6iJdFXlWSa5wlnM8QiXXUuS6xg9Sr7DelgJTnEl-L_SoroVSUm_qa3TRmffB3ZzmFOmF0OnKU8VSplx5NkpCD6C1YdABNezZxQ461vkJaR2NmCW-H8VgmRmXLXGujW1sgULgoI2TgDlqjT9FcDxr-90w9K5r9v3rh-l_GiDNX59m7NOc-jSHl0fn7ujsvvf_wH8BW8RhFQ</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Lee, Haekyung</creator><creator>Yang, Wonmi</creator><creator>Kim, Hyoungnae</creator><creator>Jeon, Jin Seok</creator><creator>Noh, Hyunjin</creator><creator>Han, Dong cheol</creator><creator>Byun, Dong Won</creator><creator>Kim, Hye Jeong</creator><creator>Suh, Kyoil</creator><creator>Park, Hyeong Kyu</creator><creator>Kwon, Soon hyo</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20200601</creationdate><title>P1016EMPAGLIFLOZIN REDUCES URINARY MITOCHONDRIAL DNA IN PATIENTS WITH TYPE 2 DIABETES MELLITUS</title><author>Lee, Haekyung ; Yang, Wonmi ; Kim, Hyoungnae ; Jeon, Jin Seok ; Noh, Hyunjin ; Han, Dong cheol ; Byun, Dong Won ; Kim, Hye Jeong ; Suh, Kyoil ; Park, Hyeong Kyu ; Kwon, Soon hyo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c796-11dc64f12a5be8e1f5f390de275c033781c5a2a5d0eed8c8c1214e1d8945e2ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Haekyung</creatorcontrib><creatorcontrib>Yang, Wonmi</creatorcontrib><creatorcontrib>Kim, Hyoungnae</creatorcontrib><creatorcontrib>Jeon, Jin Seok</creatorcontrib><creatorcontrib>Noh, Hyunjin</creatorcontrib><creatorcontrib>Han, Dong cheol</creatorcontrib><creatorcontrib>Byun, Dong Won</creatorcontrib><creatorcontrib>Kim, Hye Jeong</creatorcontrib><creatorcontrib>Suh, Kyoil</creatorcontrib><creatorcontrib>Park, Hyeong Kyu</creatorcontrib><creatorcontrib>Kwon, Soon hyo</creatorcontrib><collection>CrossRef</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Haekyung</au><au>Yang, Wonmi</au><au>Kim, Hyoungnae</au><au>Jeon, Jin Seok</au><au>Noh, Hyunjin</au><au>Han, Dong cheol</au><au>Byun, Dong Won</au><au>Kim, Hye Jeong</au><au>Suh, Kyoil</au><au>Park, Hyeong Kyu</au><au>Kwon, Soon hyo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P1016EMPAGLIFLOZIN REDUCES URINARY MITOCHONDRIAL DNA IN PATIENTS WITH TYPE 2 DIABETES MELLITUS</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><date>2020-06-01</date><risdate>2020</risdate><volume>35</volume><issue>Supplement_3</issue><issn>0931-0509</issn><eissn>1460-2385</eissn><abstract>Abstract
Background and Aims
Recent evidences has shown that sodium-glucose co-transporter 2 (SGLT2) inhibitors improve cardiovascular and renal outcomes of type 2 diabetes mellitus (T2DM) patients. However, the mechanisms by which SGLT2 inhibitors improve clinical outcomes are unclear. Mitochondrial dysfunction plays a principal role in the pathophysiology of T2DM and its complications. We hypothesized empagliflozin, an SGLT2 inhibitor improves mitochondrial dysfunction in T2DM patients.
Method
We prospectively recruited healthy volunteers (n = 22) and SGLT2 naïve T2DM patients (n = 21). Copy numbers of urinary and serum mitochondrial DNA (mtDNA) nicotinamide adenine dinucleotide dehydrogenase subunit-1 (mtND-1) and cytochrome-c oxidase 3 (mtCOX-3) were measured using quantitative polymerase chain reaction in healthy volunteers and T2DM patients at baseline and in T2DM patients after 3 months of treatment with empagliflozin (10 mg, n = 17 or 25 mg, n = 4).
Results
Patients with T2DM were older than healthy volunteers and had higher body mass index and systolic blood pressure, but lower estimated glomerular filtration rate. Urinary mtND-1 and mtCOX-3 copy numbers were significantly higher in the T2DM group than in healthy volunteers. Urinary mtDNA copy numbers were correlated with diabetes duration (8.74 ± 7.60 years, r = 0.54, P = 0.01 for mtND-1, r = 0.50, P = 0.02 for mtCOX-3). Urinary copy numbers of mtND-1 and mtCOX-3 decreased after empagliflozin treatment. The amount of reduction of urinary mtDNA copy number did not differ according to empagliflozin dose (P = 0.897 for mtND-1, P = 0.462 for mtCOX-3).
Conclusion
In this study, we found that T2DM is associated with elevated urinary mtND-1 and mtCOX-3 copy numbers. Empagliflozin reduces the elevated urinary mtND-1 and mtCOX-3 copy numbers in patients with T2DM. Our results suggest that empagliflozin could attenuate mitochondrial damage in the kidney cells of T2DM patients.</abstract><pub>Oxford University Press</pub><doi>10.1093/ndt/gfaa142.P1016</doi></addata></record> |
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| title | P1016EMPAGLIFLOZIN REDUCES URINARY MITOCHONDRIAL DNA IN PATIENTS WITH TYPE 2 DIABETES MELLITUS |
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