Effect of empagliflozin on ectopic fat stores and myocardial energetics in type 2 diabetes: the EMPACEF study
Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) d...
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| Published in: | Cardiovascular diabetology Vol. 20; no. 1; pp. 57 - 14 |
|---|---|
| Main Authors: | , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
England
BioMed Central
01-03-2021
BMC |
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| Abstract | Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) diet mice and in type 2 diabetics (T2D).
C57BL/6 HFHS mice (n = 24) and T2D subjects (n = 56) were randomly assigned to 12 weeks of treatment with EMPA (30 mg/kg in mice, 10 mg/day in humans) or with placebo. A 4.7 T or 3 T MRI with
H-MRS evaluation-myocardial fat (primary endpoint) and liver fat content (LFC)-were performed at baseline and at 12 weeks. In humans, standard cardiac MRI was coupled with myocardial energetics (PCr/ATP) measured with
P-MRS. Subcutaneous (SAT) abdominal, visceral (VAT), epicardial and pancreatic fat were also evaluated. The primary efficacy endpoint was the change in epicardial fat volume between EMPA and placebo from baseline to 12 weeks. Secondary endpoints were the differences in PCr/ATP ratio, myocardial, liver and pancreatic fat content, SAT and VAT between groups at 12 weeks.
In mice fed HFHS, EMPA significantly improved glucose tolerance and increased blood ketone bodies (KB) and β-hydroxybutyrate levels (p < 0.05) compared to placebo. Mice fed HFHS had increased myocardial and liver fat content compared to standard diet mice. EMPA significantly attenuated liver fat content by 55%, (p < 0.001) but had no effect on myocardial fat. In the human study, all the 56 patients had normal LV function with mean LVEF = 63.4 ± 7.9%. Compared to placebo, T2D patients treated with EMPA significantly lost weight (- 2.6 kg [- 1.2; - 3.7]) and improved their HbA1c by 0.88 ± 0.74%. Hematocrit and EPO levels were significantly increased in the EMPA group compared to placebo (p < 0.0001, p = 0.041). EMPA significantly increased glycosuria and plasma KB levels compared to placebo (p < 0.0001, p = 0.012, respectively), and significantly reduced liver fat content (- 27 ± 23 vs. - 2 ± 24%, p = 0.0005) and visceral fat (- 7.8% [- 15.3; - 5.6] vs. - 0.1% [- 1.1;6.5], p = 0.043), but had no effect on myocardial or epicardial fat. At 12 weeks, no significant change was observed in the myocardial PCr/ATP (p = 0.57 between groups).
EMPA effectively reduced liver fat in mice and humans without changing epicardial, myocardial fat or myocardial energetics, rebutting the thrifty substrate hypothesis for cardiovascular protection of SGLT2 inhibitors. Trial registration NCT, NCT03118336. Registered 18 April 2017, https://clinicaltrials.gov/ct2/show/NCT03118336. |
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| AbstractList | Abstract
Background
Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) diet mice and in type 2 diabetics (T2D).
Methods
C57BL/6 HFHS mice (
n
= 24) and T2D subjects (
n
= 56) were randomly assigned to 12 weeks of treatment with EMPA (30 mg/kg in mice, 10 mg/day in humans) or with placebo. A 4.7 T or 3 T MRI with
1
H-MRS evaluation–myocardial fat (primary endpoint) and liver fat content (LFC)–were performed at baseline and at 12 weeks. In humans, standard cardiac MRI was coupled with myocardial energetics (PCr/ATP) measured with
31
P-MRS. Subcutaneous (SAT) abdominal, visceral (VAT), epicardial and pancreatic fat were also evaluated.
The primary efficacy endpoint was the change in epicardial fat volume between EMPA and placebo from baseline to 12 weeks. Secondary endpoints were the differences in PCr/ATP ratio, myocardial, liver and pancreatic fat content, SAT and VAT between groups at 12 weeks.
Results
In mice fed HFHS, EMPA significantly improved glucose tolerance and increased blood ketone bodies (KB) and β-hydroxybutyrate levels (
p
< 0.05) compared to placebo. Mice fed HFHS had increased myocardial and liver fat content compared to standard diet mice. EMPA significantly attenuated liver fat content by 55%, (
p
< 0.001) but had no effect on myocardial fat.
In the human study, all the 56 patients had normal LV function with mean LVEF = 63.4 ± 7.9%. Compared to placebo, T2D patients treated with EMPA significantly lost weight (− 2.6 kg [− 1.2; − 3.7]) and improved their HbA1c by 0.88 ± 0.74%. Hematocrit and EPO levels were significantly increased in the EMPA group compared to placebo (
p
< 0.0001,
p
= 0.041). EMPA significantly increased glycosuria and plasma KB levels compared to placebo (
p
< 0.0001,
p
= 0.012, respectively), and significantly reduced liver fat content (− 27 ± 23 vs. − 2 ± 24%,
p
= 0.0005) and visceral fat (− 7.8% [− 15.3; − 5.6] vs. − 0.1% [− 1.1;6.5],
p
= 0.043), but had no effect on myocardial or epicardial fat. At 12 weeks, no significant change was observed in the myocardial PCr/ATP (
p
= 0.57 between groups).
Conclusions
EMPA effectively reduced liver fat in mice and humans without changing epicardial, myocardial fat or myocardial energetics, rebutting the thrifty substrate hypothesis for cardiovascular protection of SGLT2 inhibitors.
Trial registration
NCT, NCT03118336. Registered 18 April 2017,
https://clinicaltrials.gov/ct2/show/NCT03118336 Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) diet mice and in type 2 diabetics (T2D). C57BL/6 HFHS mice (n = 24) and T2D subjects (n = 56) were randomly assigned to 12 weeks of treatment with EMPA (30 mg/kg in mice, 10 mg/day in humans) or with placebo. A 4.7 T or 3 T MRI with H-MRS evaluation-myocardial fat (primary endpoint) and liver fat content (LFC)-were performed at baseline and at 12 weeks. In humans, standard cardiac MRI was coupled with myocardial energetics (PCr/ATP) measured with P-MRS. Subcutaneous (SAT) abdominal, visceral (VAT), epicardial and pancreatic fat were also evaluated. The primary efficacy endpoint was the change in epicardial fat volume between EMPA and placebo from baseline to 12 weeks. Secondary endpoints were the differences in PCr/ATP ratio, myocardial, liver and pancreatic fat content, SAT and VAT between groups at 12 weeks. In mice fed HFHS, EMPA significantly improved glucose tolerance and increased blood ketone bodies (KB) and β-hydroxybutyrate levels (p < 0.05) compared to placebo. Mice fed HFHS had increased myocardial and liver fat content compared to standard diet mice. EMPA significantly attenuated liver fat content by 55%, (p < 0.001) but had no effect on myocardial fat. In the human study, all the 56 patients had normal LV function with mean LVEF = 63.4 ± 7.9%. Compared to placebo, T2D patients treated with EMPA significantly lost weight (- 2.6 kg [- 1.2; - 3.7]) and improved their HbA1c by 0.88 ± 0.74%. Hematocrit and EPO levels were significantly increased in the EMPA group compared to placebo (p < 0.0001, p = 0.041). EMPA significantly increased glycosuria and plasma KB levels compared to placebo (p < 0.0001, p = 0.012, respectively), and significantly reduced liver fat content (- 27 ± 23 vs. - 2 ± 24%, p = 0.0005) and visceral fat (- 7.8% [- 15.3; - 5.6] vs. - 0.1% [- 1.1;6.5], p = 0.043), but had no effect on myocardial or epicardial fat. At 12 weeks, no significant change was observed in the myocardial PCr/ATP (p = 0.57 between groups). EMPA effectively reduced liver fat in mice and humans without changing epicardial, myocardial fat or myocardial energetics, rebutting the thrifty substrate hypothesis for cardiovascular protection of SGLT2 inhibitors. Trial registration NCT, NCT03118336. Registered 18 April 2017, https://clinicaltrials.gov/ct2/show/NCT03118336. Abstract Background Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) diet mice and in type 2 diabetics (T2D). Methods C57BL/6 HFHS mice (n = 24) and T2D subjects (n = 56) were randomly assigned to 12 weeks of treatment with EMPA (30 mg/kg in mice, 10 mg/day in humans) or with placebo. A 4.7 T or 3 T MRI with 1H-MRS evaluation–myocardial fat (primary endpoint) and liver fat content (LFC)–were performed at baseline and at 12 weeks. In humans, standard cardiac MRI was coupled with myocardial energetics (PCr/ATP) measured with 31P-MRS. Subcutaneous (SAT) abdominal, visceral (VAT), epicardial and pancreatic fat were also evaluated. The primary efficacy endpoint was the change in epicardial fat volume between EMPA and placebo from baseline to 12 weeks. Secondary endpoints were the differences in PCr/ATP ratio, myocardial, liver and pancreatic fat content, SAT and VAT between groups at 12 weeks. Results In mice fed HFHS, EMPA significantly improved glucose tolerance and increased blood ketone bodies (KB) and β-hydroxybutyrate levels (p < 0.05) compared to placebo. Mice fed HFHS had increased myocardial and liver fat content compared to standard diet mice. EMPA significantly attenuated liver fat content by 55%, (p < 0.001) but had no effect on myocardial fat. In the human study, all the 56 patients had normal LV function with mean LVEF = 63.4 ± 7.9%. Compared to placebo, T2D patients treated with EMPA significantly lost weight (− 2.6 kg [− 1.2; − 3.7]) and improved their HbA1c by 0.88 ± 0.74%. Hematocrit and EPO levels were significantly increased in the EMPA group compared to placebo (p < 0.0001, p = 0.041). EMPA significantly increased glycosuria and plasma KB levels compared to placebo (p < 0.0001, p = 0.012, respectively), and significantly reduced liver fat content (− 27 ± 23 vs. − 2 ± 24%, p = 0.0005) and visceral fat (− 7.8% [− 15.3; − 5.6] vs. − 0.1% [− 1.1;6.5], p = 0.043), but had no effect on myocardial or epicardial fat. At 12 weeks, no significant change was observed in the myocardial PCr/ATP (p = 0.57 between groups). Conclusions EMPA effectively reduced liver fat in mice and humans without changing epicardial, myocardial fat or myocardial energetics, rebutting the thrifty substrate hypothesis for cardiovascular protection of SGLT2 inhibitors. Trial registration NCT, NCT03118336. Registered 18 April 2017, https://clinicaltrials.gov/ct2/show/NCT03118336 Abstract Background Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) diet mice and in type 2 diabetics (T2D). Methods C57BL/6 HFHS mice ( n = 24) and T2D subjects ( n = 56) were randomly assigned to 12 weeks of treatment with EMPA (30 mg/kg in mice, 10 mg/day in humans) or with placebo. A 4.7 T or 3 T MRI with 1 H-MRS evaluation–myocardial fat (primary endpoint) and liver fat content (LFC)–were performed at baseline and at 12 weeks. In humans, standard cardiac MRI was coupled with myocardial energetics (PCr/ATP) measured with 31 P-MRS. Subcutaneous (SAT) abdominal, visceral (VAT), epicardial and pancreatic fat were also evaluated. The primary efficacy endpoint was the change in epicardial fat volume between EMPA and placebo from baseline to 12 weeks. Secondary endpoints were the differences in PCr/ATP ratio, myocardial, liver and pancreatic fat content, SAT and VAT between groups at 12 weeks. Results In mice fed HFHS, EMPA significantly improved glucose tolerance and increased blood ketone bodies (KB) and β-hydroxybutyrate levels ( p < 0.05) compared to placebo. Mice fed HFHS had increased myocardial and liver fat content compared to standard diet mice. EMPA significantly attenuated liver fat content by 55%, ( p < 0.001) but had no effect on myocardial fat. In the human study, all the 56 patients had normal LV function with mean LVEF = 63.4 ± 7.9%. Compared to placebo, T2D patients treated with EMPA significantly lost weight (− 2.6 kg [− 1.2; − 3.7]) and improved their HbA1c by 0.88 ± 0.74%. Hematocrit and EPO levels were significantly increased in the EMPA group compared to placebo ( p < 0.0001, p = 0.041). EMPA significantly increased glycosuria and plasma KB levels compared to placebo ( p < 0.0001, p = 0.012, respectively), and significantly reduced liver fat content (− 27 ± 23 vs. − 2 ± 24%, p = 0.0005) and visceral fat (− 7.8% [− 15.3; − 5.6] vs. − 0.1% [− 1.1;6.5], p = 0.043), but had no effect on myocardial or epicardial fat. At 12 weeks, no significant change was observed in the myocardial PCr/ATP ( p = 0.57 between groups). Conclusions EMPA effectively reduced liver fat in mice and humans without changing epicardial, myocardial fat or myocardial energetics, rebutting the thrifty substrate hypothesis for cardiovascular protection of SGLT2 inhibitors. Trial registration NCT, NCT03118336. Registered 18 April 2017, https://clinicaltrials.gov/ct2/show/NCT03118336 Background Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes (T2D). We hypothesized that empaglifozin (EMPA) could modulate ectopic fat stores and myocardial energetics in high-fat-high-sucrose (HFHS) diet mice and in type 2 diabetics (T2D). Methods C57BL/6 HFHS mice (n = 24) and T2D subjects (n = 56) were randomly assigned to 12 weeks of treatment with EMPA (30 mg/kg in mice, 10 mg/day in humans) or with placebo. A 4.7 T or 3 T MRI with 1H-MRS evaluation–myocardial fat (primary endpoint) and liver fat content (LFC)–were performed at baseline and at 12 weeks. In humans, standard cardiac MRI was coupled with myocardial energetics (PCr/ATP) measured with 31P-MRS. Subcutaneous (SAT) abdominal, visceral (VAT), epicardial and pancreatic fat were also evaluated. The primary efficacy endpoint was the change in epicardial fat volume between EMPA and placebo from baseline to 12 weeks. Secondary endpoints were the differences in PCr/ATP ratio, myocardial, liver and pancreatic fat content, SAT and VAT between groups at 12 weeks. Results In mice fed HFHS, EMPA significantly improved glucose tolerance and increased blood ketone bodies (KB) and β-hydroxybutyrate levels (p < 0.05) compared to placebo. Mice fed HFHS had increased myocardial and liver fat content compared to standard diet mice. EMPA significantly attenuated liver fat content by 55%, (p < 0.001) but had no effect on myocardial fat. In the human study, all the 56 patients had normal LV function with mean LVEF = 63.4 ± 7.9%. Compared to placebo, T2D patients treated with EMPA significantly lost weight (− 2.6 kg [− 1.2; − 3.7]) and improved their HbA1c by 0.88 ± 0.74%. Hematocrit and EPO levels were significantly increased in the EMPA group compared to placebo (p < 0.0001, p = 0.041). EMPA significantly increased glycosuria and plasma KB levels compared to placebo (p < 0.0001, p = 0.012, respectively), and significantly reduced liver fat content (− 27 ± 23 vs. − 2 ± 24%, p = 0.0005) and visceral fat (− 7.8% [− 15.3; − 5.6] vs. − 0.1% [− 1.1;6.5], p = 0.043), but had no effect on myocardial or epicardial fat. At 12 weeks, no significant change was observed in the myocardial PCr/ATP (p = 0.57 between groups). Conclusions EMPA effectively reduced liver fat in mice and humans without changing epicardial, myocardial fat or myocardial energetics, rebutting the thrifty substrate hypothesis for cardiovascular protection of SGLT2 inhibitors. Trial registration NCT, NCT03118336. Registered 18 April 2017, https://clinicaltrials.gov/ct2/show/NCT03118336 |
| ArticleNumber | 57 |
| Author | Gaborit, B Abdullah, A E Abdesselam, I Houssays, M Varlet, I Rapacchi, S Eisinger, M Soghomonian, A Kober, F Calen, A Resseguier, N Darmon, P Peiretti, F Ancel, P Bornet, C E Bernard, M Lefur, Y Pini, L Maurice, F Lasbleiz, A Dutour, A |
| Author_xml | – sequence: 1 givenname: B orcidid: 0000-0002-4180-158X surname: Gaborit fullname: Gaborit, B organization: Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Hôpital Nord, Chemin Des Bourrely, 13915, Marseille cedex 20, France – sequence: 2 givenname: P surname: Ancel fullname: Ancel, P organization: Aix Marseille Univ, INSERM, INRAE, C2VN, Marseille, France – sequence: 3 givenname: A E surname: Abdullah fullname: Abdullah, A E organization: Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Hôpital Nord, Chemin Des Bourrely, 13915, Marseille cedex 20, France – sequence: 4 givenname: F surname: Maurice fullname: Maurice, F organization: Aix Marseille Univ, INSERM, INRAE, C2VN, Marseille, France – sequence: 5 givenname: I surname: Abdesselam fullname: Abdesselam, I organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 6 givenname: A surname: Calen fullname: Calen, A organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 7 givenname: A surname: Soghomonian fullname: Soghomonian, A organization: Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Hôpital Nord, Chemin Des Bourrely, 13915, Marseille cedex 20, France – sequence: 8 givenname: M surname: Houssays fullname: Houssays, M organization: Assistance-Publique Hôpitaux de Marseille, Medical Evaluation Department, CIC-CPCET, 13005, Marseille, France – sequence: 9 givenname: I surname: Varlet fullname: Varlet, I organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 10 givenname: M surname: Eisinger fullname: Eisinger, M organization: Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Hôpital Nord, Chemin Des Bourrely, 13915, Marseille cedex 20, France – sequence: 11 givenname: A surname: Lasbleiz fullname: Lasbleiz, A organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 12 givenname: F surname: Peiretti fullname: Peiretti, F organization: Aix Marseille Univ, INSERM, INRAE, C2VN, Marseille, France – sequence: 13 givenname: C E surname: Bornet fullname: Bornet, C E organization: Support Unit for Clinical Research and Economic Evaluation, Assistance Publique-Hôpitaux de Marseille, 13385, Marseille, France – sequence: 14 givenname: Y surname: Lefur fullname: Lefur, Y organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 15 givenname: L surname: Pini fullname: Pini, L organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 16 givenname: S surname: Rapacchi fullname: Rapacchi, S organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 17 givenname: M surname: Bernard fullname: Bernard, M organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 18 givenname: N surname: Resseguier fullname: Resseguier, N organization: Aix-Marseille Univ, EA 3279 CEReSS-Health Service Research and Quality of Life Center, Marseille, France – sequence: 19 givenname: P surname: Darmon fullname: Darmon, P organization: Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Hôpital Nord, Chemin Des Bourrely, 13915, Marseille cedex 20, France – sequence: 20 givenname: F surname: Kober fullname: Kober, F organization: Aix Marseille Univ, CNRS, CRMBM, Marseille, France – sequence: 21 givenname: A surname: Dutour fullname: Dutour, A email: anne.dutour@ap-hm.fr, anne.dutour@ap-hm.fr organization: Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Hôpital Nord, Chemin Des Bourrely, 13915, Marseille cedex 20, France. anne.dutour@ap-hm.fr |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33648515$$D View this record in MEDLINE/PubMed https://hal.inrae.fr/hal-03328849$$DView record in HAL |
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| Cites_doi | 10.1148/radiology.191.3.8184033 10.2337/dc18-1569 10.2147/DMSO.S223629 10.1172/JCI57426 10.1038/nrendo.2015.58 10.1093/cvr/cvx186 10.1161/CIRCULATIONAHA.119.042375 10.1371/journal.pone.0146337 10.1002/jcb.28141 10.2337/dc16-0542 10.1126/scitranslmed.3007328 10.1056/NEJMoa1504720 10.1016/j.jacc.2019.01.056 10.1002/nbm.4085 10.1007/s00125-016-3984-6 10.1016/j.jacbts.2018.07.006 10.1016/j.bbadis.2020.165807 10.1172/JCI72227 10.2337/dc17-0518 10.1007/s00125-015-3544-5 10.1016/j.jacc.2012.06.016 10.1016/j.phrs.2020.104870 10.1111/jdi.13237 10.1038/s41598-019-51949-5 10.1056/NEJMra063052 10.1007/s10334-009-0186-y 10.1007/s00125-018-4675-2 10.1186/s12933-019-0849-6 10.1186/s12916-014-0123-4 10.2337/dc16-0330 10.1016/j.jacbts.2020.02.004 10.1002/mrm.22347 10.1016/j.jacc.2012.11.062 10.1016/S2213-8587(20)30303-X 10.1016/j.jhep.2015.11.004 10.1056/NEJMoa1611925 10.1093/eurheartj/ehw106 10.1161/01.CIR.96.7.2190 10.1161/ATVBAHA.119.311904 10.1111/dom.12680 10.1056/NEJMoa1812389 10.1038/ijo.2011.117 10.1111/dom.13061 10.1002/mrm.21867 10.1161/CIRCULATIONAHA.119.042770 10.1186/s12933-020-00997-7 10.1007/s00125-017-4509-7 10.2337/dc20-S005 10.1186/s12933-017-0658-8 10.1002/hep.21983 10.2337/db20-0921 10.1006/jmre.1997.1244 10.1002/cphy.c160034 |
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| References | G Perseghin (1237_CR9) 2008; 47 G Iacobellis (1237_CR31) 2015; 11 E Ferrannini (1237_CR16) 2016; 39 PA Bottomley (1237_CR13) 2013; 5 B Xing (1237_CR48) 2020; 11 B Zinman (1237_CR1) 2015; 373 PA Bottomley (1237_CR25) 1994; 191 J-W Kim (1237_CR46) 2018; 120 AA Mahabadi (1237_CR32) 2013; 61 1237_CR21 B Gaborit (1237_CR11) 2012; 60 JW Eriksson (1237_CR51) 2018; 61 S Verma (1237_CR38) 2019; 140 E Díaz-Rodríguez (1237_CR37) 2018; 114 CG Santos-Gallego (1237_CR49) 2019; 73 P Begovatz (1237_CR43) 2015; 58 SD Wiviott (1237_CR3) 2019; 380 D Abdurrachim (1237_CR57) 2018; 114 L Vanhamme (1237_CR27) 1997; 129 S Neubauer (1237_CR15) 1997; 96 T Fukuda (1237_CR36) 2017; 8 J Moellmann (1237_CR39) 2020; 1866 A Braha (1237_CR35) 2019; 12 S Mudaliar (1237_CR17) 2016; 39 WT Clarke (1237_CR30) 2019; 32 B Neal (1237_CR2) 2017; 377 B Gaborit (1237_CR10) 2012; 36 J-C Hsu (1237_CR34) 2019; 9 1237_CR55 A-M El-Sharkawy (1237_CR28) 2009; 61 B Gaborit (1237_CR8) 2017; 7 Y Le Fur (1237_CR26) 2010; 23 A Dutour (1237_CR24) 2016; 18 GD Lopaschuk (1237_CR4) 2020; 5 MMY Lee (1237_CR19) 2020; 40 T Sato (1237_CR33) 2018; 17 S Verma (1237_CR58) 2018; 3 A Al-Mrabeh (1237_CR45) 2016; 59 D Ito (1237_CR53) 2017; 40 American Diabetes Association (1237_CR22) 2020; S43 A Al-Mrabeh (1237_CR44) 2020; 8 S-H Park (1237_CR7) 2020; 19 Y Honda (1237_CR47) 2016; 11 T Shibuya (1237_CR54) 2018; 20 S Kahl (1237_CR50) 2020; 43 H-C Lee (1237_CR5) 2019; 18 M Schär (1237_CR29) 2010; 63 A Latva-Rasku (1237_CR52) 2019; 42 KM Lauritsen (1237_CR18) 2020 L Uthman (1237_CR56) 2018; 61 CN Koyani (1237_CR6) 2020; 158 I Abdesselam (1237_CR20) 2015; 17 E Ferrannini (1237_CR40) 2014; 124 JJ Rayner (1237_CR59) 2020; 141 F Maurice (1237_CR23) 2018; 22 S Neubauer (1237_CR14) 2007; 356 N Sattar (1237_CR41) 2014; 12 B Gaborit (1237_CR42) 2005; 2015 A Gupta (1237_CR12) 2012; 122 MF Piepoli (1237_CR60) 2016; 37 |
| References_xml | – volume: 191 start-page: 593 year: 1994 ident: 1237_CR25 publication-title: Radiology doi: 10.1148/radiology.191.3.8184033 contributor: fullname: PA Bottomley – volume: 22 start-page: 1551 year: 2018 ident: 1237_CR23 publication-title: J Am Coll Cardiol. contributor: fullname: F Maurice – volume: 42 start-page: 931 year: 2019 ident: 1237_CR52 publication-title: Diabetes Care doi: 10.2337/dc18-1569 contributor: fullname: A Latva-Rasku – volume: 12 start-page: 2559 year: 2019 ident: 1237_CR35 publication-title: Diabetes Metab Syndr Obes Targets Ther doi: 10.2147/DMSO.S223629 contributor: fullname: A Braha – volume: 122 start-page: 291 year: 2012 ident: 1237_CR12 publication-title: J Clin Invest doi: 10.1172/JCI57426 contributor: fullname: A Gupta – volume: 11 start-page: 363 year: 2015 ident: 1237_CR31 publication-title: Nat Rev Endocrinol doi: 10.1038/nrendo.2015.58 contributor: fullname: G Iacobellis – volume: 2015 start-page: 480 issue: 39 year: 2005 ident: 1237_CR42 publication-title: Int J Obes contributor: fullname: B Gaborit – volume: 114 start-page: 336 year: 2018 ident: 1237_CR37 publication-title: Cardiovasc Res doi: 10.1093/cvr/cvx186 contributor: fullname: E Díaz-Rodríguez – volume: 140 start-page: 1693 year: 2019 ident: 1237_CR38 publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.119.042375 contributor: fullname: S Verma – volume: 11 start-page: e0146337 year: 2016 ident: 1237_CR47 publication-title: PLoS ONE doi: 10.1371/journal.pone.0146337 contributor: fullname: Y Honda – volume: 120 start-page: 8534 year: 2018 ident: 1237_CR46 publication-title: J Cell Biochem. doi: 10.1002/jcb.28141 contributor: fullname: J-W Kim – volume: 39 start-page: 1115 year: 2016 ident: 1237_CR17 publication-title: A Unify Hypothesis Diabetes Care doi: 10.2337/dc16-0542 contributor: fullname: S Mudaliar – volume: 5 start-page: 215re3 year: 2013 ident: 1237_CR13 publication-title: Sci Transl Med. doi: 10.1126/scitranslmed.3007328 contributor: fullname: PA Bottomley – volume: 373 start-page: 2117 year: 2015 ident: 1237_CR1 publication-title: N Engl J Med doi: 10.1056/NEJMoa1504720 contributor: fullname: B Zinman – volume: 73 start-page: 1931 year: 2019 ident: 1237_CR49 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2019.01.056 contributor: fullname: CG Santos-Gallego – volume: 32 start-page: e4085 year: 2019 ident: 1237_CR30 publication-title: NMR Biomed doi: 10.1002/nbm.4085 contributor: fullname: WT Clarke – volume: 59 start-page: 1753 year: 2016 ident: 1237_CR45 publication-title: Diabetologia doi: 10.1007/s00125-016-3984-6 contributor: fullname: A Al-Mrabeh – volume: 3 start-page: 575 year: 2018 ident: 1237_CR58 publication-title: JACC Basic Transl Sci doi: 10.1016/j.jacbts.2018.07.006 contributor: fullname: S Verma – volume: 1866 start-page: 165807 year: 2020 ident: 1237_CR39 publication-title: Biochim Biophys Acta Mol Basis Dis doi: 10.1016/j.bbadis.2020.165807 contributor: fullname: J Moellmann – volume: 124 start-page: 499 year: 2014 ident: 1237_CR40 publication-title: J Clin Invest doi: 10.1172/JCI72227 contributor: fullname: E Ferrannini – volume: 40 start-page: 1364 year: 2017 ident: 1237_CR53 publication-title: Diabetes Care doi: 10.2337/dc17-0518 contributor: fullname: D Ito – volume: 58 start-page: 1646 year: 2015 ident: 1237_CR43 publication-title: Diabetologia doi: 10.1007/s00125-015-3544-5 contributor: fullname: P Begovatz – volume: 60 start-page: 1381 year: 2012 ident: 1237_CR11 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2012.06.016 contributor: fullname: B Gaborit – volume: 158 start-page: 104870 year: 2020 ident: 1237_CR6 publication-title: Pharmacol Res doi: 10.1016/j.phrs.2020.104870 contributor: fullname: CN Koyani – volume: 43 start-page: 298 year: 2020 ident: 1237_CR50 publication-title: Placebo-Controlled Trial Diabetes Care contributor: fullname: S Kahl – volume: 11 start-page: 1238 year: 2020 ident: 1237_CR48 publication-title: J Diabetes Investig. doi: 10.1111/jdi.13237 contributor: fullname: B Xing – volume: 9 start-page: 15348 year: 2019 ident: 1237_CR34 publication-title: Sci Rep. doi: 10.1038/s41598-019-51949-5 contributor: fullname: J-C Hsu – volume: 356 start-page: 1140 year: 2007 ident: 1237_CR14 publication-title: N Engl J Med doi: 10.1056/NEJMra063052 contributor: fullname: S Neubauer – volume: 23 start-page: 23 year: 2010 ident: 1237_CR26 publication-title: Magma N Y N doi: 10.1007/s10334-009-0186-y contributor: fullname: Y Le Fur – volume: 61 start-page: 1923 year: 2018 ident: 1237_CR51 publication-title: Diabetologia doi: 10.1007/s00125-018-4675-2 contributor: fullname: JW Eriksson – volume: 18 start-page: 45 year: 2019 ident: 1237_CR5 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-019-0849-6 contributor: fullname: H-C Lee – volume: 12 start-page: 123 year: 2014 ident: 1237_CR41 publication-title: BMC Med doi: 10.1186/s12916-014-0123-4 contributor: fullname: N Sattar – volume: 39 start-page: 1108 year: 2016 ident: 1237_CR16 publication-title: Diabetes Care doi: 10.2337/dc16-0330 contributor: fullname: E Ferrannini – volume: 5 start-page: 632 year: 2020 ident: 1237_CR4 publication-title: JACC Basic Transl Sci doi: 10.1016/j.jacbts.2020.02.004 contributor: fullname: GD Lopaschuk – volume: 63 start-page: 1493 year: 2010 ident: 1237_CR29 publication-title: Magn Reson Med. doi: 10.1002/mrm.22347 contributor: fullname: M Schär – volume: 61 start-page: 1388 year: 2013 ident: 1237_CR32 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2012.11.062 contributor: fullname: AA Mahabadi – volume: 8 start-page: 939 year: 2020 ident: 1237_CR44 publication-title: Lancet Diabetes Endocrinol doi: 10.1016/S2213-8587(20)30303-X contributor: fullname: A Al-Mrabeh – volume: 8 start-page: 851 year: 2017 ident: 1237_CR36 publication-title: Diabetes Ther Res Treat Educ Diabetes Relat Disord contributor: fullname: T Fukuda – ident: 1237_CR55 doi: 10.1016/j.jhep.2015.11.004 – ident: 1237_CR21 – volume: 377 start-page: 644 year: 2017 ident: 1237_CR2 publication-title: N Engl J Med doi: 10.1056/NEJMoa1611925 contributor: fullname: B Neal – volume: 37 start-page: 2315 year: 2016 ident: 1237_CR60 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehw106 contributor: fullname: MF Piepoli – volume: 96 start-page: 2190 year: 1997 ident: 1237_CR15 publication-title: Circulation doi: 10.1161/01.CIR.96.7.2190 contributor: fullname: S Neubauer – volume: 40 start-page: 506 year: 2020 ident: 1237_CR19 publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.119.311904 contributor: fullname: MMY Lee – volume: 18 start-page: 882 year: 2016 ident: 1237_CR24 publication-title: Diabetes Obes Metab doi: 10.1111/dom.12680 contributor: fullname: A Dutour – volume: 380 start-page: 347 year: 2019 ident: 1237_CR3 publication-title: N Engl J Med doi: 10.1056/NEJMoa1812389 contributor: fullname: SD Wiviott – volume: 36 start-page: 422 year: 2012 ident: 1237_CR10 publication-title: Int J Obes doi: 10.1038/ijo.2011.117 contributor: fullname: B Gaborit – volume: 20 start-page: 438 year: 2018 ident: 1237_CR54 publication-title: Diabetes Obes Metab doi: 10.1111/dom.13061 contributor: fullname: T Shibuya – volume: 61 start-page: 785 year: 2009 ident: 1237_CR28 publication-title: Magn Reson Med doi: 10.1002/mrm.21867 contributor: fullname: A-M El-Sharkawy – volume: 141 start-page: 1152 year: 2020 ident: 1237_CR59 publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.119.042770 contributor: fullname: JJ Rayner – volume: 19 start-page: 19 year: 2020 ident: 1237_CR7 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-020-00997-7 contributor: fullname: S-H Park – volume: 61 start-page: 722 year: 2018 ident: 1237_CR56 publication-title: Diabetologia doi: 10.1007/s00125-017-4509-7 contributor: fullname: L Uthman – volume: S43 start-page: 48 year: 2020 ident: 1237_CR22 publication-title: Diabetes Care doi: 10.2337/dc20-S005 contributor: fullname: American Diabetes Association – volume: 17 start-page: 6 year: 2018 ident: 1237_CR33 publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-017-0658-8 contributor: fullname: T Sato – volume: 114 start-page: 1843 year: 2018 ident: 1237_CR57 publication-title: Cardiovasc Res contributor: fullname: D Abdurrachim – volume: 47 start-page: 51 year: 2008 ident: 1237_CR9 publication-title: Hepatol Baltim Md doi: 10.1002/hep.21983 contributor: fullname: G Perseghin – volume: 17 start-page: 95 year: 2015 ident: 1237_CR20 publication-title: J Cardiovasc Magn Reson Off J Soc Cardiovasc Magn Reson contributor: fullname: I Abdesselam – year: 2020 ident: 1237_CR18 publication-title: Diabetes doi: 10.2337/db20-0921 contributor: fullname: KM Lauritsen – volume: 129 start-page: 35 year: 1997 ident: 1237_CR27 publication-title: J Magn Reson San Diego Calif. doi: 10.1006/jmre.1997.1244 contributor: fullname: L Vanhamme – volume: 7 start-page: 1051 year: 2017 ident: 1237_CR8 publication-title: Compr Physiol doi: 10.1002/cphy.c160034 contributor: fullname: B Gaborit |
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| Snippet | Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type 2 diabetes... Abstract Background Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients... Background Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients with type... Abstract Background Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor that has demonstrated cardiovascular and renal protection in patients... |
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| Title | Effect of empagliflozin on ectopic fat stores and myocardial energetics in type 2 diabetes: the EMPACEF study |
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