Combination of Linagliptin and Empagliflozin Preserves Cardiac Systolic Function in an Ischemia-Reperfusion Injury Mice With Diabetes Mellitus.

Cardiac systolic function Diabetes mellitus Empagliflozin Linagliptin Myocardial reperfusion injury

Journal

Cardiology research
ISSN: 1923-2829
Titre abrégé: Cardiol Res
Pays: Canada
ID NLM: 101557543

Informations de publication

Date de publication:
Apr 2021
Historique:
received: 04 11 2020
accepted: 10 12 2020
entrez: 19 3 2021
pubmed: 20 3 2021
medline: 20 3 2021
Statut: ppublish

Résumé

Sodium-glucose co-transporter 2 inhibitor (SGLT2i) and dipeptidyl peptidase 4 inhibitor (DPP4i) are oral hypoglycemic agents. Although SGLT2i has been shown having the beneficial effects on heart failure in basic and clinical studies, the combined effects of SGLT2i and DPP4i have not been established well. We investigated the effects of SGLT2i and DPP4i against diabetes mice model of myocardial ischemia-reperfusion injury. Streptozotocin-induced diabetic C57BL/6J mice were divided into control (vehicle), empagliflozin (30 mg/kg/day), linagliptin (3 mg/kg/day) and combination (30 mg/kg/day and 3 mg/kg/day, respectively) groups. After 7 days of drug administration, 30 min of myocardial ischemia was performed. We investigated body weight, heart weight, blood glucose, and cardiac functions by pressure-volume Millar catheter followed by 28 days of additional drug administration. Blood glucose levels, body weight, and heart weight were not significantly different between the groups. In Millar catheter analysis, left ventricular volume at the peak left ventricular ejection rate which is one of the cardiac systolic parameters in combination group was significantly preserved than that in control (P = 0.036). The cardiac index in the combination group tended to be preserved compared to that in the control (P = 0.06). The pathological fibrotic area in the left ventricle in the combination group also tended to be smaller (P = 0.08). Combination therapy with linagliptin and empagliflozin preserved cardiac systolic function on the diabetes mice model of myocardial ischemia-reperfusion injury independent of blood glucose levels.

Sections du résumé

BACKGROUND BACKGROUND
Sodium-glucose co-transporter 2 inhibitor (SGLT2i) and dipeptidyl peptidase 4 inhibitor (DPP4i) are oral hypoglycemic agents. Although SGLT2i has been shown having the beneficial effects on heart failure in basic and clinical studies, the combined effects of SGLT2i and DPP4i have not been established well. We investigated the effects of SGLT2i and DPP4i against diabetes mice model of myocardial ischemia-reperfusion injury.
METHODS METHODS
Streptozotocin-induced diabetic C57BL/6J mice were divided into control (vehicle), empagliflozin (30 mg/kg/day), linagliptin (3 mg/kg/day) and combination (30 mg/kg/day and 3 mg/kg/day, respectively) groups. After 7 days of drug administration, 30 min of myocardial ischemia was performed. We investigated body weight, heart weight, blood glucose, and cardiac functions by pressure-volume Millar catheter followed by 28 days of additional drug administration.
RESULTS RESULTS
Blood glucose levels, body weight, and heart weight were not significantly different between the groups. In Millar catheter analysis, left ventricular volume at the peak left ventricular ejection rate which is one of the cardiac systolic parameters in combination group was significantly preserved than that in control (P = 0.036). The cardiac index in the combination group tended to be preserved compared to that in the control (P = 0.06). The pathological fibrotic area in the left ventricle in the combination group also tended to be smaller (P = 0.08).
CONCLUSIONS CONCLUSIONS
Combination therapy with linagliptin and empagliflozin preserved cardiac systolic function on the diabetes mice model of myocardial ischemia-reperfusion injury independent of blood glucose levels.

Identifiants

pubmed: 33738012
doi: 10.14740/cr1194
pmc: PMC7935637
doi:

Types de publication

Journal Article

Langues

eng

Pagination

91-97

Informations de copyright

Copyright 2021, Ideishi et al.

Déclaration de conflit d'intérêts

S.M. has received grants and lecture honoraria from Boehringer Ingelheim.

Références

Circ Res. 2018 May 11;122(10):1439-1459
pubmed: 29748368
Circulation. 1977 Nov;56(5):820-9
pubmed: 912845
Ann Nucl Med. 2005 Sep;19(6):447-54
pubmed: 16248380
Cardiovasc Diabetol. 2020 Feb 8;19(1):13
pubmed: 32035482
Physiol Rep. 2017 Mar;5(6):
pubmed: 28351966
Circulation. 1975 Sep;52(3):378-89
pubmed: 125632
J Clin Med. 2019 Nov 01;8(11):
pubmed: 31683785
Exp Physiol. 2015 Jun;100(6):667-79
pubmed: 25823534
Am J Cardiol. 1989 Jan 15;63(3):256-7
pubmed: 2910003
JACC Basic Transl Sci. 2019 Oct 23;4(7):831-840
pubmed: 31998851
Cardiovasc Drugs Ther. 2019 Oct;33(5):547-555
pubmed: 31418140
Eur J Heart Fail. 2016 Apr;18(4):386-93
pubmed: 26749570
Diabetes Metab Syndr. 2019 May - Jun;13(3):2001-2008
pubmed: 31235127
Magn Reson Imaging. 1994;12(5):711-7
pubmed: 7934657
Yakugaku Zasshi. 2013;133(7):773-82
pubmed: 23811765
Diabetol Metab Syndr. 2016 Jul 26;8:45
pubmed: 27462372
J Pharmacol Sci. 2005 Sep;99(1):95-104
pubmed: 16177543
Basic Res Cardiol. 2019 Aug 6;114(5):35
pubmed: 31388770
Front Immunol. 2018 Dec 18;9:2996
pubmed: 30619349
N Engl J Med. 2015 Nov 26;373(22):2117-28
pubmed: 26378978
Diabetes Metab Rev. 1987 Jul;3(3):751-78
pubmed: 2956075
Eur Heart J Cardiovasc Pharmacother. 2020 Nov 1;6(6):364-371
pubmed: 31816038
Eur J Pharmacol. 2020 May 15;875:173040
pubmed: 32114052
Life Sci. 2018 Oct 1;210:47-54
pubmed: 30170072
Am Heart J. 1971 Jun;81(6):799-808
pubmed: 4253442
J Diabetes. 2016 Jan;8(1):63-75
pubmed: 25565455
Cardiovasc Diabetol. 2019 Nov 28;18(1):165
pubmed: 31779619
Jpn Circ J. 1977 Oct;41(10):1085-97
pubmed: 592471
J Nucl Med. 1979 Jan;20(1):1-6
pubmed: 430171
Cardiol Rev. 2012 Jan-Feb;20(1):45-51
pubmed: 22143285
Ann Endocrinol (Paris). 2016 Oct;77(5):557-562
pubmed: 27062036
Biol Pharm Bull. 2006 Jun;29(6):1110-9
pubmed: 16755002
Diabetes Obes Metab. 2018 Mar;20(3):740-744
pubmed: 29053207
J Nucl Med. 2006 Jun;47(6):974-80
pubmed: 16741307
Diabetes Obes Metab. 2020 Jul;22(7):1141-1150
pubmed: 32227432
Int Heart J. 2019 Mar 20;60(2):411-418
pubmed: 30745531
Biochem Biophys Rep. 2019 Apr 19;18:100640
pubmed: 31032431
Diabetes Care. 2015 Mar;38(3):384-93
pubmed: 25583754

Auteurs

Akihito Ideishi (A)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.
Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka, 564-8565, Japan.
These authors were equally contributed as first authors.

Yasunori Suematsu (Y)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.
These authors were equally contributed as first authors.

Kohei Tashiro (K)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.

Hidetaka Morita (H)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.

Takashi Kuwano (T)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.

Sayo Tomita (S)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.

Kanji Nakai (K)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.

Shin-Ichiro Miura (SI)

Department of Cardiology, Fukuoka University School of Medicine, 7-45-1, Nanakuma, Jonan-ku, Fukuoka, Japan.
Department of Cardiology, Fukuoka University Nishijin Hospital, Fukuoka, Japan.

Classifications MeSH