Metformin Improves Cardiac Metabolism and Function, and Prevents Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats.
AMP-Activated Protein Kinases
/ metabolism
Animals
Arterial Pressure
/ drug effects
Cardiovascular Agents
/ pharmacology
Disease Models, Animal
Energy Metabolism
/ drug effects
Fatty Acids
/ metabolism
Glucose
/ metabolism
Hypertension
/ drug therapy
Hypertrophy, Left Ventricular
/ metabolism
Metformin
/ pharmacology
Myocardium
/ metabolism
Oxidation-Reduction
Oxidative Stress
/ drug effects
Rats, Inbred SHR
Rats, Inbred WKY
TOR Serine-Threonine Kinases
/ metabolism
Ventricular Function, Left
/ drug effects
Ventricular Remodeling
/ drug effects
cardiac MRI
cardiac hypertrophy
dynamic FDG PET
metformin
spontaneously hypertensive rats
Journal
Journal of the American Heart Association
ISSN: 2047-9980
Titre abrégé: J Am Heart Assoc
Pays: England
ID NLM: 101580524
Informations de publication
Date de publication:
07 04 2020
07 04 2020
Historique:
entrez:
7
4
2020
pubmed:
7
4
2020
medline:
9
3
2021
Statut:
ppublish
Résumé
Background In spontaneously hypertensive rats (SHR) we observed profound myocardial metabolic changes during early hypertension before development of cardiac dysfunction and left ventricular hypertrophy. In this study, we evaluated whether metformin improved myocardial metabolic abnormalities and simultaneously prevented contractile dysfunction and left ventricular hypertrophy in SHR. Methods and Results SHR and control Wistar-Kyoto rats were treated with metformin from 2 to 5 months of age, when SHR hearts exhibit metabolic abnormalities and develop cardiac dysfunction and left ventricular hypertrophy. We evaluated the effect of metformin on myocardial glucose uptake rates with dynamic 2-[
Identifiants
pubmed: 32248762
doi: 10.1161/JAHA.119.015154
pmc: PMC7428616
doi:
Substances chimiques
Cardiovascular Agents
0
Fatty Acids
0
Metformin
9100L32L2N
mTOR protein, rat
EC 2.7.1.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
AMP-Activated Protein Kinases
EC 2.7.11.31
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e015154Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL123627
Pays : United States
Organisme : NIBIB NIH HHS
ID : R01 EB001763
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL061483
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128189
Pays : United States
Organisme : NIH HHS
ID : S10 OD021672
Pays : United States
Commentaires et corrections
Type : ErratumIn
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