TY - JOUR
T1 - Targeting fatty acid metabolism in heart failure
T2 - Is it a suitable therapeutic approach?
AU - Arumugam, Somasundaram
AU - Sreedhar, Remya
AU - Thandavarayan, Rajarajan A.
AU - Karuppagounder, Vengadeshprabhu
AU - Watanabe, Kenichi
N1 - Publisher Copyright:
© 2016 Elsevier Ltd. All rights reserved.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2016/6/1
Y1 - 2016/6/1
N2 - The energy substrate preference of the human heart is well regulated and is modified upon aging, in that the fetal heart uses glucose, whereas the adult heart utilizes fatty acids. Various human and animal studies suggest a shift in myocardial substrate utilization and decreased rate of myocardial fatty acid uptake and oxidation in heart failure. Given that fatty acids provide greater capacity for energy production compared with glucose, reverting the heart back to using fatty acids might be a therapeutic option for treating heart failure. Targeting the enzymes and/or genes responsible for, or controlling, fatty acid metabolism in the heart, such as peroxisome proliferator-activated receptors (PPARs), mitochondrial fatty acid metabolizing proteins, AMP-activated protein kinase (AMPK), and glucose transporters (GLUTs), could provide novel therapeutic insights for treating heart failure.
AB - The energy substrate preference of the human heart is well regulated and is modified upon aging, in that the fetal heart uses glucose, whereas the adult heart utilizes fatty acids. Various human and animal studies suggest a shift in myocardial substrate utilization and decreased rate of myocardial fatty acid uptake and oxidation in heart failure. Given that fatty acids provide greater capacity for energy production compared with glucose, reverting the heart back to using fatty acids might be a therapeutic option for treating heart failure. Targeting the enzymes and/or genes responsible for, or controlling, fatty acid metabolism in the heart, such as peroxisome proliferator-activated receptors (PPARs), mitochondrial fatty acid metabolizing proteins, AMP-activated protein kinase (AMPK), and glucose transporters (GLUTs), could provide novel therapeutic insights for treating heart failure.
UR - http://www.scopus.com/inward/record.url?scp=84959470387&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84959470387&partnerID=8YFLogxK
U2 - 10.1016/j.drudis.2016.02.010
DO - 10.1016/j.drudis.2016.02.010
M3 - Review article
C2 - 26905600
AN - SCOPUS:84959470387
SN - 1359-6446
VL - 21
SP - 1003
EP - 1008
JO - Drug Discovery Today
JF - Drug Discovery Today
IS - 6
ER -