Myocardial Metabolic Abnormalities and Cardiac Dysfunction

Author(s):  
Petra C. Kienesberger
Nutrition ◽  
2012 ◽  
Vol 28 (5) ◽  
pp. 520-526 ◽  
Author(s):  
Peter A. Hecker ◽  
Tatiana F. Galvao ◽  
Karen M. O’Shea ◽  
Bethany H. Brown ◽  
Reney Henderson ◽  
...  

Metabolites ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 846
Author(s):  
Satoshi Kawaguchi ◽  
Motoi Okada

The mechanism of sepsis-induced cardiac dysfunction is believed to be different from that of myocardial ischemia. In sepsis, chemical mediators, such as endotoxins, cytokines, and nitric oxide, cause metabolic abnormalities, mitochondrial dysfunction, and downregulation of β-adrenergic receptors. These factors inhibit the production of ATP, essential for myocardial energy metabolism, resulting in cardiac dysfunction. This review focuses on the metabolic changes in sepsis, particularly in the heart. In addition to managing inflammation, interventions focusing on metabolism may be a new therapeutic strategy for cardiac dysfunction due to sepsis.


2005 ◽  
Vol 288 (6) ◽  
pp. E1229-E1235 ◽  
Author(s):  
Priya Pillutla ◽  
Yuying C. Hwang ◽  
Ayanna Augustus ◽  
Masayoshi Yokoyama ◽  
Hiroaki Yagyu ◽  
...  

Hearts with overexpression of anchored lipoprotein lipase (LpL) by cardiomyocytes (hLpLGPI mice) develop a lipotoxic cardiomyopathy. To characterize cardiac fatty acid (FA) and triglyceride (TG) metabolism in these mice and to determine whether changes in lipid metabolism precede cardiac dysfunction, hearts from young mice were perfused in Langendorff mode with [14C]palmitate. In hLpLGPI hearts, FA uptake and oxidation were decreased by 59 and 82%, respectively. This suggests reliance on an alternative energy source, such as TG. Indeed, these hearts oxidized 88% more TG. Hearts from young hLpLGPI mice also had greater uptake of intravenously injected cholesteryl ester-labeled Intralipid and VLDL. To determine whether perfusion of normal hearts would mimic the metabolic alterations found in hLpLGPI mouse hearts, wild-type hearts were perfused with [14C]palmitate and either human VLDL or Intralipid (0.4 mM TG). Both sources of TG reduced [14C]palmitate uptake (48% with VLDL and 45% with Intralipid) and FA oxidation (71% with VLDL and 65% with Intralipid). Addition of either heparin or LpL inhibitor P407 to Intralipid-containing perfusate restored [14C]palmitate uptake and confirmed that Intralipid inhibition requires local LpL. Our data demonstrate that reduced FA uptake and oxidation occur before mechanical dysfunction in hLpLGPI lipotoxicity. This physiology is reproduced with perfusion of hearts with TG-containing particles. Together, the results demonstrate that cardiac uptake of TG-derived FA reduces utilization of albumin-FA.


Author(s):  
V. Pelliccia ◽  
C. Pizzanelli ◽  
S. Pini ◽  
P. Malacarne ◽  
U. Bonuccelli

2000 ◽  
Vol 6 (2) ◽  
pp. 130-139 ◽  
Author(s):  
Duncan J. Campbell ◽  
Kenneth I. Mitchelhill ◽  
Stephen M. Schlicht ◽  
Russell J. Booth

2005 ◽  
Vol 38 (05) ◽  
Author(s):  
B Reisinger ◽  
E Mueller ◽  
B Kropp-Hartmann ◽  
D Wölflick ◽  
C Zimmerer ◽  
...  

2020 ◽  
Author(s):  
Elnoza Adilkhodjaeva ◽  
Zulaykho Shamansurova ◽  
Ismailov Said

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