Serum Peroxisome Proliferator-activated Receptor Gamma Coactivator-1α Related to Myocardial Energy Expenditure in Patients With Chronic Heart Failure

被引:7
作者
Chen, Pingan [1 ,2 ,3 ,4 ]
Zhan, Qiong [1 ,2 ,3 ]
Bai, Yujia [2 ]
Huang, Xingfu [2 ]
Wang, Peng [2 ]
Pan, Yizhi [4 ]
Li, Shaonan [4 ]
Fu, Shenshen [5 ]
Lai, Wenyan [1 ,2 ,3 ]
Zeng, Qingchun [1 ,2 ,3 ]
Ren, Hao [6 ]
Xu, Dingli [1 ,2 ,3 ]
机构
[1] Southern Med Univ, Nanfang Hosp, Dept Cardiol, State Key Lab Organ Failure Res, Guangzhou, Guangdong, Peoples R China
[2] Southern Med Univ, Nanfang Hosp, Dept Cardiol, 1838 Northern Guangzhou Ave, Guangzhou 510515, Guangdong, Peoples R China
[3] Minist Educ Peoples Republ China, Key Lab Organ Failure Res, Guangzhou, Guangdong, Peoples R China
[4] Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Dept Cardiol, Guangzhou, Guangdong, Peoples R China
[5] Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Ultrason Dept, Guangzhou, Guangdong, Peoples R China
[6] Southern Med Univ, Nanfang Hosp, Dept Rheumatol, 1838 Northern Guangzhou Ave, Guangzhou 510515, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Peroxisome proliferator-activated receptor gamma coactivator-1 alpha; Heart failure; Cardiac energy metabolism; FATTY-ACID OXIDATION; SUBSTRATE METABOLISM; BODY-COMPOSITION; PGC-1-ALPHA; CONTRACTILE; TARGET;
D O I
10.1016/j.amjms.2018.12.002
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Background: Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) plays key roles in controlling cardiac metabolism and function. Myocardial energy expenditure (MEE) can reflect myocardial energy metabolism and cardiac function. Whether the variation of PGC-1 alpha can influence MEE levels in chronic heart failure (CHF) is unclear. Therefore, we investigated the relationship between PGC-1 alpha and MEE. Material and Methods: We studied 219 patients with CHF and 66 healthy controls. MEE was measured according to echocardiographic parameters. Serum PGC-1 alpha, N-terminal pro-B-type natriuretic peptide and other parameters were detected. Patients with CHF were divided into different groups according to the left ventricular ejection fraction (LVEF) and the tertile range of MEE. Results: Serum PGC-1 alpha was lower in the MEE 2 and 3 groups compared with controls (both P < 0.05). Patients in the MEE 2 (1.73 +/- 0.83 versus 2.16 +/- 0.82 ng/mL, P = 0.001) and 3 groups (1.65 +/- 0.73 versus 2.16 +/- 0.82 ng/mL, P < 0.001) possessed lower levels of PGC-1 alpha than those in the MEE 1 group. Compared with high LVEF, patients with low LVEF had higher MEE (median, 167 versus 73 cal/minute, P < 0.05) and lower PGC-1 alpha (1.71 +/- 0.65 versus 1.95 +/- 0.91 ng/mL, P = 0.032). Multivariate logistic regression analysis showed that MEE (OR = 0.517, 95% CI = 0.267-0.998, P = 0.049) and creatinine (OR = 2.704, 95% CI = 1.144-6.391, P = 0.023) were independently associated with increased PGC-1 alpha. Conclusions: Serum PGC-1 alpha was related to MEE and LVEF in patients with CHF and can reflect the degree of MEE and the systolic function of the left ventricle.
引用
收藏
页码:205 / 212
页数:8
相关论文
共 29 条
[1]
[Anonymous], 1984, Br J Clin Pharmacol, V18, P51
[2]
Energy Metabolism in Cardiac Remodeling and Heart Failure [J].
Azevedo, Paula S. ;
Minicucci, Marcos F. ;
Santos, Priscila P. ;
Paiva, Sergio A. R. ;
Zornoff, Leonardo A. M. .
CARDIOLOGY IN REVIEW, 2013, 21 (03) :135-140
[3]
Evidence for Intramyocardial Disruption of Lipid Metabolism and Increased Myocardial Ketone Utilization in Advanced Human Heart Failure [J].
Bedi, Kenneth C., Jr. ;
Snyder, Nathaniel W. ;
Brandimarto, Jeffrey ;
Aziz, Moez ;
Mesaros, Clementina ;
Worth, Andrew J. ;
Wang, Linda L. ;
Javaheri, Ali ;
Blair, Ian A. ;
Margulies, Kenneth B. ;
Rame, J. Eduardo .
CIRCULATION, 2016, 133 (08) :706-716
[4]
Angiotensin II induces skeletal muscle wasting through enhanced protein degradation and down-regulates autocrine insulin-like growth factor I [J].
Brink, M ;
Price, SR ;
Chrast, J ;
Bailey, JL ;
Anwar, A ;
Mitch, WE ;
Delafontaine, P .
ENDOCRINOLOGY, 2001, 142 (04) :1489-1496
[5]
Mitochondrial function as a therapeutic target in heart failure [J].
Brown, David A. ;
Perry, Justin B. ;
Allen, Mitchell E. ;
Sabbah, Hani N. ;
Stauffer, Brian L. ;
Shaikh, Saame Raza ;
Cleland, John G. F. ;
Colucci, Wilson S. ;
Butler, Javed ;
Voors, Adriaan A. ;
Anker, Stefan D. ;
Pitt, Bertram ;
Pieske, Burkert ;
Filippatos, Gerasimos ;
Greene, Stephen J. ;
Gheorghiade, Mihai .
NATURE REVIEWS CARDIOLOGY, 2017, 14 (04) :238-250
[6]
Coronary slow flow phenomenon: Not only low in flow rate but also in myocardial energy expenditure [J].
Cetin, M. S. ;
Cetin, E. H. Ozcan ;
Aras, D. ;
Topaloglu, S. ;
Aydogdu, S. .
NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES, 2015, 25 (10) :931-936
[7]
Increased serum 2-oxoglutarate associated with high myocardial energy expenditure and poor prognosis in chronic heart failure patients [J].
Chen, Ping-An ;
Xu, Zhi-Hao ;
Huang, Yu-Li ;
Luo, Yi ;
Zhu, Ding-Ji ;
Wang, Peng ;
Du, Zhi-Yong ;
Yang, Yang ;
Wu, Dai-Hong ;
Lai, Wen-Yan ;
Ren, Hao ;
Xu, Ding-Li .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2014, 1842 (11) :2120-2125
[8]
PGC-1/Spargel Counteracts High-Fat-Diet-Induced Obesity and Cardiac Lipotoxicity Downstream of TOR and Brummer ATGL Lipase [J].
Diop, Soda Balla ;
Bisharat-Kernizan, Jumana ;
Birse, Ryan Tyge ;
Oldham, Sean ;
Ocorr, Karen ;
Bodmer, Rolf .
CELL REPORTS, 2015, 10 (09) :1572-1584
[9]
Myocardial Energy Substrate Metabolism in Heart Failure: From Pathways to Therapeutic Targets [J].
Fukushima, Arata ;
Milner, Kenneth ;
Gupta, Abhishek ;
Lopaschuk, Gary D. .
CURRENT PHARMACEUTICAL DESIGN, 2015, 21 (25) :3654-3664
[10]
Chronic ethanol consumption increases cardiomyocyte fatty acid uptake and decreases ventricular contractile function in C57BL/6J mice [J].
Hu, Chunguang ;
Ge, Fengxia ;
Hyodo, Eiichi ;
Arai, Kotaro ;
Iwata, Shinichi ;
Lobdell, Harrison ;
Walewski, Jose L. ;
Zhou, Shengli ;
Clugston, Robin D. ;
Jiang, Hongfeng ;
Zizola, Cynthia P. ;
Bharadwaj, Kalyani G. ;
Blaner, William S. ;
Homma, Shunichi ;
Schulze, P. Christian ;
Goldberg, Ira J. ;
Berk, Paul D. .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2013, 59 :30-40