Substrate and Energy Metabolism in Heart Failure

2015 ◽  
pp. 186-199
Author(s):  
W. Lamprecht
Keyword(s):  
Heart Failure ◽  
Energy Metabolism

scholarly journals Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in heart failure patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Kagami Hirabayashi ◽  
Mayumi Yamato ◽  
Shingo Takada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Aerobic Capacity ◽  
Plantar Flexion ◽  
Exercise Intolerance ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Systemic Oxidative Stress

AbstractOxidative stress plays a role in the progression of chronic heart failure (CHF). We investigated whether systemic oxidative stress is linked to exercise intolerance and skeletal muscle abnormalities in patients with CHF. We recruited 30 males: 17 CHF patients, 13 healthy controls. All participants underwent blood testing, cardiopulmonary exercise testing, and magnetic resonance spectroscopy (MRS). The serum thiobarbituric acid reactive substances (TBARS; lipid peroxides) were significantly higher (5.1 ± 1.1 vs. 3.4 ± 0.7 μmol/L, p < 0.01) and the serum activities of superoxide dismutase (SOD), an antioxidant, were significantly lower (9.2 ± 7.1 vs. 29.4 ± 9.7 units/L, p < 0.01) in the CHF cohort versus the controls. The oxygen uptake (VO2) at both peak exercise and anaerobic threshold was significantly depressed in the CHF patients; the parameters of aerobic capacity were inversely correlated with serum TBARS and positively correlated with serum SOD activity. The phosphocreatine loss during plantar-flexion exercise and intramyocellular lipid content in the participants' leg muscle measured by 31phosphorus- and 1proton-MRS, respectively, were significantly elevated in the CHF patients, indicating abnormal intramuscular energy metabolism. Notably, the skeletal muscle abnormalities were related to the enhanced systemic oxidative stress. Our analyses revealed that systemic oxidative stress is related to lowered whole-body aerobic capacity and skeletal muscle dysfunction in CHF patients.

Energy Metabolism in Cardiac Remodeling and Heart Failure

2013 ◽  
Vol 21 (3) ◽  
pp. 135-140 ◽  
Author(s):  
Paula S. Azevedo ◽  
Marcos F. Minicucci ◽  
Priscila P. Santos ◽  
Sergio A. R. Paiva ◽  
Leonardo A. M. Zornoff
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Cardiac Remodeling

Abstract 14459: The Cardioprotective Effect on Energy Metabolism of Empagliflozin in Heart of Type 2 Diabetes Model Mouse in vivo

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Masamichi Yamamoto ◽  
Yuichirou Kitai ◽  
Shigenori Yamamoto ◽  
Michael P Pieper ◽  
Yutaro Kotobuki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Placebo Group ◽  
Energy Metabolism ◽  
Treated Group ◽  
Atp Level ◽  
Intracellular Atp ◽  
Atp Levels

Chronic pathological conditions, such as type 2 diabetes mellitus, involve various mechanisms in promoting heart failure by remodelling energy metabolic pathways and impairing cardiac contractility. The major source of myocardial energetics has been reported to shifts from OXPHOS in normal conditions to glycolysis in heart failure. Therefore, we decided to focus on the effect of empagliflozin on energy metabolic status in the heart.Recently, we generated two types of transgenic mice to monitor energy metabolism, intracellular ATP levels (iATP Tg) and mitochondrial ATP levels (mATP Tg) using FRET biosensor “ATeam” in the whole body, organ, and cellular levels as well as in beating heart. We intercrossed these mice with db/db, a mouse model of type 2 diabetes, and examined the energy metabolism of the heart in the empagliflozin -treated or non-treated groups.db/db;iATP Tg mice were fed EMPA-containing diets (30 mg/kg b.w., day) from 7 weeks of age for 10 weeks, and the ATP levels in the heart were measured by imaging with a fluorescence microscope. The results showed that, unlike the lowered ATP levels in the placebo group, the intracellular ATP level in the heart was significantly increased in the empagliflozin-treated group. Also, the ATP level was recovered in this empagliflozin-treated group to the same level as the wild type.Next, 8 weeks-old db/db;mATP Tg mice received a single dose of empagliflozin (30 mg/kg b.w.) via oral gavage after 4 hr of fasting. After another 3 hr of fasting, monitor the mitochondrial ATP level of the heart in vivo under the fluorescent microscope. The results showed that, unlike the placebo group, the ATP level in the mitochondria of the heart was significantly increased in the empagliflozin-treated group.These results suggest that empagliflozin may restore normal remodelling of energy metabolism in type 2 diabetic hearts.

Barth Syndrome-Related Cardiomyopathy is Associated with a Reduction in Myocardial Glucose Oxidation

2021 ◽  
Author(s):  
Amanda A. Greenwell ◽  
Keshav Gopal ◽  
Tariq Altamimi ◽  
Christina T. Saed ◽  
Faqi Wang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Glucose Oxidation ◽  
Genetic Disorder ◽  
Left Ventricular ◽  
Barth Syndrome ◽  
Acid Oxidation ◽  
Functional Impairments ◽  
Myocardial Energy Metabolism ◽  
Oxidation Rates

Heart failure presents as the leading cause of infant mortality in individuals with Barth syndrome (BTHS), a rare genetic disorder due to mutations in the tafazzin (TAZ) gene affecting mitochondrial structure and function. Investigations into the perturbed bioenergetics in the BTHS heart remain limited. Hence, our objective was to identify the potential alterations in myocardial energy metabolism and molecular underpinnings that may contribute to the early cardiomyopathy and heart failure development in BTHS. Cardiac function and myocardial energy metabolism were assessed via ultrasound echocardiography and isolated working heart perfusions, respectively, in a mouse model of BTHS (doxycycline-inducible Taz knockdown (TazKD) mice). In addition, we also performed mRNA/protein expression profiling for key regulators of energy metabolism in hearts from TazKD mice and their wild-type (WT) littermates. TazKD mice developed hypertrophic cardiomyopathy as evidenced by increased left ventricular anterior and posterior wall thickness, as well as increased cardiac myocyte cross sectional area, though no functional impairments were observed. Glucose oxidation rates were markedly reduced in isolated working hearts from TazKD mice compared to their WT littermates in the presence of insulin, which was associated with decreased pyruvate dehydrogenase activity. Conversely, myocardial fatty acid oxidation rates were elevated in TazKD mice, whereas no differences in glycolytic flux or ketone body oxidation rates were observed. Our findings demonstrate that myocardial glucose oxidation is impaired prior to the development of overt cardiac dysfunction in TazKD mice, and may thus represent a pharmacological target for mitigating the development of cardiomyopathy in BTHS.

scholarly journals Regulation of energy metabolism by combination therapy attenuates cardiac metabolic remodeling in heart failure

2020 ◽  
Vol 16 (16) ◽  
pp. 3133-3148
Author(s):  
Yuting Huang ◽  
Kai Zhang ◽  
Miaomiao Jiang ◽  
Jingyu Ni ◽  
Jingrui Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Combination Therapy ◽  
Metabolic Remodeling
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