Structural and biochemical analyses of cardiac ventricular enlargement in cold-acclimated striped bass

1997 ◽  
Vol 273 (1) ◽  
pp. R252-R258 ◽  
Author(s):  
K. J. Rodnick ◽  
B. D. Sidell
Keyword(s):  
Striped Bass ◽  
Cardiac Tissue ◽  
Citrate Synthase ◽  
Temperature Acclimation ◽  
Circulatory Support ◽  
Ventricular Enlargement ◽  
Cold Temperatures ◽  
Atp Production ◽  
Ventricular Mass ◽  
Biochemical Analyses

We examined effects of temperature acclimation on ultrastructural characteristics of cardiac myocytes and maximal activities of metabolic enzymes in cardiac tissue of striped bass (Morone saxatilis). Ventricular mass and ventricular mass divided by body weight were significantly increased (29% and 40%, respectively) in animals acclimated to cold (5 degrees C) vs. warm temperatures (25 degrees C). Mean myocyte diameter was increased at cold temperature (3.47 +/- 0.14 vs. 2.98 +/- 0.08 microns), which is sufficient to explain the increase in ventricular mass. Ventricular enlargement did not alter volume densities of mitochondria, myofibrils, protein concentration, or citrate synthase activity. Thus total volume of mitochondria and myofibrils increased proportionately with cardiac mass in cold animals. Activities of hexokinase (34%) and carnitine palmitoyltransferase (42%) increased in cold animals, suggesting positive compensation and increased aerobic capacity for utilization of glucose and fatty acids for energy production. Enlargement of the ventricle and an increased capacity for ATP production in striped bass may help compensate for kinetic constraints at cold temperatures and maintain circulatory support to oxidative axial musculature for swimming activity.

Sex differences in energy metabolism and performance of teleost cardiac tissue

2007 ◽  
Vol 292 (2) ◽  
pp. R827-R836 ◽  
Author(s):  
Pavan K. Battiprolu ◽  
Kelli J. Harmon ◽  
Kenneth J. Rodnick
Keyword(s):  
Sex Differences ◽  
Rainbow Trout ◽  
Cardiac Tissue ◽  
Citrate Synthase ◽  
Isometric Force ◽  
Force Production ◽  
Ringer Solution ◽  
Lactate Dehydrogenase Activity ◽  
Atp Production ◽  
Exogenous Glucose

This study examined the effects of different oxygenation levels and substrate availability on cardiac performance, metabolism, and biochemistry in sexually immature male and female rainbow trout ( Oncorhynchus mykiss). Ventricle strips were electrically paced (0.5 Hz, 14°C) in hyperoxic or hypoxic Ringer solution. Our results demonstrate that 1) males sustain isometric force production ( F) longer than females under hyperoxia (Po2 = 640 mmHg) with exogenous glucose present; 2) contractility is not maintained under moderate (Po2 = 130 mmHg) or severe hypoxia (Po2 = 10–20 mmHg) with glucose in either sex; however, following reoxygenation, F is higher in females compared with males; and 3) female tissue has higher lactate levels, net lactate efflux, and lactate dehydrogenase activity than males, whereas males have higher glycogen, citrate synthase, and β-hydroxy acyl-CoA dehydrogenase activities, and greater inotropic responses to exogenous glucose and octanoate. No sex differences were detected in responsiveness to epinephrine and inhibitors of glucose transport or activities of hexokinase and pyruvate kinase. We conclude that sex differences exist in rainbow trout cardiac tissue: females appear to prefer glycolysis for ATP production, whereas males have a higher capacity for aerobic and lipid metabolism.

scholarly journals DNA methyltransferase 3a mediates developmental thermal plasticity

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Isabella Loughland ◽  
Alexander Little ◽  
Frank Seebacher
Keyword(s):  
Environmental Change ◽  
Dna Methyltransferase ◽  
Developmental Plasticity ◽  
Citrate Synthase ◽  
Thermal Sensitivity ◽  
Short Term ◽  
Cold Temperatures ◽  
Knock Out ◽  
Thermal Plasticity ◽  
Dna Methyltransferase 3A

Abstract Background Thermal plasticity is pivotal for evolution in changing climates and in mediating resilience to its potentially negative effects. The efficacy to respond to environmental change depends on underlying mechanisms. DNA methylation induced by DNA methyltransferase 3 enzymes in the germline or during early embryonic development may be correlated with responses to environmental change. This developmental plasticity can interact with reversible acclimation within adult organisms, which would increase the speed of response and could alleviate potential mismatches between parental or early embryonic environments and those experienced at later life stages. Our aim was to determine whether there is a causative relationship between DNMT3 enzyme and developmental thermal plasticity and whether either or both interact with short-term acclimation to alter fitness and thermal responses in zebrafish (Danio rerio). Results We developed a novel DNMT3a knock-out model to show that sequential knock-out of DNA methyltransferase 3a isoforms (DNMT3aa−/− and DNMT3aa−/−ab−/−) additively decreased survival and increased deformities when cold developmental temperatures in zebrafish offspring mismatched warm temperatures experienced by parents. Interestingly, short-term cold acclimation of parents before breeding rescued DNMT3a knock-out offspring by restoring survival at cold temperatures. DNMT3a knock-out genotype interacted with developmental temperatures to modify thermal performance curves in offspring, where at least one DNMT3a isoform was necessary to buffer locomotion from increasing temperatures. The thermal sensitivity of citrate synthase activity, an indicator of mitochondrial density, was less severely affected by DNMT3a knock-out, but there was nonetheless a significant interaction between genotype and developmental temperatures. Conclusions Our results show that DNMT3a regulates developmental thermal plasticity and that the phenotypic effects of different DNMT3a isoforms are additive. However, DNMT3a interacts with other mechanisms, such as histone (de)acetylation, induced during short-term acclimation to buffer phenotypes from environmental change. Interactions between these mechanisms make phenotypic compensation for climate change more efficient and make it less likely that thermal plasticity incurs a cost resulting from environmental mismatches.

Abstract 126: Peroxisomal Proliferator Activated Receptor Alpha Overexpression in Hypertrophied Cardiomyocytes Restores Mitochondrial Integrity and Function

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Sagartirtha Sarkar ◽  
Santanu Rana
Keyword(s):  
Energy Demand ◽  
Cardiac Tissue ◽  
Structural Integrity ◽  
Heart Function ◽  
Ros Generation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Atp Production ◽  
Receptor Alpha ◽  
And Function

Cardiac tissue engineering is an interdisciplinary field that engineers modulation of viable molecular milieu to restore, maintain or improve heart function. Myocardial workload (energy demand) and energy substrate availability (supply) are in continual flux to maintain specialized cellular processes, yet the heart has a limited capacity for substrate storage and utilization during pathophysiological conditions. Damage to heart muscle, acute or chronic, leads to dysregulation of cardiac metabolic processes associated with gradual but progressive decline in mitochondrial respiratory pathways resulting in diminished ATP production. The Peroxisome Proliferator Activated Receptor Alpha ( PPARα ) is known to regulate fatty acid to glucose metabolic balance as well as mitochondrial structural integrity. In this study, a non-canonical pathway of PPARα was analyzed by cardiomyocyte targeted PPARα overexpression during cardiac hypertrophy that showed significant downregulation in p53 acetylation as well as GSK3β activation levels. Targeted PPARα overexpression during hypertrophy resulted in restoration of mitochondrial structure and function along with significantly improved mitochondrial ROS generation and membrane potential. This is the first report of myocyte targeted PPARα overexpression in hypertrophied myocardium that results in an engineered heart with significantly improved function with increased muscle mitochondrial endurance and reduced mitochondrial apoptotic load, thus conferring a greater resistance to pathological stimuli within cardiac microenvironment.

T3 increases mitochondrial ATP production in oxidative muscle despite increased expression of UCP2 and -3

2001 ◽  
Vol 280 (5) ◽  
pp. E761-E769 ◽  
Author(s):  
Kevin R. Short ◽  
Jonas Nygren ◽  
Rocco Barazzoni ◽  
James Levine ◽  
K. Sreekumaran Nair
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Atp Synthesis ◽  
Nutrient Flux ◽  
Oxidative Enzymes ◽  
Mrna Levels ◽  
Plantaris Muscle ◽  
Atp Production ◽  
Protein Levels ◽  
Different Types

Triiodothyronine (T3) increases O2 and nutrient flux through mitochondria (Mito) of many tissues, but it is unclear whether ATP synthesis is increased, particularly in different types of skeletal muscle, because variable changes in uncoupling proteins (UCP) and enzymes have been reported. Thus Mito ATP production was measured in oxidative and glycolytic muscles, as well as in liver and heart, in rats administered T3 for 14 days. Relative to saline-treated controls, T3 rats had 80, 168, and 62% higher ATP production in soleus muscle, liver, and heart, respectively, as well as higher activities of citrate synthase (CS; 63, 90, 25%) and cytochrome c oxidase (COX; 119, 225, 52%) in the same tissues (all P < 0.01). In plantaris muscle of T3 rats, CS was only slightly higher (17%, P < 0.05) than in controls, and ATP production and COX were unaffected. mRNA levels of COX I and III were 33 and 47% higher in soleus of T3 rats ( P < 0.01), but there were no differences in plantaris. In contrast, UCP2 and -3 mRNAs were 2.5- to 14-fold higher, and protein levels were 3- to 10-fold higher in both plantaris and soleus of the T3 group. We conclude that T3 increases oxidative enzymes and Mito ATP production and Mito-encoded transcripts in oxidative but not glycolytic rodent tissues. Despite large increases in UCP expression, ATP production was enhanced in oxidative tissues and maintained in glycolytic muscle of hyperthyroid rats.

scholarly journals Senescence-associated changes in respiration and oxidative phosphorylation in primary human fibroblasts

2004 ◽  
Vol 380 (3) ◽  
pp. 919-928 ◽  
Author(s):  
Eveline HUTTER ◽  
Kathrin RENNER ◽  
Gerald PFISTER ◽  
Petra STÖCKL ◽  
Pidder JANSEN-DÜRR ◽  
...  
Keyword(s):  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Replicative Senescence ◽  
Citrate Synthase ◽  
Human Fibroblasts ◽  
Respiratory Control ◽  
Compensatory Mechanisms ◽  
Intact Cells ◽  
Atp Production ◽  
Human Diploid Fibroblasts

Limitation of lifespan in replicative senescence is related to oxidative stress, which is probably both the cause and consequence of impaired mitochondrial respiratory function. The respiration of senescent human diploid fibroblasts was analysed by highresolution respirometry. To rule out cell-cycle effects, proliferating and growth-arrested young fibroblasts were used as controls. Uncoupled respiration, as normalized to citrate synthase activity, remained unchanged, reflecting a constant capacity of the respiratory chain. Oligomycin-inhibited respiration, however, was significantly increased in mitochondria of senescent cells, indicating a lower coupling of electron transport with phosphorylation. In contrast, growth-arrested young fibroblasts exhibited a higher coupling state compared with proliferating controls. In intact cells, partial uncoupling may lead to either decreased oxidative ATP production or a compensatory increase in routine respiration. To distinguish between these alternatives, we subtracted oligomycin-inhibited respiration from routine respiration, which allowed us to determine the part of respiratory activity coupled with ATP production. Despite substantial differences in the respiratory control ratio, ranging from 4 to 11 in the different experimental groups, a fixed proportion of respiratory capacity was maintained for coupled oxidative phosphorylation in all the experimental groups. This finding indicates that the senescent cells fully compensate for increased proton leakage by enhanced electron-transport activity in the routine state. These results provide a new insight into age-associated defects in mitochondrial function and compensatory mechanisms in intact cells.

scholarly journals Effect of short-term training on mitochondrial ATP production rate in human skeletal muscle

1999 ◽  
Vol 86 (2) ◽  
pp. 450-454 ◽  
Author(s):  
Emma C. Starritt ◽  
Damien Angus ◽  
Mark Hargreaves
Keyword(s):  
Glutamate Dehydrogenase ◽  
Production Rate ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Muscle Sample ◽  
Atp Production ◽  
Exercise Training Program ◽  
Before And After ◽  
Resting Muscle ◽  
Total Muscle

Seven untrained volunteers [3 men, 4 women, 20.1 ± 2.0 (SD) yr, 66.0 ± 11.0 kg, 171 ± 13 cm] participated in a 10-day cycle exercise training program. Resting muscle samples were obtained from vastus lateralis before and after 5 and 10 days of training. Mitochondrial ATP production rate (MAPR) was assayed in isolated mitochondria by using a bioluminescence technique and referenced to the activity of glutamate dehydrogenase in the muscle sample. MAPR increased 136 and 161% after 10 days of training for the mitochondrial substrate combinations pyruvate + palmitoyl-l-carnitine + α-ketoglutarate + malate and palmitoyl-l-carnitine + malate, respectively. Total muscle glutamate dehydrogenase and citrate synthase activity increased 53 and 16%, respectively, after 5 days but did not significantly increase further after 10 days. The results from the present study indicate that MAPR, measured by using the substrate combinations pyruvate + palmitoyl-l-carnitine + α-ketoglutarate + malate and palmitoyl-l-carnitine + malate, can rapidly increase in response to endurance training.

scholarly journals Adaptation of mitochondrial ATP production in human skeletal muscle to endurance training and detraining

1992 ◽  
Vol 73 (5) ◽  
pp. 2004-2010 ◽  
Author(s):  
R. Wibom ◽  
E. Hultman ◽  
M. Johansson ◽  
K. Matherei ◽  
D. Constantin-Teodosiu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cytochrome C ◽  
Endurance Training ◽  
Enzyme Activities ◽  
Citrate Synthase ◽  
Mitochondrial Fraction ◽  
Mitochondrial Enzyme ◽  
Atp Production ◽  
Before And After ◽  
Training And Detraining

The adaptation of mitochondrial ATP production rate (MAPR) to training and detraining was evaluated in nine healthy men. Muscle samples (approximately 60 mg) were obtained before and after 6 wk of endurance training and after 3 wk of detraining. MAPR was measured in isolated mitochondria by a bioluminometric method. In addition, the activities of mitochondrial and glycolytic enzymes were determined in skeletal muscle. In response to training, MAPR increased by 70%, with a substrate combination of pyruvate + palmitoyl-L-carnitine + alpha-ketoglutarate + malate, by 50% with only pyruvate + malate, and by 92% with palmitoyl-L-carnitine + malate. With detraining MAPR decreased by 12–28% from the posttraining rate (although not significantly for all substrates). No differences were found when MAPR was related to the protein content in the mitochondrial fraction. The largest increase in mitochondrial enzyme activities induced by training was observed for cytochrome-c oxidase (78%), whereas succinate cytochrome c reductase showed only an 18% increase. The activity of citrate synthase increased by 40% and of glutamate dehydrogenase by 45%. Corresponding changes in maximal O2 uptake were a 9.6% increase by training and a 6.0% reversion after detraining. In conclusion, both MAPR and mitochondrial enzyme activities are shown to increase with endurance training and to decrease with detraining.

scholarly journals IL-15 Mediates Mitochondrial Activity through a PPARδ-Dependent-PPARα-Independent Mechanism in Skeletal Muscle Cells

PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Shantaé M. Thornton ◽  
James E. Krolopp ◽  
Marcia J. Abbott
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Metabolic Effects ◽  
Mitochondrial Activity ◽  
Mrna Levels ◽  
Metabolic Processes ◽  
Atp Production ◽  
Positive Effects ◽  
Increase Energy Expenditure ◽  
Interleukin 15

Molecular mediators of metabolic processes, to increase energy expenditure, have become a focus for therapies of obesity. The discovery of cytokines secreted from the skeletal muscle (SKM), termed “myokines,” has garnered attention due to their positive effects on metabolic processes. Interleukin-15 (IL-15) is a myokine that has numerous positive metabolic effects and is linked to the PPAR family of mitochondrial regulators. Here, we aimed to determine the importance of PPARαand/or PPARδas targets of IL-15 signaling. C2C12 SKM cells were differentiated for 6 days and treated every other day with IL-15 (100 ng/mL), a PPARαinhibitor (GW-6471), a PPARδinhibitor (GSK-3787), or both IL-15 and the inhibitors. IL-15 increased mitochondrial activity and induced PPARα, PPARδ, PGC1α, PGC1β, UCP2, and Nrf1 expression. There was no effect of inhibiting PPARα, in combination with IL-15, on the aforementioned mRNA levels except for PGC1βand Nrf1. However, with PPARδinhibition, IL-15 failed to induce the expression levels of PGC1α, PGC1β, UCP2, and Nrf1. Further, inhibition of PPARδabolished IL-15 induced increases in citrate synthase activity, ATP production, and overall mitochondrial activity. IL-15 had no effects on mitochondrial biogenesis. Our data indicates that PPARδactivity is required for the beneficial metabolic effects of IL-15 signaling in SKM.

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