A comparison of fuel preferences of mitochondria from vertebrates and invertebrates

1990 ◽  
Vol 68 (7) ◽  
pp. 1337-1349 ◽  
Author(s):  
C. D. Moyes ◽  
R. K. Suarez ◽  
P. W. Hochachka ◽  
J. S. Ballantyne
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Fatty Acids ◽  
Energy Metabolism ◽  
Ketone Bodies ◽  
Mitochondrial Enzymes ◽  
Tissue Specific ◽  
Isolated Mitochondria ◽  
Mitochondrial Oxidation ◽  
Aerobic Energy Metabolism

Knowledge of tissue-specific mitochondrial properties is important in understanding cellular aerobic energy metabolism. Studies employing isolated mitochondria offer the advantage of direct and controlled manipulation of extramitochondrial conditions, while minimizing disruption of interactions between mitochondrial enzymes, transporters, and membranes. In this review, we compare the oxidative properties of mitochondria isolated from liver, heart, and skeletal muscle of vertebrates and invertebrates. The observed differences between tissues and species in the capacities for mitochondrial oxidation of fatty acids, ketone bodies, pyruvate, and amino acids reflect fundamentally different adaptations for the assimilation, storage, and utilization of metabolic fuels.

scholarly journals Different variations of tissue B-group vitamin concentrations in short- and long-term starved rats

2011 ◽  
Vol 107 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Aya Moriya ◽  
Tsutomu Fukuwatari ◽  
Mitsue Sano ◽  
Katsumi Shibata
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Fatty Acids ◽  
Energy Metabolism ◽  
Metabolic Response ◽  
Pantothenic Acid ◽  
Vitamin B ◽  
Short And Long Term ◽  
Kidney Liver

Prolonged starvation changes energy metabolism; therefore, the metabolic response to starvation is divided into three phases according to changes in glucose, lipid and protein utilisation. B-group vitamins are involved in energy metabolism via metabolism of carbohydrates, fatty acids and amino acids. To determine how changes in energy metabolism alter B-group vitamin concentrations during starvation, we measured the concentration of eight kinds of B-group vitamins daily in rat blood, urine and in nine tissues including cerebrum, heart, lung, stomach, kidney, liver, spleen, testis and skeletal muscle during 8 d of starvation. Vitamin B1, vitamin B6, pantothenic acid, folate and biotin concentrations in the blood reduced after 6 or 8 d of starvation, and other vitamins did not change. Urinary excretion was decreased during starvation for all B-group vitamins except pantothenic acid and biotin. Less variation in B-group vitamin concentrations was found in the cerebrum and spleen. Concentrations of vitamin B1, vitamin B6, nicotinamide and pantothenic acid increased in the liver. The skeletal muscle and stomach showed reduced concentrations of five vitamins including vitamin B1, vitamin B2, vitamin B6, pantothenic acid and folate. Concentrations of two or three vitamins decreased in the kidney, testis and heart, and these changes showed different patterns in each tissue and for each vitamin. The concentration of pantothenic acid rapidly decreased in the heart, stomach, kidney and testis, whereas concentrations of nicotinamide were stable in all tissues except the liver. Different variations in B-group vitamin concentrations in the tissues of starved rats were found. The present findings will lead to a suitable supplementation of vitamins for the prevention of the re-feeding syndrome.

ATPase Effects on pro-nutrients-mTOR release long fatty acids chains which under mitochondrial phospholipase, synthase & synthetase effects form three ROR-alpha, beta, gamma isoform

2021 ◽  
Vol 1 (2) ◽  
Author(s):  
Ashraf Marzouk El Tantawi
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Lipid Metabolism ◽  
Mitochondrial Genes ◽  
Biological Molecules ◽  
Mitochondrial Enzymes ◽  
Mitochondrial Enzyme ◽  
Alpha Beta

RORs isoforms are so active biological molecules in lipid metabolism and in fat biosynthesis, that strongly dependent on and regulated by OPA1 mitochondrial genes and its active mitochondrial enzymes where each of mitochondrial enzyme (phospholipase, synthase, and synthetase) is responsible for its own ROR isoform {phospholipase responsible for ROR-alpha synthesis, synthase responsible for ROR[1]beta synthesis, and synthetase responsible for ROR-gamma synthesis} for acting and functioning the long fatty acids molecules “which produced from the effects of ATPase and COX enzyme on lipid molecules which accompanied and associated with absorbed nutrient molecules (pro-lipo-nutrient -mTOR molecules) “, and then will follow its own pathway in fatty and amino acids biosynthesis, in active anti[1]inflammations biosynthesis, and then will follow its own functions in original cells proliferations.

scholarly journals Systemic, Cerebral and Skeletal Muscle Ketone Body and Energy Metabolism During Acute Hyper-D-β-Hydroxybutyratemia in Post-Absorptive Healthy Males

2015 ◽  
Vol 100 (2) ◽  
pp. 636-643 ◽  
Author(s):  
Kristian H. Mikkelsen ◽  
Thomas Seifert ◽  
Niels H. Secher ◽  
Thomas Grøndal ◽  
Gerrit van Hall
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Ketone Bodies ◽  
Glucose Production ◽  
Epileptic Seizures ◽  
Energy Utilization ◽  
Glucose Turnover ◽  
Dependent Manner ◽  
Oxidation Rates ◽  
Healthy Males

Abstract Context: Ketone bodies are substrates during fasting and when on a ketogenic diet not the least for the brain and implicated in the management of epileptic seizures and dementia. Moreover, D-β-hydroxybutyrate (HOB) is suggested to reduce blood glucose and fatty acid levels. Objectives: The objectives of this study were to quantitate systemic, cerebral, and skeletal muscle HOB utilization and its effect on energy metabolism. Design: Single trial. Setting: Hospital. Participant: Healthy post-absorptive males (n = 6). Interventions: Subjects were studied under basal condition and three consecutive 1-hour periods with a 3-, 6-, and 12-fold increased HOB concentration via HOB infusion. Main Outcome Measures: Systemic, cerebral, and skeletal muscle HOB kinetics, oxidation, glucose turnover, and lipolysis via arterial, jugular, and femoral venous differences in combination with stable isotopically labeled HOB, glucose, and glycerol, infusion. Results: An increase in HOB from the basal 160–450 μmol/L elicited 14 ± 2% reduction (P = .03) in glucose appearance and 37 ± 4% decrease (P = .03) in lipolytic rate while insulin and glucagon were unchanged. Endogenous HOB appearance was reduced in a dose-dependent manner with complete inhibition at the highest HOB concentration (1.7 mmol/L). Cerebral HOB uptake and subsequent oxidation was linearly related to the arterial HOB concentration. Resting skeletal muscle HOB uptake showed saturation kinetics. Conclusion: A small increase in the HOB concentration decreases glucose production and lipolysis in post-absorptive healthy males. Moreover, cerebral HOB uptake and oxidation rates are linearly related to the arterial HOB concentration of importance for modifying brain energy utilization, potentially of relevance for patients with epileptic seizures and dementia.

scholarly journals The putative electrogenic nitrate-proton symport of the yeast Candida utilis. Comparison with the systems absorbing glucose or lactate

1985 ◽  
Vol 231 (2) ◽  
pp. 291-297 ◽  
Author(s):  
A A Eddy ◽  
P G Hopkins
Keyword(s):  
Amino Acids ◽  
Energy Metabolism ◽  
Candida Utilis ◽  
Membrane Depolarization ◽  
Yeast Cells ◽  
Charge Balance ◽  
Proton Symport ◽  
Limiting Nutrient ◽  
Proton Uptake ◽  
Aerobic Energy Metabolism

Strain N.C.Y.C. 193 of Candida utilis was grown aerobically at 30 degrees C with nitrate as limiting nutrient in a chemostat. The washed yeast cells depleted of ATP absorbed up to 5 nmol of nitrate/mg dry wt. of yeast. At pH 4-6, extra protons and nitrate entered the yeast cells together, in a ratio of about 2:1. Charge balance was maintained by an outflow of about 1 equiv. of K+. Nitrate stimulated the uptake of about 1 proton equivalent during glycolysis or aerobic energy metabolism. Studies with 3,3′-dipropylthiadicarbocyanine indicated that the proton-linked absorption of nitrate, amino acids or glucose depolarized the yeast cells. Proton uptake along with lactate led neither to net expulsion of K+ nor to membrane depolarization.

scholarly journals Fatty Acids in Energy Metabolism of the Central Nervous System

2014 ◽  
Vol 2014 ◽  
pp. 1-22 ◽  
Author(s):  
Alexander Panov ◽  
Zulfiya Orynbayeva ◽  
Valentin Vavilin ◽  
Vyacheslav Lyakhovich
Keyword(s):  
Fatty Acids ◽  
Energy Metabolism ◽  
De Novo ◽  
Aerobic Glycolysis ◽  
Metabolic Phenotype ◽  
Neuronal Excitation ◽  
Palmitoyl Carnitine ◽  
The Central Nervous System ◽  
Mitochondrial Oxidation ◽  
The Brain

In this review, we analyze the current hypotheses regarding energy metabolism in the neurons and astroglia. Recently, it was shown that up to 20% of the total brain’s energy is provided by mitochondrial oxidation of fatty acids. However, the existing hypotheses consider glucose, or its derivative lactate, as the only main energy substrate for the brain. Astroglia metabolically supports the neurons by providing lactate as a substrate for neuronal mitochondria. In addition, a significant amount of neuromediators, glutamate and GABA, is transported into neurons and also serves as substrates for mitochondria. Thus, neuronal mitochondria may simultaneously oxidize several substrates. Astrocytes have to replenish the pool of neuromediators by synthesis de novo, which requires large amounts of energy. In this review, we made an attempt to reconcileβ-oxidation of fatty acids by astrocytic mitochondria with the existing hypothesis on regulation of aerobic glycolysis. We suggest that, under condition of neuronal excitation, both metabolic pathways may exist simultaneously. We provide experimental evidence that isolated neuronal mitochondria may oxidize palmitoyl carnitine in the presence of other mitochondrial substrates. We also suggest that variations in the brain mitochondrial metabolic phenotype may be associated with different mtDNA haplogroups.

3,5-Diiodo-l-thyronine rapidly enhances mitochondrial fatty acid oxidation rate and thermogenesis in rat skeletal muscle: AMP-activated protein kinase involvement

2009 ◽  
Vol 296 (3) ◽  
pp. E497-E502 ◽  
Author(s):  
A. Lombardi ◽  
P. de Lange ◽  
E. Silvestri ◽  
R. A. Busiello ◽  
A. Lanni ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Energy Metabolism ◽  
Fatty Acid Oxidation ◽  
Atp Synthesis ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid ◽  
Amp Activated Protein Kinase

Triiodothyronine regulates energy metabolism and thermogenesis. Among triiodothyronine derivatives, 3,5-diiodo-l-thyronine (T2) has been shown to exert marked effects on energy metabolism by acting mainly at the mitochondrial level. Here we investigated the capacity of T2 to affect both skeletal muscle mitochondrial substrate oxidation and thermogenesis within 1 h after its injection into hypothyroid rats. Administration of T2 induced an increase in mitochondrial oxidation when palmitoyl-CoA (+104%), palmitoylcarnitine (+80%), or succinate (+30%) was used as substrate, but it had no effect when pyruvate was used. T2 was able to 1) activate the AMPK-ACC-malonyl-CoA metabolic signaling pathway known to direct lipid partitioning toward oxidation and 2) increase the importing of fatty acids into the mitochondrion. These results suggest that T2 stimulates mitochondrial fatty acid oxidation by activating several metabolic pathways, such as the fatty acid import/β-oxidation cycle/FADH2-linked respiratory pathways, where fatty acids are imported. T2 also enhanced skeletal muscle mitochondrial thermogenesis by activating pathways involved in the dissipation of the proton-motive force not associated with ATP synthesis (“proton leak”), the effect being dependent on the presence of free fatty acids inside mitochondria. We conclude that skeletal muscle is a target for T2, and we propose that, by activating processes able to enhance mitochondrial fatty acid oxidation and thermogenesis, T2 could play a role in protecting skeletal muscle against excessive intramyocellular lipid storage, possibly allowing it to avoid functional disorders.

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