scholarly journals The contribution of uncoupling protein and ATP synthase to state 3 respiration in Acanthamoeba castellanii mitochondria.

2004 ◽  
Vol 51 (2) ◽  
pp. 533-538 ◽  
Author(s):  
Wiesława Jarmuszkiewicz ◽  
Małgorzata Czarna ◽  
Claudine Sluse-Goffart ◽  
Francis E Sluse
Keyword(s):  
Fatty Acid ◽  
Linoleic Acid ◽  
Free Fatty Acid ◽  
Respiratory Rate ◽  
Atp Synthase ◽  
Acid Concentration ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Mitochondrial Uncoupling ◽  
Linoleic Acid Concentration

Mitochondria of the amoeba Acanthamoeba castellanii possess a free fatty acid-activated uncoupling protein (AcUCP) that mediates proton re-uptake driven by the mitochondrial proton electrochemical gradient. We show that AcUCP activity diverts energy from ATP synthesis during state 3 mitochondrial respiration in a fatty acid-dependent way. The efficiency of AcUCP in mitochondrial uncoupling increases when the state 3 respiratory rate decreases as the AcUCP contribution is constant at a given linoleic acid concentration while the ATP synthase contribution decreases with respiratory rate. Respiration sustained by this energy-dissipating process remains constant at a given linoleic acid concentration until more than 60% inhibition of state 3 respiration by n-butyl malonate is achieved. The present study supports the validity of the ADP/O method to determine the actual contributions of AcUCP (activated with various linoleic acid concentrations) and ATP synthase in state 3 respiration of A.castellanii mitochondria fully depleted of free fatty acid-activated and describes how the two contributions vary when the rate of succinate dehydrogenase is decreased by succinate uptake limitation.

Hydroxynonenal-stimulated activity of the uncoupling protein in Acanthamoeba castellanii mitochondria under phosphorylating conditions

2013 ◽  
Vol 394 (5) ◽  
pp. 649-658 ◽  
Author(s):  
Andrzej Woyda-Ploszczyca ◽  
Wieslawa Jarmuszkiewicz
Keyword(s):  
Respiratory Rate ◽  
Atp Synthase ◽  
Redox State ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Complex Iii ◽  
Dependent Manner ◽  
Mitochondrial Uncoupling ◽  
Concentration Dependent Manner ◽  
Succinate Oxidation

Abstract The influence of 4-hydroxy-2-nonenal (HNE), a lipid peroxidation end product, on the activity of the amoeba Acanthamoeba castellanii uncoupling protein (AcUCP) in isolated phosphorylating mitochondria was studied. Under phosphorylating conditions, exogenously added HNE induced GTP-sensitive AcUCP-mediated mitochondrial uncoupling. The HNE-induced proton leak decreased the yield of oxidative phosphorylation in an HNE concentration-dependent manner. The present study describes how the contributions of ATP synthase and HNE-induced AcUCP in phosphorylating respiration vary when the rate of succinate oxidation is decreased by limiting succinate uptake or inhibiting complex III activity within the range of a constant membrane potential. In phosphorylating mitochondria, at a given HNE concentration (100 μm), the efficiency of AcUCP in mitochondrial uncoupling increased as the respiratory rate decreased because the AcUCP contribution remained constant while the ATP synthase contribution decreased with the respiratory rate. HNE-induced uncoupling can be inhibited by GTP only when ubiquinone is sufficiently oxidized, indicating that in phosphorylating A. castellanii mitochondria, the sensitivity of AcUCP activity to GTP depends on the redox state of the membranous ubiquinone.

Redox state of quinone affects sensitivity of Acanthamoeba castellanii mitochondrial uncoupling protein to purine nucleotides

2008 ◽  
Vol 413 (2) ◽  
pp. 359-367 ◽  
Author(s):  
Aleksandra Swida ◽  
Andrzej Woyda-Ploszczyca ◽  
Wieslawa Jarmuszkiewicz
Keyword(s):  
Respiratory Rate ◽  
Redox State ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Inhibitory Effect ◽  
Proton Conductance ◽  
Purine Nucleotides ◽  
Protein Activity ◽  
Mitochondrial Uncoupling ◽  
Quinone Reduction

We studied FFA (free fatty acid)-induced uncoupling activity in Acanthamoeba castellanii mitochondria in the non-phosphorylating state. Either succinate or external NADH was used as a respiratory substrate to determine the proton conductance curves and the relationships between respiratory rate and the quinone reduction level. Our determinations of the membranous quinone reduction level in non-phosphorylating mitochondria show that activation of UCP (uncoupling protein) activity leads to a PN (purine nucleotide)-sensitive decrease in the quinone redox state. The gradual decrease in the rate of quinone-reducing pathways (using titration of dehydrogenase activities) progressively leads to a full inhibitory effect of GDP on LA (linoleic acid) induced proton conductance. This inhibition cannot be attributed to changes in the membrane potential. Indeed, the lack of GDP inhibitory effect observed when the decrease in respiratory rate is accompanied by an increase in the quinone reduction level (using titration of the quinol-oxidizing pathway) proves that the inhibition by nucleotides can be revealed only for a low quinone redox state. It must be underlined that, in A. castellanii non-phosphorylating mitochondria, the transition of the inhibitory effect of GDP on LA-induced UCP-mediated uncoupling is observed for the same range of quinone reduction levels (between 50% and 40%) as that observed previously for phosphorylating conditions. This observation, drawn from the two different metabolic states of mitochondria, indicates that quinone could affect UCP activity through sensitivity to PNs.

Effect of Preexercise Meals with Different Glycemic Indices and Loads on Metabolic Responses and Endurance Running

2008 ◽  
Vol 18 (3) ◽  
pp. 281-300 ◽  
Author(s):  
Ya Jun Chen ◽  
Stephen H. Wong ◽  
Chun Kwok Wong ◽  
Ching Wan Lam ◽  
Ya Jun Huang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Acid Concentration ◽  
Metabolic Changes ◽  
Metabolic Responses ◽  
Free Fatty Acid Concentration ◽  
Endurance Running ◽  
Postprandial Period ◽  
Glycemic Indices ◽  
Endurance Running Performance

This study examined the effect of ingesting 3 isocaloric meals with different glycemic indices (GI) and glycemic loads (GL) 2 hr before exercise on metabolic responses and endurance running performance. Eight male runners completed 3 trials in a randomized order, separated by at least 7 days. Carbohydrate (CHO) content (%), GI, and GL were, respectively, 65%, 79, and 82 for the high-GI/high-GL meal (H-H); 65%, 40, and 42 for the low-GI/low-GL meal (L-L); and 36%, 78, and 44 for the high-GI/low-GL meal (H-L). Each trial consisted of a 1-hr run at 70% VO2max, followed by a 10-km performance run. Low-GL diets (H-L and L-L) were found to induce smaller metabolic changes during the postprandial period and during exercise, which were characterized by a lower CHO oxidation in the 2 trials (p < .05) and a concomitant, higher glycerol and free-fatty-acid concentration in the H-L trial (p < .05). There was no difference, however, in time to complete the preloaded 10-km performance run between trials. This suggests that the GL of the preexercise meal has an important role in determining subsequent metabolic responses.

scholarly journals Enhanced Fatty Acid Flux Triggered by Adiponectin Overexpression

Endocrinology ◽  
2012 ◽  
Vol 153 (1) ◽  
pp. 113-122 ◽  
Author(s):  
Shoba Shetty ◽  
Maria A. Ramos-Roman ◽  
You-Ree Cho ◽  
Jonathan Brown ◽  
Jorge Plutzky ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Uncoupling Protein ◽  
Retinol Binding Protein ◽  
Peroxisome Proliferator ◽  
Tissue Mass ◽  
Triglyceride Synthesis ◽  
Peroxisome Proliferator Activated Receptor ◽  
Brown Adipose

Adiponectin overexpression in mice increases insulin sensitivity independent of adiposity. Here, we combined stable isotope infusion and in vivo measurements of lipid flux with transcriptomic analysis to characterize fatty acid metabolism in transgenic mice that overexpress adiponectin via the aP2-promoter (ADNTg). Compared with controls, fasted ADNTg mice demonstrated a 31% reduction in plasma free fatty acid concentrations (P = 0.008), a doubling of ketones (P = 0.028), and a 68% increase in free fatty acid turnover in plasma (15.1 ± 1.5 vs. 25.3 ± 6.8 mg/kg · min, P = 0.011). ADNTg mice had 2-fold more brown adipose tissue mass, and triglyceride synthesis and turnover were 5-fold greater in this organ (P = 0.046). Epididymal white adipose tissue was slightly reduced, possibly due to the approximately 1.5-fold increase in the expression of genes involved in oxidation (peroxisome proliferator-activated receptor α, peroxisome proliferator-activated receptor-γ coactivator 1α, and uncoupling protein 3). In ADNTg liver, lipogenic gene expression was reduced, but there was an unexpected increase in the expression of retinoid pathway genes (hepatic retinol binding protein 1 and retinoic acid receptor beta and adipose Cyp26A1) and liver retinyl ester content (64% higher, P &lt; 0.02). Combined, these data support a physiological link between adiponectin signaling and increased efficiency of triglyceride synthesis and hydrolysis, a process that can be controlled by retinoids. Interactions between adiponectin and retinoids may underlie adiponectin's effects on intermediary metabolism.

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