Abstract:Juvenile king penguins develop adaptive thermogenesis after repeated immersion in cold water. However, the mechanisms of such metabolic adaptation in birds are unknown, as they lack brown adipose tissue and uncoupling protein-1 (UCP1), which mediate adaptive non-shivering thermogenesis in mammals. We used three different groups of juvenile king penguins to investigate the mitochondrial basis of avian adaptive thermogenesis in vitro. Skeletal muscle mitochondria isolated from penguins that had never been immers… Show more
“…The ability of HCF1 pretreatment to partially reverse the mitochondrial GSH depletion induced by I/R challenge likely involved the upregulation of cellular glutathione redox cycling through the intermediacy of mitochondrial ROS production, as was the case in H9c2 cardiomyocytes (Yim & Ko, 1999;Ramires & Ji, 2001). While the reduction of tissue ATP level by long-term, low-dose HCF1 pretreatment in non-I/R rat hearts might be due to the induction of a sustained mitochondrial uncoupling, the significant reduction of tissue ATP level in ischemic/reperfused rat hearts was likely due to the impaired mitochondrial electron transport and oxidative phosphorylation (Talbot et al, 2004;Brennan et al, 2006). The reduced extent of I/Rinduced myocardial ATP depletion in HCF1-pretreated rat hearts, as observed in the present study, was likely related to the increased ATP-GC that compensated the enhanced ATP consumption for cellular homeostasis during reperfusion (Plaschke et al, 1998;Young, 2008).…”
“…The ability of HCF1 pretreatment to partially reverse the mitochondrial GSH depletion induced by I/R challenge likely involved the upregulation of cellular glutathione redox cycling through the intermediacy of mitochondrial ROS production, as was the case in H9c2 cardiomyocytes (Yim & Ko, 1999;Ramires & Ji, 2001). While the reduction of tissue ATP level by long-term, low-dose HCF1 pretreatment in non-I/R rat hearts might be due to the induction of a sustained mitochondrial uncoupling, the significant reduction of tissue ATP level in ischemic/reperfused rat hearts was likely due to the impaired mitochondrial electron transport and oxidative phosphorylation (Talbot et al, 2004;Brennan et al, 2006). The reduced extent of I/Rinduced myocardial ATP depletion in HCF1-pretreated rat hearts, as observed in the present study, was likely related to the increased ATP-GC that compensated the enhanced ATP consumption for cellular homeostasis during reperfusion (Plaschke et al, 1998;Young, 2008).…”
“…However, the loss of the phylogenetic and allometric differences in proton conductance found with liposomes made from the mitochondrial membrane (Brookes et al, 1997) further highlights that the presence of mitochondrial membrane proteins plays an important role in determining proton permeability (Stuart et al, 2001). For example, this has been suggested for the content of adenine nucleotide translocase (Talbot et al, 2004;Brand et al, 2005;Shabalina et al, 2006). In amphibians, some studies have shown that the mitochondrial inner membrane surface area might be greater in the mitochondria of liver and muscle from smaller species (Brookes et al, 1998;Hulbert et al, 2006;Berner et al, 2009).…”
Body size is a central biological parameter affecting most biological processes (especially energetics) and the mitochondrion is a key organelle controlling metabolism and is also the cell's main source of chemical energy. However, the link between body size and mitochondrial function is still unclear, especially in ectotherms. In this study, we investigated several parameters of mitochondrial bioenergetics in the liver of three closely related species of frog (the common frog Rana temporaria, the marsh frog Pelophylax ridibundus and the bull frog Lithobates catesbeiana). These particular species were chosen because of their differences in adult body mass. We found that mitochondrial coupling efficiency was markedly increased with animal size, which led to a higher ATP production (+70%) in the larger frogs (L. catesbeiana) compared with the smaller frogs (R. temporaria). This was essentially driven by a strong negative dependence of mitochondrial proton conductance on body mass. Liver mitochondria from the larger frogs (L. catesbeiana) displayed 50% of the proton conductance of mitochondria from the smaller frogs (R. temporaria). Contrary to our prediction, the low mitochondrial proton conductance measured in L. catesbeiana was not associated with higher reactive oxygen species production. Instead, liver mitochondria from the larger individuals produced significantly lower levels of radical oxygen species than those from the smaller frogs. Collectively, the data show that key bioenergetics parameters of mitochondria (proton leak, ATP production efficiency and radical oxygen species production) are correlated with body mass in frogs. This research expands our understanding of the relationship between mitochondrial function and the evolution of allometric scaling in ectotherms.
“…Increased expression of avUCP in cold-acclimated ducklings [24], chickens [25] and king penguins [26] has been demonstrated. Moreover, we also reported the negative correlation between avUCP content and mitochondrial superoxide production in chicken skeletal muscle during acute heat stress [27].…”
Little is known about the precise physiological roles of uncoupling protein 1 (UCP1) homologs (UCP2, UCP3, avian UCP) whose levels are up-regulated during fasting. UCPs in skeletal muscle are thought to play a role in the regulation of lipids as fuel substrates, and/or in controlling the production of reactive oxygen species (ROS). The aim of this investigation, using skeletal muscle from fasted chickens, was to examine alterations in the expression of genes encoding for avian UCP and key enzymes relevant to lipid flux across the mitochondrial b-oxidation pathway. We also clarified whether an increase in avUCP content could be associated with altered ROS production by mitochondria. Transcription levels of avUCP and CPT-I genes were increased 7.7-and 9.5-fold after a 24 h fast and slightly diminished but remained about 5.0-and 7.7-fold higher than baseline levels, respectively, after 48 h of fasting. In contrast, members of the b-oxidation pathway, LCAD and 3HADH, were gradually up-regulated from 12 to 48 h of fasting. This suggests that processes involved in the transfer and oxidation of fatty acids are up-regulated differently during the initial stage of fasting. Analysis of ROS production by lucigenin-derived chemiluminescence showed that the FFA-sensitive portion of carboxyatractyloside-upregulated ROS production was greater in skeletal muscle mitochondria from 24 h-fasted chickens compared with control, which leads us to postulate that ROS production is potentially down-regulated by UCP. The possible involvement of a backlog of fatty acid for oxidation, observed in chickens after a 24 h fast, in a transmembrane gradient of free non-oxidized fatty acids is also discussed.
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