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1
RAIMBAULT, Serge, Sami DRIDI, Frédérique DENJEAN, Joël LACHUER, Elodie COUPLAN, Frédéric BOUILLAUD, André BORDAS, Claude DUCHAMP, Mohamed TAOUIS, and Daniel RICQUIER. "An uncoupling protein homologue putatively involved in facultative muscle thermogenesis in birds." Biochemical Journal 353, no. 3 (January 25, 2001): 441–44. http://dx.doi.org/10.1042/bj3530441.
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The cDNA of an uncoupling protein (UCP) homologue was obtained by screening a chicken skeletal-muscle library. The predicted 307-amino-acid sequence of avian UCP (avUCP) is 55, 70, 70 and 46% identical with mammalian UCP1, UCP2 and UCP3 and plant UCP respectively. avUCP mRNA expression is restricted to skeletal muscle and its abundance was increased 1.3-fold in a chicken line showing diet-induced thermogenesis, and 3.6- and 2.6-fold in cold-acclimated and glucagon-treated ducklings developing muscle non-shivering thermogenesis respectively. The present data support the implication of avUCP in avian energy expenditure.
2
Schwartz, Tonia S., Shauna Murray, and Frank Seebacher. "Novel reptilian uncoupling proteins: molecular evolution and gene expression during cold acclimation." Proceedings of the Royal Society B: Biological Sciences 275, no. 1637 (January 29, 2008): 979–85. http://dx.doi.org/10.1098/rspb.2007.1761.
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Many animals upregulate metabolism in response to cold. Uncoupling proteins (UCPs) increase proton conductance across the mitochondrial membrane and can thereby alleviate damage from reactive oxygen species that may form as a result of metabolic upregulation. Our aim in this study was to determine whether reptiles ( Crocodylus porosus ) possess UCP genes. If so, we aimed to place reptilian UCP genes within a phylogenetic context and to determine whether the expression of UCP genes is increased during cold acclimation. We provide the first evidence that UCP2 and UCP3 genes are present in reptiles. Unlike in other vertebrates, UCP2 and UPC3 are expressed in liver and skeletal muscle of the crocodile, and both are upregulated in liver during cold acclimation but not in muscle. We identified two transcripts of UCP3, one of which produces a truncated protein similar to the UCP3S transcript in humans, and the resulting protein lacks the predicted nucleotide-binding regulatory domain. Our molecular phylogeny suggests that uncoupling protein 1 (UCP1) is ancestral and has been lost in archosaurs. In birds, UCP3 may have assumed a similar function as UCP1 in mammals, which has important ramifications for understanding endothermic heat production.
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Masaki, Takayuki, Hironobu Yoshimatsu, Seiichi Chiba, and Toshiie Sakata. "Impaired response of UCP family to cold exposure in diabetic (db/db) mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 4 (October 1, 2000): R1305—R1309. http://dx.doi.org/10.1152/ajpregu.2000.279.4.r1305.
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Impaired activity of the uncoupling protein (UCP) family has been proposed to promote obesity development. The present study examined differences in UCP responses to cold exposure between leptin-resistance obese ( db/db) mice and their lean (C57Ksj) littermates. Basal UCP1 and UCP3 mRNA expression in brown adipose tissue was lower in obese mice compared with lean mice, but UCP2 expression in white adipose tissue (WAT) was higher. Basal skeletal muscle UCP3 did not change remarkably. The UCP family mRNAs, which were upregulated 12 and 24 h after cold exposure (4°C), were returned to prior levels 12 h after rewarming exposure (21°C) in lean mice. The accelerating effects of cold exposure on the UCP family were impaired in db/db obese mice. Together with these changes, WAT lipoprotein lipase mRNA was downregulated, and the concentration of serum free fatty acid was increased in response to cold exposure in the lean mice but not in db/db obese littermates. The impaired function of the UCP family and diminished lipolysis in response to cold exposure indicate that the reduced lipolytic activity may contribute to the inactivation of the UCP family in db/db obese mice.
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Keller, Patrick A., Lorenz Lehr, Jean-Paul Giacobino, Yves Charnay, Françoise Assimacopoulos-Jeannet, and Natalia Giovannini. "Cloning, ontogenesis, and localization of an atypical uncoupling protein 4 in Xenopus laevis." Physiological Genomics 22, no. 3 (August 11, 2005): 339–45. http://dx.doi.org/10.1152/physiolgenomics.00012.2005.
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Uncoupling protein 1 (UCP1) is the first UCP described. It belongs to the family of mitochondrial carrier proteins and is expressed mainly in brown adipose tissue. Recently, the family of the UCPs has rapidly been growing due to the successive cloning of UCP2, UCP3, UCP4, and UCP5, also called brain mitochondrial carrier protein 1. Phylogenetic studies suggest that UCP1/UCP2/UCP3 on one hand and UCP4/UCP5 on the other hand belong to separate subfamilies. In this study, we report the cloning from a frog Xenopus laevis (Xl) oocyte cDNA library of a novel UCP that was shown, by sequence homology, to belong to the family of ancestral UCP4. This cloning provides a milestone in the gap between Drosophila melanogaster or Caenorhabditis elegans on one hand and mammalian UCP4 on the other. Xl UCP4 is already expressed in the oocyte, being the first UCP described in germ cell lineage. During development, it segregates in the neural cord, and, in the adult, in situ hybridization shows its expression in the neurons and also in the choroid plexus of the brain. By RT-PCR analysis, it was found that Xl UCP4 is present in all the subdivisions of the brain and also that it differs from mammalian UCP4 by a very high relative level of expression in peripheral tissues such as the liver and kidney. The peripheral tissue distribution of Xl UCP4 reinforces the hypothesis that UCP4 might be the ancestral UCP from which other UCPs diverged from.
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Villarroya, Francesc, Roser Iglesias, and Marta Giralt. "PPARs in the Control of Uncoupling Proteins Gene Expression." PPAR Research 2007 (2007): 1–12. http://dx.doi.org/10.1155/2007/74364.
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Uncoupling proteins (UCPs) are mitochondrial membrane transporters involved in the control of energy conversion in mitochondria. Experimental and genetic evidence relate dysfunctions of UCPs with metabolic syndrome and obesity. The PPAR subtypes mediate to a large extent the transcriptional regulation of the UCP genes, with a distinct relevance depending on the UCP gene and the tissue in which it is expressed. UCP1 gene is under the dual control of PPARγand PPARαin relation to brown adipocyte differentiation and lipid oxidation, respectively. UCP3 gene is regulated by PPARαand PPARδin the muscle, heart, and adipose tissues. UCP2 gene is also under the control of PPARs even in tissues in which it is the predominantly expressed UCP (eg, the pancreas and liver). This review summarizes the current understanding of the role of PPARs in UCPs gene expression in normal conditions and also in the context of type-2 diabetes or obesity.
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Monemdjou, Shadi, Leslie P. Kozak, and Mary-Ellen Harper. "Mitochondrial proton leak in brown adipose tissue mitochondria of Ucp1-deficient mice is GDP insensitive." American Journal of Physiology-Endocrinology and Metabolism 276, no. 6 (June 1, 1999): E1073—E1082. http://dx.doi.org/10.1152/ajpendo.1999.276.6.e1073.
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Mice deficient in mitochondrial uncoupling protein (UCP) 1 are cold sensitive, despite abundant expression of the homologues, Ucp2 and Ucp3 (S. Enerbäck, A. Jacobsson, E. M. Simpson, C. Guerra, H. Yamashita, M.-E. Harper, and L. P. Kozak. Nature 387: 90–94, 1997). We have analyzed characteristics of mitochondrial proton leak from brown adipose tissue (BAT) of Ucp1-deficient mice and normal controls and conducted the first top-down metabolic control analysis of oxidative phosphorylation in BAT mitochondria. Because purine nucleotides inhibit UCP1 and because UCP2 and the long form of UCP3 have putative purine nucleotide-binding regions, we predicted that proton leak in BAT mitochondria from Ucp1-deficient mice would be sensitive to GDP. On the contrary, although control over mitochondrial oxygen consumption and proton leak reactions at state 4 are strongly affected by 1 mM GDP in mitochondria from normal mice, there is no effect in UCP1-deficient mitochondria. In the presence of GDP, the overall kinetics of proton leak were not significantly different between Ucp1-deficient mice and controls. In its absence, state 4 respiration in normal BAT mitochondria was double that in its presence. Leak-dependent oxygen consumption was higher over a range of membrane potentials in its absence than in its presence. Thus proton leak, potentially including that through UCP2 and UCP3, is GDP insensitive. However, our measurements were made in the presence of albumin and may not allow for the detection of any fatty acid-induced UCP-mediated leak; this possibility requires investigation.
7
RICQUIER, Daniel, and Frédéric BOUILLAUD. "The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP." Biochemical Journal 345, no. 2 (January 10, 2000): 161–79. http://dx.doi.org/10.1042/bj3450161.
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Animal and plant uncoupling protein (UCP) homologues form a subfamily of mitochondrial carriers that are evolutionarily related and possibly derived from a proton/anion transporter ancestor. The brown adipose tissue (BAT) UCP1 has a marked and strongly regulated uncoupling activity, essential to the maintenance of body temperature in small mammals. UCP homologues identified in plants are induced in a cold environment and may be involved in resistance to chilling. The biochemical activities and biological functions of the recently identified mammalian UCP2 and UCP3 are not well known. However, recent data support a role for these UCPs in State 4 respiration, respiration uncoupling and proton leaks in mitochondria. Moreover, genetic studies suggest that UCP2 and UCP3 play a part in energy expenditure in humans. The UCPs may also be involved in adaptation of cellular metabolism to an excessive supply of substrates in order to regulate the ATP level, the NAD+/NADH ratio and various metabolic pathways, and to contain superoxide production. A major goal will be the analysis of mice that either lack the UCP2 or UCP3 gene or overexpress these genes. Other aims will be to investigate the possible roles of UCP2 and UCP3 in response to oxidative stress, lipid peroxidation, inflammatory processes, fever and regulation of temperature in certain specific parts of the body.
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Mozo, Julien, Yalin Emre, Frederic Bouillaud, Daniel Ricquier, and Francois Criscuolo. "Thermoregulation: What Role for UCPs in Mammals and Birds?" Bioscience Reports 25, no. 3-4 (June 8, 2005): 227–49. http://dx.doi.org/10.1007/s10540-005-2887-4.
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Mammals and birds are endotherms and respond to cold exposure by the means of regulatory thermogenesis, either shivering or non-shivering. In this latter case, waste of cell energy as heat can be achieved by uncoupling of mitochondrial respiration. Uncoupling proteins, which belong to the mitochondrial carrier family, are able to transport protons and thus may assume a thermogenic function. The mammalian UCP1 physiological function is now well understood and gives to the brown adipose tissue the capacity for heat generation. But is it really the case for its more recently discovered isoforms UCP2 and UCP3? Additionally, whereas more and more evidence suggests that non-shivering also exists in birds, is the avian UCP also involved in response to cold exposure? In this review, we consider the latest advances in the field of UCP biology and present putative functions for UCP1 homologues.
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Viengchareun, Say, Patrice Penfornis, Maria-Christina Zennaro, and Marc Lombès. "Mineralocorticoid and glucocorticoid receptors inhibit UCP expression and function in brown adipocytes." American Journal of Physiology-Endocrinology and Metabolism 280, no. 4 (April 1, 2001): E640—E649. http://dx.doi.org/10.1152/ajpendo.2001.280.4.e640.
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Uncoupling proteins (UCP), specific mitochondrial proton transporters that function by uncoupling oxidative metabolism from ATP synthesis, are involved in thermoregulation and control of energy expenditure. The hibernoma-derived T37i cells, which possess functional endogenous mineralocorticoid receptors (MR), can undergo differentiation into brown adipocytes. In differentiated T37i cells, UCP1 mRNA levels increased 10- to 20-fold after retinoic acid or β-adrenergic treatment. Interestingly, UCP2 and UCP3 mRNA was also detected. Aldosterone treatment induced a drastic decrease in isoproterenol- and retinoic acid-stimulated UCP1 mRNA levels in a time- and dose-dependent manner (IC50≈ 1 nM aldosterone). This inhibition was unaffected by cycloheximide and did not modify UCP1 mRNA stability (half-life time = 5 h), indicating that it occurs at the transcriptional level. It involves both the MR and/or the glucocorticoid receptor (GR), depending on the retinoic or catecholamine induction pathway. Basal UCP3 expression was also significantly reduced by aldosterone, whereas UCP2 mRNA levels were not modified. Finally, as demonstrated by JC1 aggregate formation in living cells, aldosterone restored mitochondrial membrane potential abolished by isoproterenol or retinoic acid. Our results demonstrate that MR and GR inhibit expression of UCP1 and UCP3, thus participating in the control of energy expenditure.
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Klingenberg, M., E. Winkler, and K. Echtay. "Uncoupling protein, H+ transport and regulation." Biochemical Society Transactions 29, no. 6 (November 1, 2001): 806–11. http://dx.doi.org/10.1042/bst0290806.
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The biochemical functions of uncoupling proteins (UCPs) are discussed with the view of UCP1 as a paradigm. In contrast with UCP1, the heterologous expression of UCP3 in yeast is found to result primarily in extra-mitochondrial deposits and thus is unsuitable for studying UCP3 function. On expression in Escherichia coli inclusion bodies, UCPs extracted and incorporated into vesicles showed no H+ transport, only Cl– transport. Only after addition of coenzyme Q was fully nucleotide-sensitive high-H+ transport reconstituted, with UCP1 as well as with UCP2 and UCP3. The newly discovered cofactor role of coenzyme Q in H+ transport is proposed to imply co-operation with fatty acids for the injection of H+ into the UCP channel.
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Yu, Xing Xian, Jamie L. Barger, Bert B. Boyer, Martin D. Brand, Guohua Pan, and Sean H. Adams. "Impact of endotoxin on UCP homolog mRNA abundance, thermoregulation, and mitochondrial proton leak kinetics." American Journal of Physiology-Endocrinology and Metabolism 279, no. 2 (August 1, 2000): E433—E446. http://dx.doi.org/10.1152/ajpendo.2000.279.2.e433.
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Linking tissue uncoupling protein (UCP) homolog abundance with functional metabolic outcomes and with expression of putative genetic regulators promises to better clarify UCP homolog physiological function. A murine endotoxemia model characterized by marked alterations in thermoregulation was employed to examine the association between heat production, UCP homolog expression, and mitochondrial proton leak (“uncoupling”). After intraperitoneal lipopolysaccharide (LPS, ∼6 mg/kg) injection, colonic temperature (Tc) in adult female C57BL6/J mice dropped to a nadir of ∼30°C by 8 h, preceded by a four- to fivefold drop in liver UCP2 and UCP5/brain mitochondrial carrier protein 1 mRNA levels, with no change in their hindlimb skeletal muscle (SKM) expression. SKM UCP3 mRNA rose fivefold during development of hypothermia and was correlated with an LPS-induced increase in plasma free fatty acid concentration. UCP2 and UCP5 transcripts recovered about three- to sixfold in both tissues starting at 6–8 h, preceding a recovery of Tc between 16 and 24 h. SKM UCP3 followed an opposite pattern. Such results are not consistent with an important influence of UCP3 in driving heat production but do not preclude a role for UCP2 or UCP5 in this process. The transcription coactivator PGC-1 displayed a transient LPS-evoked rise (threefold) or drop (two- to fivefold) in SKM and liver expression, respectively. No differences between control and LPS-treated mouse liver or SKM in vitro mitochondrial proton leak were evident at time points corresponding to large differences in UCP homolog expression.
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VIANNA, CLAUDIA R., THILO HAGEN, CHEN-YU ZHANG, ERIC BACHMAN, OLIVIER BOSS, BALAZS GEREBEN, ANSELMO S. MORISCOT, BRADFORD B. LOWELL, JOSÉ EDUARDO P. W. BICUDO, and ANTONIO C. BIANCO. "Cloning and functional characterization of an uncoupling protein homolog in hummingbirds." Physiological Genomics 5, no. 3 (April 2, 2001): 137–45. http://dx.doi.org/10.1152/physiolgenomics.2001.5.3.137.
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The cDNA of an uncoupling protein (UCP) homolog has been cloned from the swallow-tailed hummingbird, Eupetomena macroura. The hummingbird uncoupling protein (HmUCP) cDNA was amplified from pectoral muscle (flight muscle) using RT-PCR and primers for conserved domains of various known UCP homologs. The rapid amplification of cDNA ends (RACE) method was used to complete the cloning of the 5′ and 3′ ends of the open reading frame. The HmUCP coding region contains 915 nucleotides, and the deduced protein sequence consists of 304 amino acids, being ∼72, 70, and 55% identical to human UCP3, UCP2, and UCP1, respectively. The uncoupling activity of this novel protein was characterized in yeast. In this expression system, the 12CA5-tagged HmUCP fusion protein was detected by Western blot in the enriched mitochondrial fraction. Similarly to rat UCP1, HmUCP decreased the mitochondrial membrane potential as measured in whole yeast by uptake of the fluorescent potential-sensitive dye 3′,3-dihexyloxacarbocyanine iodide. The HmUCP mRNA is primarily expressed in skeletal muscle, but high levels can also be detected in heart and liver, as assessed by Northern blot analysis. Lowering the room’s temperature to 12–14°C triggered the cycle torpor/rewarming, typical of hummingbirds. Both in the pectoral muscle and heart, HmUCP mRNA levels were 1.5- to 3.4-fold higher during torpor. In conclusion, this is the first report of an UCP homolog in birds. The data indicate that HmUCP has the potential to function as an UCP and could play a thermogenic role during rewarming.
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Boyer, Bert B., Brian M. Barnes, Bradford B. Lowell, and Danica Grujic. "Differential regulation of uncoupling protein gene homologues in multiple tissues of hibernating ground squirrels." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 4 (October 1, 1998): R1232—R1238. http://dx.doi.org/10.1152/ajpregu.1998.275.4.r1232.
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Nonshivering thermogenesis in brown adipose tissue (BAT) provides heat through activation of a mitochondrial uncoupling protein (UCP1), which causes futile electron transport cycles without the production of ATP. Recent discovery of two molecular homologues, UCP2, expressed in multiple tissues, and UCP3, expressed in muscle, has resulted in investigation of their roles in thermoregulatory physiology and energy balance. To determine the expression pattern of Ucp homologues in hibernating mammals, we compared relative mRNA levels of Ucp1, -2, and -3 in BAT, white adipose tissue (WAT), and skeletal muscle of arctic ground squirrels ( Spermophilus parryii) hibernating at different ambient and body temperatures, with levels determined in tissues from ground squirrels not in hibernation. Here we report significant increases in mRNA levels for Ucp2 in WAT (1.6-fold) and Ucp3 in skeletal muscle (3-fold) during hibernation. These results indicate the potential for a role of UCP2 and UCP3 in thermal homeostasis during hibernation and indicate that parallel mechanisms and multiple tissues could be important for nonshivering thermoregulation in mammals.
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Barger, Jamie L., Brian M. Barnes, and Bert B. Boyer. "Regulation of UCP1 and UCP3 in arctic ground squirrels and relation with mitochondrial proton leak." Journal of Applied Physiology 101, no. 1 (July 2006): 339–47. http://dx.doi.org/10.1152/japplphysiol.01260.2005.
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Uncoupling protein (UCP) 1 (UCP1) catalyzes a proton leak in brown adipose tissue (BAT) mitochondria that results in nonshivering thermogenesis (NST), but the extent to which UCP homologs mediate NST in other tissues is controversial. To clarify the role of UCP3 in mediating NST in a hibernating species, we measured Ucp3 expression in skeletal muscle of arctic ground squirrels in one of three activity states (not hibernating, not hibernating and fasted for 48 h, or hibernating) and housed at 5°C or −10°C. We then compared Ucp3 mRNA levels in skeletal muscle with Ucp1 mRNA and UCP1 protein levels in BAT in the same animals. Ucp1 mRNA and UCP1 protein levels were increased on cold exposure and decreased with fasting, with the highest UCP1 levels in thermogenic hibernators. In contrast, Ucp3 mRNA levels were not affected by temperature but were increased 10-fold during fasting and >3-fold during hibernation. UCP3 protein levels were increased nearly fivefold in skeletal muscle mitochondria isolated from fasted squirrels compared with nonhibernators, but proton leak kinetics in the presence of BSA were unchanged. Proton leak in BAT mitochondria also did not differ between fed and fasted animals but did show classical inhibition by the purine nucleotide GDP. Levels of nonesterified fatty acids were highest during hibernation, and tissue temperatures during hibernation were related to Ucp1, but not Ucp3, expression. Taken together, these results do not support a role for UCP3 as a physiologically relevant mediator of NST in muscle.
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Mozo, Julien, Gilles Ferry, Aurélie Studeny, Claire Pecqueur, Marianne Rodriguez, Jean A. Boutin, and Frédéric Bouillaud. "Expression of UCP3 in CHO cells does not cause uncoupling, but controls mitochondrial activity in the presence of glucose." Biochemical Journal 393, no. 1 (December 12, 2005): 431–39. http://dx.doi.org/10.1042/bj20050494.
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The proton-transport activity of UCP1 (uncoupling protein 1) triggers mitochondrial uncoupling and thermogenesis. The exact role of its close homologues, UCP2 and UCP3, is unclear. Mounting evidence associates them with the control of mitochondrial superoxide production. Using CHO (Chinese-hamster ovary) cells stably expressing UCP3 or UCP1, we found no evidence for respiration uncoupling. The explanation lies in the absence of an appropriate activator of UCP protonophoric function. Accordingly, the addition of retinoic acid uncouples the respiration of the UCP1-expressing clone, but not that of the UCP3-expressing ones. In a glucose-containing medium, the extent of the hyperpolarization of mitochondria by oligomycin was close to 22 mV in the five UCP3-expressing clones, contrasting with the variable values observed with the 15 controls. Our observations suggest that, when glycolysis and mitochondria generate ATP, and in the absence of appropriate activators of proton transport, UCPs do not transport protons (uncoupling), but rather other ions of physiological relevance that control mitochondrial activity. A model is proposed using the known passive transport of pyruvate by UCP1.
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Villarroya, F., S. Brun, M. Giralt, Y. Cámara, G. Solanes, and R. Iglesias. "Gene expression of leptin and uncoupling proteins: molecular end-points of fetal development." Biochemical Society Transactions 29, no. 2 (May 1, 2001): 76–80. http://dx.doi.org/10.1042/bst0290076.
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Uncoupling proteins (UCPs) are considered to be major determinants of energy expenditure in mammals. During development in rodents, the expression of the UCP genes occurs sequentially. UCP2 mRNA is expressed long before birth. UCP1 mRNA expression in brown adipose tissue (BAT) starts in the late fetal period, and the expression of UCP3 mRNA begins immediately after birth in BAT and skeletal muscle. The postnatal induction of UCP1 gene expression is due mainly to cold stimuli, whereas the switch-on of UCP3 mRNA expression after birth requires the stimulus of food intake, specifically of lipids in the mother's milk. However, UCP3 mRNA expression after birth is also highly sensitive to leptin, and administration of a single injection of leptin to neonatal mice that were not allowed to suckle partly mimicked the natural induction of UCP3 gene expression in BAT and skeletal muscle. The speed of the effects of leptin on UCP3 mRNA expression suggests a direct action on skeletal muscle and BAT. The injection of leptin produced minor effects on UCP1 mRNA expression, and no effects were observed on UCP2 mRNA. In summary, leptin appears to contribute to the regulation of UCP3 gene expression in the perinatal period. Whatever the mechanism of action of leptin in BAT and skeletal muscle, it is already functional at birth.
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Boschini, Renata Polessi, and Jair Rodrigues Garcia Júnior. "Regulação da expressão gênica das UCP2 e UCP3 pela restrição energética,jejum e exercício físico." Revista de Nutrição 18, no. 6 (December 2005): 753–64. http://dx.doi.org/10.1590/s1415-52732005000600006.
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O tecido adiposo marrom, onde se localiza a proteína desacopladora 1 (UCP1 - uncoupling protein 1), é um tecido termogênico presente somente nos pequenos mamíferos e neonatos, com função de manter temperatura e peso corporal estáveis quando da exposição ao frio ou consumo de dietas hipercalóricas. Como a UCP1 está localizada exclusivamente no tecido adiposo marrom, tecido pouco expressado em adultos, os estudos dão ênfase às proteínas desacopladoras 2 e 3 (UCP2 e UCP3), proteínas homólogas à UCP1, expressas em múltiplos tecidos e nos músculos esqueléticos, respectivamente. A atividade física provoca aumento do RNAm da UCP2 e UCP3, questiona-se, porém, se este aumento é devido a mudanças no metabolismo de gordura ou a mudanças no metabolismo energético. Durante a restrição energética ou jejum, há depleção de gordura corporal e aumento da concentração plasmática de ácidos graxos livres, com regulação positiva da UCP2 e da UCP3 no músculo e aumento da oxidação lipídica. A concentração elevada de ácidos graxos representa sinal intracelular importante na indução da expressão das UCP no músculo, o que pode estar ligado à sua utilização como combustível até que ocorra aumento da demanda do organismo para dissipação da energia. No entanto, discute-se se a UCP2 e a UCP3 no músculo esquelético têm como função mediar a termogênese ou regular a oxidação de lipídios.
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Shigematsu, Mei, Tomoya Yamada, Yun Yi Wong, Yohei Kanamori, Masaru Murakami, Yusuke Fujimoto, Mika Suzuki, et al. "Dietary regulation of Ucp2 and Ucp3 expressions in white adipose tissues of beef cattle." Canadian Journal of Animal Science 96, no. 4 (December 1, 2016): 457–60. http://dx.doi.org/10.1139/cjas-2016-0020.
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Expression of uncoupling protein (Ucp) 2 but not Ucp3 in subcutaneous fat was significantly higher in cattle fed the concentrate diet than in those fed the roughage diet. Ucp2 expression in mesenteric fat was higher in cattle fed the vitamin A-deficient diet than in those fed the control diet.
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Jastroch, Martin, Sven Wuertz, Werner Kloas, and Martin Klingenspor. "Uncoupling protein 1 in fish uncovers an ancient evolutionary history of mammalian nonshivering thermogenesis." Physiological Genomics 22, no. 2 (July 14, 2005): 150–56. http://dx.doi.org/10.1152/physiolgenomics.00070.2005.
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Uncoupling proteins (UCPs) increase proton leakage across the inner mitochondrial membrane. Thereby, UCP1 in brown adipose tissue dissipates proton motive force as heat. This mechanism of nonshivering thermogenesis is considered as a monophyletic trait of endothermic placental mammals that emerged about 140 million years ago and provided a crucial advantage for life in the cold. The paralogues UCP2 and UCP3 are probably not thermogenic proteins but convey mild uncoupling, which may serve to reduce the rate of mitochondrial reactive oxygen species production. Both are present in endotherms (mammals and birds), but so far only UCP2 has been identified in ectothermic vertebrates (fish and amphibia). The evolution of UCPs is of general interest in the search for the origin of mammalian UCP1-mediated nonshivering thermogenesis. We here show the presence of UCP1 and UCP3 in ectothermic teleost fish species using comparative genomics, phylogenetic inference, and gene expression analysis. In the common carp ( Cyprinus carpio), UCP1 is predominantly expressed in the liver and strongly diminished in response to cold exposure, thus contrasting the cold-induced expression of mammalian UCP1 in brown adipose tissue. UCP3 mRNA is only found in carp skeletal muscle with expression levels increased fivefold in response to fasting. Our findings disprove the monophyletic nature of UCP1 in placental mammals and demonstrate that all three members of the core UCP family were already present before the divergence of ray-finned and lobe-finned vertebrate lineages about 420 million years ago.
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Lengacher, Sylvain, Pierre J. Magistretti, and Luc Pellerin. "Quantitative RT-PCR Analysis of Uncoupling Protein Isoforms in Mouse Brain Cortex: Methodological Optimization and Comparison of Expression with Brown Adipose Tissue and Skeletal Muscle." Journal of Cerebral Blood Flow & Metabolism 24, no. 7 (July 2004): 780–88. http://dx.doi.org/10.1097/01.wcb.0000122743.72175.52.
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Uncoupling proteins (UCPs) present in the inner mitochondrial membrane are involved in uncoupling respiration from ATP synthesis. Five UCP isoforms have been identified but information about their presence and level of expression in the central nervous system remains incomplete. To determine the nature and proportion of UCP isoform mRNAs present in brain cortex, we developed and optimized a specific quantitative reverse-transcription polymerase chain reaction procedure. Optimal range of RNA concentrations to be used in the reverse-transcriptase reaction was determined. Primer design and concentration were optimized for each target gene while polymerase chain reaction efficiency was assessed for a range of reverse-transcriptase dilutions. Genomic contribution to the quantitative signal was evaluated for each isoform and minimized. Three reference genes were tested for normalization, and β-actin was found to be the most stable among tissues. Results indicate that brain cortex contains significant amounts of all UCP mRNAs, with UCP5 and UCP4 being the most abundant, as opposed to brown adipose tissue and skeletal muscle, which predominantly express UCP1 and UCP3, respectively. These data provide a first quantitative assessment of UCP mRNA expression in mouse brain, showing the presence of all five isoforms with distinct proportions, thus suggesting specific roles in the central nervous system.
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Bui, Linh Le Thuc. "Independence principle and its exception in letter of credit law: Suggestions for Vietnam." Science & Technology Development Journal - Economics - Law and Management 4, no. 4 (October 4, 2020): First. http://dx.doi.org/10.32508/stdjelm.v4i4.591.
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Even though the letter of credit was invented from a long time ago, however, its legal personalities are very new to the Vietnam Legal Framework. The International Chamber of Commerce (``ICC'') has issued principles for the documentary credit which is the Uniform of Customs and Practice (``UCP'') since 1933 and kept updating it until now, the latest version of UCP is UCP 600 which is presented in 2007. However, the UCP has not systematized many aspects of documentary credit yet and ICC considered those problems as subjects of domestic regulations. The diversification in different national laws leads to confusion thus causing many problems to merchants in international trade. Some countries do not have specified codifications to regulate the letter of credit so these countries treat UCP as ``quasi-law'' while other countries have their own legal framework for letter of credit law and even have fraud rules included. It is quite interesting that the United States which is a common law country is the first country to embody the operation of letter of credit in the Uniform of Commercial Code (``UCC'') and regulates the fraud rule within the same Code. This paper will try to explain and compare the principle of independence in the UCP and UCC, clarify the definition and regulations of fraud rule in UCC and evaluate the legal regulations of Vietnam law for the independence principle in a letter of credit.
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Borecký, Jirí, Ivan G. Maia, and Paulo Arruda. "Mitochondrial Uncoupling Proteins in Mammals and Plants." Bioscience Reports 21, no. 2 (April 1, 2001): 201–12. http://dx.doi.org/10.1023/a:1013604526175.
Full textAbstract:
Uncoupling proteins (UCPs) belong to a distinct cluster of the mitochondrial anion carrier family. Up to five different uncoupling protein types were found in mitochondria of mammals and plants, and recently in fishes, fungi and protozoa. They exhibit a significantly conserved structure with several motifs specific to either the whole cluster or protein type. Uncoupling proteins, as well as the whole mitochondrial anion carrier gene family, probably emerged in evolution before the separation of animal, fungi, and plant kingdoms and originate from an anion/nucleotide or anion/anion transporter ancestor. Mammalian UCP1, UCP2, UCP3, and plant uncoupling proteins pUCP1 and pUCP2 are similar and seem to form one subgroup, whereas UCP4 and BMCP1 belong to a different group. Molecular, biochemical, and phylogenic data suggest that UCP2 could be considered as an UCP-prototype. UCP1 plays its biological role mainly in the non-shivering thermogenesis while the role of the other types is unknown. However, hypotheses have suggested that they are involved in the general balance of basic energy expenditure, protection from reactive oxygen species, and, in plants, in fruit ripening and seed ontogeny.
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Kotz, Catherine M., Chuanfeng Wang, Allen S. Levine, and Charles J. Billington. "Urocortin in the hypothalamic PVN increases leptin and affects uncoupling proteins-1 and -3 in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 2 (February 1, 2002): R546—R551. http://dx.doi.org/10.1152/ajpregu.00436.2001.
Full textAbstract:
The hypothalamic paraventricular nucleus (PVN) plays a primary role in energy homeostasis, and urocortin (UCN) decreases feeding after injection into the PVN. Peripheral uncoupling proteins (UCPs) may influence energy metabolism. The effect of UCN administered into the PVN on UCPs is unknown. We injected PVN-cannulated rats with either UCN (200 pmol) or artificial cerebrospinal fluid (aCSF) at 0800, 2000, and again at 0800. An aCSF-injected group with food intake restricted to the level of UCN-treated animals was included to control for decreased feeding in the UCN-treated rats. Two hours after the final set of injections, rats were killed, and white adipose tissue, brown adipose tissue, and biceps femoris and acromiotrapezius muscle tissues were taken for analysis of UCP-1, -2, and -3. Trunk blood was collected for measurement of plasma leptin. Relative to food-restricted control animals, UCN in the PVN significantly increased plasma leptin and UCP-1 mRNA in brown adipose tissue and decreased UCP-3 mRNA in acromiotrapezius muscle, suggesting a role for PVN UCN in the regulation of energy balance.
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Dulloo, Abdul G., and Sonia Samec. "Uncoupling proteins: their roles in adaptive thermogenesis and substrate metabolism reconsidered." British Journal of Nutrition 86, no. 2 (August 2001): 123–39. http://dx.doi.org/10.1079/bjn2001412.
Full textAbstract:
During the past few years, there have been two major developments, if not revolutions, in the field of energy balance and weight regulation. The first at the molecular level, which was catalysed by developments in DNA screening technology together with the mapping of the human genome, has been the tremendous advances made in the identification of molecules that play a role in the control of food intake and metabolic rate. The second, at the systemic level, which centered upon the use of modern technologies or more robust analytical techniques for assessing human energy expenditure in response to starvation and overfeeding, has been the publication of several papers providing strong evidence that adaptive thermogenesis plays a much more important role in the regulation of body weight and body composition than previously thought. Within these same few years, several new members of the mitochondrial carrier protein family have been identified in a variety of tissues and organs. All apparently possess uncoupling properties in genetically-modified systems, with two of them (uncoupling protein (UCP) 2 and UCP3) being expressed in adipose tissues and skeletal muscles, which are generally recognised as important sites for variations in thermogenesis and/or in substrate oxidation. Considered as breakthrough discoveries, the cloning of these genes has generated considerable optimism for rapid advances in our molecular understanding of adaptive thermogenesis, and for the identification of new targets for pharmacological management of obesity and cachexia. The present paper traces first, from a historical perspective, the landmark events in the field of thermogenesis that led to the identification of these genes encoding candidate UCP, and then addresses the controversies and on-going debate about their physiological importance in adaptive thermogenesis, in lipid oxidation or in oxidative stress. The general conclusion is that UCP2 and UCP3 may have distinct primary functions, with UCP3 implicated in regulating the flux of lipid substrates across the mitochondria and UCP2 in the control of mitochondrial generation of reactive oxygen species. The distinct functions of these two UCP1 homologues have been incorporated in a conceptual model to illustrate how UCP2 and UCP3 may act in concert in the overall regulation of lipid oxidation concomitant to the prevention of lipid-induced oxidative damage.
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Xiao, Xiao Qiu, Kevin L. Grove, Bernadette E. Grayson, and M. Susan Smith. "Inhibition of Uncoupling Protein Expression during Lactation: Role of Leptin." Endocrinology 145, no. 2 (February 1, 2004): 830–38. http://dx.doi.org/10.1210/en.2003-0836.
Full textAbstract:
Abstract Uncoupling proteins (UCPs) are mitochondrial proteins that play a role in regulation of energy expenditure by uncoupling respiration from ATP synthesis. Lactation is a physiological condition characterized by negative energy balance due to the loss of energy sources to the production of milk. The objective of the current study was to investigate whether UCP mRNA and protein expressions were altered during lactation compared with those after 48 h of fasting. Lactation significantly reduced serum leptin levels, and removal of pups for 48 h increased serum leptin to higher levels than those observed in control rats. Compared with control rats, mRNA expression of UCP1 and UCP3 in brown adipose tissue (BAT) was dramatically reduced during lactation and fasting. The reduction in mRNAs was reflected by a lowered UCP1 protein level, and to some extent, UCP3 protein. Treatment of lactating rats with exogenous leptin (3 mg/kg) or removal of pups for 48 h completely reversed the down-regulation of UCP1 and UCP3 mRNA expression in BAT, and pup removal led to a recovery of protein expression. In contrast to BAT, UCP3 expression in skeletal muscle was increased in fasted rats and decreased during lactation. Similar changes were observed in serum free fatty acid levels. These changes are consistent with the idea that the utilization of free fatty acids as a fuel source is spared during lactation. As in BAT, leptin treatment and removal of pups were able to restore changes in mRNA expression of UCP3 in skeletal muscle during lactation. The present results suggest that the inhibition of leptin secretion during lactation is involved in the down-regulation of UCP expression in BAT and skeletal muscle, which, in turn, is responsible for the decrease in metabolic fuel oxidation and thermogenesis.
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Gnanalingham, M. G., D. A. Giussani, P. Sivathondan, A. J. Forhead, T. Stephenson, M. E. Symonds, and D. S. Gardner. "Chronic umbilical cord compression results in accelerated maturation of lung and brown adipose tissue in the sheep fetus during late gestation." American Journal of Physiology-Endocrinology and Metabolism 289, no. 3 (September 2005): E456—E465. http://dx.doi.org/10.1152/ajpendo.00053.2005.
Full textAbstract:
Umbilical cord compression (UCC) sufficient to reduce umbilical blood flow by 30% for 3 days, results in increased fetal plasma cortisol and catecholamines that are likely to promote maturation of the fetal lung and brown adipose tissue (BAT). We determined the effect of UCC on the abundance of uncoupling protein (UCP)1 (BAT only) and -2, glucocorticoid receptor (GR), and 11β-hydroxysteroid dehydrogenase (11β-HSD)1 and -2 mRNA, and mitochondrial protein voltage-dependent anion channel (VDAC) and cytochrome c in these tissues. At 118 ± 2 days of gestation (dGA; term ∼145 days), 14 fetuses were chronically instrumented. Eight fetuses were then subjected to 3 days of UCC from 125 dGA, and the remaining fetuses were sham operated. All fetuses were then exposed to two 1-h episodes of hypoxemia at 130 ± 1 and 134 ± 1 dGA before tissue sampling at 137 ± 2 dGA. In both tissues, UCC upregulated UCP2 and GR mRNA, plus VDAC and cytochrome c mitochondrial proteins. In lung, UCC increased 11β-HSD1 mRNA but decreased 11β-HSD2 mRNA abundance, a pattern reversed for BAT. UCC increased UCP1 mRNA and its translated protein in BAT. UCP2, GR, 11β-HSD1 and -2 mRNA, plus VDAC and cytochrome c protein abundance were all significantly correlated with fetal plasma cortisol and catecholamine levels, but not thyroid hormone concentrations, in the lung and BAT of UCC fetuses. In conclusion, chronic UCC results in precocious maturation of the fetal lung and BAT mitochondria, an adaptation largely mediated by the surge in fetal plasma cortisol and catecholamines that accompanies UCC.
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Pearce, S., A. Mostyn, M. C. Alves-Guerra, C. Pecqueur, B. Miroux, R. Webb, T. Stephenson, and M. E. Symonds. "Prolactin, prolactin receptor and uncoupling proteins during fetal and neonatal development." Proceedings of the Nutrition Society 62, no. 2 (May 2003): 421–27. http://dx.doi.org/10.1079/pns2003246.
Full textAbstract:
Uncoupling proteins (UCP) 1 and 2 are members of the subfamily of inner mitochondrial membrane carriers. UCP1 is specific to brown adipose tissue (BAT), where it is responsible for the rapid production of heat at birth. In fetal sheep UCP1 is first detectable at approximately 900d of gestation; its abundance increases with gestational age and peaks at the time of birth. The mRNA and protein for both the long and short form of the prolactin (PRL) receptor (PRLR) are also highly abundant in BAT. Enhanced PRLR abundance in late gestation is associated with an increase in the abundance of UCP1. This relationship between PRLR and UCP is not only present in BAT. Similar findings are now reported in the pregnant ovine uterus, where PRLR abundance reaches a maximum just before that of UCP2. However, the role of PRLR in BAT remains undetermined. Rat studies have shown that PRL administration throughout pregnancy results in offspring with increased UCP1 at birth. Studies in newborn lambs have shown that administration of PRL (20mg/d) causes an acute response, increasing colonic temperature in the first hour by 1°. This increased colonic temperature is maintained for the first 240h of life, in conjunction with enhanced lipolysis. After 70d of treatment there is no difference in the abundance of UCP1 but an increase in UCP1 activity; this effect may be mediated by an increase in lipolysis. Taken together these findings suggest that PRL could be an important endocrine factor during pregnancy and early postnatal life.
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KRATKY, Dagmar, Juliane G. STRAUSS, and Rudolf ZECHNER. "Tissue-specific activity of lipoprotein lipase in skeletal muscle regulates the expression of uncoupling protein 3 in transgenic mouse models." Biochemical Journal 355, no. 3 (April 24, 2001): 647–52. http://dx.doi.org/10.1042/bj3550647.
Full textAbstract:
Uncoupling protein (UCP)-2 and UCP-3 are two recently discovered proteins similar to UCP-1, which regulates thermogenesis in brown adipose tissue (BAT). Whereas UCP-1 expression is restricted to BAT, UCP-2 is widely expressed. UCP-3 is found mainly in skeletal muscle and BAT. A large body of evidence exists that the expression of UCP-2 and UCP-3 in skeletal muscle of mice is regulated by feeding/fasting, and some studies have suggested that this effect might be caused by the changing concentration of plasma non-esterified fatty acids (NEFAs). In an attempt to determine whether the increased import of triacylglycerol-derived NEFAs can also affect UCP expression, we determined the mRNA levels of UCP-1, UCP-2 and UCP-3 in BAT and muscle of induced mutant mouse lines that overexpressed or lacked lipoprotein lipase (LPL) in these tissues. The expression levels of UCP-1 and UCP-2 in BAT and in skeletal and cardiac muscle respectively were not affected by variations in tissue LPL activities. In contrast, UCP-3 mRNA levels were induced 3.4-fold in mice with high levels of LPL in skeletal muscle, and down-regulated in mice that lacked LPL in skeletal muscle. The presence or absence of LPL in BAT had no effect on UCP-3 expression levels. The response of UCP-3 mRNA expression to variations in LPL activity in skeletal muscle was independent of the feeding status or of plasma NEFA concentrations. These findings indicated that NEFAs as lipolytic products of LPL-mediated triacylglycerol hydrolysis markedly affect UCP-3 expression and that increased LPL activities occurring during fasting in skeletal muscle contribute to the induction of UCP-3 expression by promoting the increased uptake of NEFAs. In addition, our results demonstrate that UCP-2 and UCP-3 are differentially regulated in response to LPL-mediated NEFA uptake in skeletal muscle of mice.
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Schrauwen, Patrick. "The role of uncoupling protein 3 in fatty acid metabolism: protection against lipotoxicity?" Proceedings of the Nutrition Society 63, no. 2 (May 2004): 287–92. http://dx.doi.org/10.1079/pns2003336.
Full textAbstract:
The physiological function of the mitochondrial uncoupling protein (UCP), UCP3, is still under debate. There is, however, ample evidence to indicate that, in contrast to UCP1, the primary function of UCP3 is not the dissipation of energy. Rather, several lines of evidence suggest that UCP3 is associated with cellular fatty acid metabolism. The highest levels of expression of UCP3 have been found in type 2 glycolytic muscle fibres, and fasting and high-fat diets up regulate UCP3. This up-regulation is most pronounced in muscle with a low fat oxidative capacity. Acute exercise also up regulates UCP3, and this effect has been shown to be a result of the exercise-induced increase in plasma fatty acid levels. In contrast, regular physical activity, which increases fat oxidative capacity, reduces UCP3 content. Based on these data it has been postulated that UCP3 functions to export those fatty acids that cannot be oxidized from the mitochondrial matrix, in order to prevent fatty acid accumulation inside the matrix. Several experiments have been conducted to test this hypothesis. Blocking carnitine palmitoyltransferase 1, thereby reducing fat oxidative capacity, rapidly induces UCP3. High-fat diets, which increase the mitochondrial supply of fatty acids, also up regulate UCP. However, feeding a similar amount of medium-chain fatty acids, which can be oxidized inside the mitochondrial matrix and therefore does not need to be exported from the matrix, does not affect UCP3 protein levels. In addition, UCP3 is increased in patients with defective β-oxidation and is reduced after restoring oxidative capacity. In conclusion, it is suggested that UCP3 has an important physiological function in facilitating outward transport from the mitochondrial matrix of fatty acid anions that cannot be oxidized, thereby protecting against lipid-induced mitochondrial damage.
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Vidal, Hubert, Dominique Langin, Fabrizio Andreelli, Laurence Millet, Dominique Larrouy, and Martine Laville. "Lack of skeletal muscle uncoupling protein 2 and 3 mRNA induction during fasting in type-2 diabetic subjects." American Journal of Physiology-Endocrinology and Metabolism 277, no. 5 (November 1, 1999): E830—E837. http://dx.doi.org/10.1152/ajpendo.1999.277.5.e830.
Full textAbstract:
Skeletal muscle uncoupling protein 2 and 3 (UCP-2 and UCP-3) mRNA levels are increased during calorie restriction in lean and nondiabetic obese subjects. In this work, we have investigated the effect of a 5-day hypocaloric diet (1,045 kJ/day) on UCP-2 and UCP-3 gene expression in the skeletal muscle of type-2 diabetic obese patients. Before the diet, UCP-2 and UCP-3 mRNA levels were more abundant in diabetic than in nondiabetic subjects. The long (UCP-3L) and short (UCP-3S) forms of UCP-3 transcripts were expressed at similar levels in nondiabetic subjects, but UCP-3S transcripts were twofold more abundant than UCP-3Ltranscripts in the muscle of diabetic patients. Calorie restriction induced a two- to threefold increase in UCP-2 and UCP-3 mRNA levels in nondiabetic patients. No change was observed in type-2 diabetic patients. Variations in plasma nonesterified fatty acid level were positively correlated with changes in skeletal muscle UCP-3L( r = 0.6, P < 0.05) and adipose tissue hormone-sensitive lipase ( r = 0.9, P < 0.001) mRNA levels. Lack of increase in plasma nonesterified fatty acid level and in hormone-sensitive lipase upregulation in diabetic patients during the diet strengthens the hypothesis that fatty acids are associated with the upregulation of uncoupling proteins during calorie restriction.
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Cortright, Ronald N., Donghai Zheng, Jared P. Jones, James D. Fluckey, Stephen E. DiCarlo, Danica Grujic, Bradford B. Lowell, and G. Lynis Dohm. "Regulation of skeletal muscle UCP-2 and UCP-3 gene expression by exercise and denervation." American Journal of Physiology-Endocrinology and Metabolism 276, no. 1 (January 1, 1999): E217—E221. http://dx.doi.org/10.1152/ajpendo.1999.276.1.e217.
Full textAbstract:
The factors that regulate gene expression of uncoupling proteins 2 and 3 (UCP-2 and UCP-3) in skeletal muscle are poorly understood, but both genes are clearly responsive to the metabolic state of the organism. Therefore, we tested the hypothesis that denervation and acute and/or chronic exercise (factors that profoundly affect metabolism) would alter UCP-2 and UCP-3 gene expression. For the denervation studies, the sciatic nerve of rat and mouse hindlimb was sectioned in one leg while the contralateral limb served as control. Northern blot analysis revealed that denervation was associated with a 331% increase ( P < 0.001) in UCP-3 mRNA and a 200% increase ( P < 0.01) in UCP-2 mRNA levels in rat mixed gastrocnemius (MG) muscle. In contrast, denervation caused a 53% decrease ( P< 0.001) in UCP-3 and a 63% increase ( P < 0.01) in UCP-2 mRNA levels in mouse MG. After acute exercise (2-h treadmill running), rat UCP-3 mRNA levels were elevated (vs. sedentary control) 252% ( P < 0.0001) in white gastrocnemius and 63% ( P < 0.05) in red gastrocnemius muscles, whereas UCP-2 levels were unaffected. To a lesser extent, elevations in UCP-3 mRNA (22%; P < 0.01) and UCP-2 mRNA (55%; P < 0.01) levels were observed after acute exercise in the mouse MG. There were no changes in either UCP-2 or UCP-3 mRNA levels after chronic exercise (9 wk of wheel running). These results indicate that acute exercise and denervation regulate gene expression of skeletal muscle UCPs.
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Scarpace, PJ, M. Nicolson, and M. Matheny. "UCP2, UCP3 and leptin gene expression: modulation by food restriction and leptin." Journal of Endocrinology 159, no. 2 (November 1, 1998): 349–57. http://dx.doi.org/10.1677/joe.0.1590349.
Full textAbstract:
To determine the effects of food restriction and leptin administration on several transcripts involved in energy homeostasis, we examined leptin, uncoupling proteins (UCP) 1, 2 and 3, lipoprotein lipase (LPL), beta3-adrenergic receptors (beta3AR) and hormone-sensitive lipase (HSL) mRNA levels in brown adipose tissue (BAT) and epididymal (EWAT) and perirenal (PWAT) white adipose tissue in three groups of rats. The groups were administered leptin for 1 week, or had food restricted to the amount of food consumed by the leptin-treated animals, or had free access to food. Leptin administration increased serum leptin concentrations 50-fold and decreased food consumption by 43%, whereas serum insulin and corticosterone concentrations were unchanged. Leptin increased LPL mRNA by 80%, UCP1 mRNA twofold, and UCP3 mRNA levels by 62% in BAT, and increased UCP2 mRNA levels twofold in EWAT. In contrast, UCP2 mRNA levels were unchanged in PWAT and BAT. In WAT from food-restricted rats, leptin gene expression was diminished by 40% compared with those fed ad libitum. With leptin administration, there was a further 50% decrease in leptin expression. LPL mRNA levels were decreased by food restriction but not by leptin in WAT, whereas beta3AR and HSL mRNA levels were unchanged with either food restriction or leptin treatment. The present study indicates that leptin increases the gene expression of UCP2 in EWAT and that of UCP1, UCP3 and LPL in BAT, whereas reduced food consumption but not leptin, decreases LPL expression in WAT. In addition, with leptin administration there is a decrease in leptin gene expression in WAT, independent of food intake and serum insulin and corticosterone concentrations.
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Ribot, Joan, Maria P. Portillo, Catalina Picó, M. Teresa Macarulla, and Andreu Palou. "Effects of trans-10, cis-12 conjugated linoleic acid on the expression of uncoupling proteins in hamsters fed an atherogenic diet." British Journal of Nutrition 97, no. 6 (June 2007): 1074–82. http://dx.doi.org/10.1017/s0007114507682932.
Full textAbstract:
It is known that conjugated linoleic acid (CLA) feeding decreases body adiposity but the mechanisms involved are not clear. The aim of this study was to analyse whether alterations in uncoupling protein (UCP) expression in white and brown adipose tissues (WAT and BAT, respectively) and in skeletal muscle may be responsible for the effect of trans-10, cis-12 CLA on the size of body fat depots in hamsters. Animals were divided into three groups and fed an atherogenic diet with different amounts of trans-10, cis-12 CLA (0 control, 0·5, or 1 g/100 g diet) for 6 weeks. CLA feeding reduced adipose depot weights, but had no effect on body weight. Leptin mRNA expression decreased in both subcutaneous and perirenal WAT depots, in accordance with lower adiposity, whereas resistin mRNA expression was not changed. Animals fed CLA had lower UCP1 mRNA levels in BAT (both doses of CLA) and in perirenal WAT (the low dose), and lower UCP3 mRNA levels in subcutaneous WAT (the high dose). UCP2 mRNA expression in WAT was not significantly affected by CLA feeding. Animals fed the high dose of CLA showed increased UCP3 and carnitine palmitoyl transferase-I (CPT-I) mRNA expression levels in skeletal muscle. In summary, induction of UCP1 or UCP2 in WAT and BAT is not likely to be responsible for the fat-reduction action of CLA, but the increased expression of UCP3 in skeletal muscle, together with a higher expression of CPT-I, may explain the previously reported effects of dietary CLA in lowering adiposity and increasing fatty acid oxidation by skeletal muscle.
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Bienengraeber, Martin, Karim S. Echtay, and Martin Klingenberg. "H+Transport by Uncoupling Protein (UCP-1) Is Dependent on a Histidine Pair, Absent in UCP-2 and UCP-3†." Biochemistry 37, no. 1 (January 1998): 3–8. http://dx.doi.org/10.1021/bi972463w.
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Armstrong, Michael B., and Howard C. Towle. "Polyunsaturated fatty acids stimulate hepatic UCP-2 expression via a PPARα-mediated pathway." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (December 1, 2001): E1197—E1204. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1197.
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The discovery of homologs of the brown fat uncoupling protein(s) (UCP) UCP-2 and UCP-3 revived the hypothesis of uncoupling protein involvement in the regulation of energy metabolism. Thus we hypothesized that UCP-2 would be regulated in the hepatocyte by fatty acids, which are known to control other energy-related metabolic processes. Treatment with 250 μM palmitic acid was without effect on UCP-2 expression, whereas 250 μM oleic acid exhibited a modest eightfold increase. Eicosapentaenoic acid (EPA), a polyunsaturated fatty acid, exerted a 50-fold upregulation of UCP-2 that was concentration dependent. This effect was seen within 12 h and was maximal by 36 h. Aspirin blocked the induction of UCP-2 by EPA, indicating involvement of the prostaglandin pathway. Hepatocytes treated with arachidonic acid, the immediate precursor to the prostaglandins, also exhibited an aspirin-inhibitable increase in UCP-2 levels, further supporting the involvement of prostaglandins in regulating hepatic UCP-2. The peroxisome proliferator-activated receptor-α (PPARα) agonist Wy-14643 stimulated UCP-2 mRNA levels as effectively as EPA. These data indicate that UCP-2 is upregulated by polyunsaturated fatty acids, potentially through a prostaglandin/PPARα-mediated pathway.
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Kotz, C. M., C. F. Wang, J. E. Briggs, A. S. Levine, and C. J. Billington. "Effect of NPY in the hypothalamic paraventricular nucleus on uncoupling proteins 1, 2, and 3 in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 2 (February 1, 2000): R494—R498. http://dx.doi.org/10.1152/ajpregu.2000.278.2.r494.
Full textAbstract:
Neuropeptide Y (NPY) injected into the hypothalamic paraventricular nucleus (PVN) stimulates feeding and decreases uncoupling protein (UCP)-1 mRNA in brown adipose tissue (BAT). The present studies were undertaken to determine whether UCP-2 in white adipose tissue (WAT) and UCP-3 in muscle are regulated by NPY in the PVN. PVN-cannulated male Sprague-Dawley rats were injected with either saline or NPY (PVN, 117 pmol, 0.5 μl) every 6 h for 24 h. NPY in the PVN stimulated feeding and decreased UCP-1 mRNA in BAT independent of NPY-induced feeding. UCP-2 mRNA in WAT was unchanged by NPY. In acromiotrapezius muscle, NPY decreased UCP-3 mRNA, but this was reversed by restricting food intake to control levels. In biceps femoris muscle, NPY alone had no effect on UCP-3 mRNA, but UCP-3 mRNA was significantly increased in the NPY-treated rats that were restricted to control levels of intake. These results suggest that UCP-2 in WAT and UCP-3 in muscle are not subject to specific regulation by NPY in the PVN.
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Depieri, Tatiane Z., Roberta R. Pinto, Juliana K. Catarin, Magda C. L. de Carli, and Jair R. Garcia Júnior. "UCP-3: regulação da expressão gênica no músculo esquelético e possível relação com o controle do peso corporal." Arquivos Brasileiros de Endocrinologia & Metabologia 48, no. 3 (June 2004): 337–44. http://dx.doi.org/10.1590/s0004-27302004000300003.
Full textAbstract:
As UCPs constituem um subgrupo das proteínas carreadoras mitocondriais que estão localizadas na membrana mitocondrial interna. Por meio da dissipação do gradiente de próton, elas desacoplam a fosforilação oxidativa e convertem combustível em calor. Foram identificadas quatro isoformas da UCP. A UCP-1 foi a primeira a ser descoberta, sendo encontrada exclusivamente no tecido adiposo marrom, a UCP-2 é encontrada em vários tecidos, a UCP-3 encontra-se no músculo esquelético em humanos e tecido adiposo marrom e músculo esquelético em roedores, enquanto a UCP-4 é expressa no cérebro. A expressão da UCP-3 no músculo esquelético e no tecido adiposo marrom pode fazer destes tecidos importantes mediadores da termogênese adaptativa. No entanto, o papel da UCP-3 quanto ao gasto de energia e como causa da obesidade ainda não passa de uma hipótese. Há evidências de que a UCP-3 seja regulada pelos substratos energéticos, tais como ácidos graxos e glicose que, ao entrarem no músculo, provocam aumento da UCP-3 e aumento no gasto de energia. Nosso objetivo nesta revisão foi descrever e discutir as informações disponíveis sobre a regulação da UCP-3, e sua possível relação com o controle do peso corporal.
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Duval, Carine, Anne Nègre-Salvayre, Alain Doglio, Robert Salvayre, Luc Pénicaud, and Louis Casteilla. "Increased reactive oxygen species production with antisense oligonucleotides directed against uncoupling protein 2 in murine endothelial cells." Biochemistry and Cell Biology 80, no. 6 (December 1, 2002): 757–64. http://dx.doi.org/10.1139/o02-158.
Full textAbstract:
Uncoupling protein 2 (UCP-2) belongs to the mitochondrial anion carrier family. It is ubiquitously expressed but is most abdundant in the reticuloendothelial system. In addition to uncoupling function, UCP-2 modulates the production of reactive oxygen species (ROS) by isolated mitochondria. Using an antisense oligonucleotide strategy, we investigated whether a defect in UCP-2 expression modulates ROS in intact endothelial cells. Murine endothelial cells (CRL 2181) pretreated by antisense oligonucleotides directed against UCP-2 mRNA exhibited a significant and specific increase in membrane potential and intracellular ROS level compared with control scrambled or anti-UCP-1 and -UCP-3 antisense oligonucleotides. These specific changes induced by UCP-2 antisense oligonucleotides were correlated with a rise in extracellular superoxide anion production and oxidative stress assessed by thiobarbituric acid reactive substance values. Taken together, these data suggest a role for UCP-2 in control of ROS production and subsequent oxidation of surrounding compounds mediating oxidative stress of endothelial cells. These data also support the notion that manipulations of UCP-2 at the genetic level could control ROS metabolism at the cellular level.Key words: UCP-2, reactive oxygen species, LDL oxidation, oxidative stress, mitochondria, endothelial cells.
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Jekabsons, Mika B., Francine M. Gregoire, Nancy A. Schonfeld-Warden, Craig H. Warden, and B. A. Horwitz. "T3 stimulates resting metabolism and UCP-2 and UCP-3 mRNA but not nonphosphorylating mitochondrial respiration in mice." American Journal of Physiology-Endocrinology and Metabolism 277, no. 2 (August 1, 1999): E380—E389. http://dx.doi.org/10.1152/ajpendo.1999.277.2.e380.
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The molecular basis for variations in resting metabolic rate (RMR) within a species is unknown. One possibility is that variations in RMR occur because of variations in uncoupling protein 2 (UCP-2) and uncoupling protein 3 (UCP-3) expression, resulting in mitochondrial proton leak differences. We tested the hypothesis that UCP-2 and -3 mRNAs positively correlate with RMR and proton leak. We treated thyroidectomized and sham-operated mice with triiodothyronine (T3) or vehicle and measured RMR, liver, and skeletal muscle mitochondrial nonphosphorylating respiration and UCP-2 and -3 mRNAs. T3 stimulated RMR and liver UCP-2 and gastrocnemius UCP-2 and -3 expression. Mitochondrial respiration was not affected by T3 and did not correlate with UCP-2 and -3 mRNAs. Gastrocnemius UCP-2 and -3 expression did correlate with RMR. We conclude 1) T3 did not influence intrinsic mitochondrial properties such as membrane structure and composition, and 2) variations in UCP-2 and -3 expression may partly explain variations in RMR. One possible explanation for these data is that T3 stimulates the leak in vivo but not in vitro because a posttranslational regulator of UCP-2 and -3 is not retained in the mitochondrial fraction.
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Rehnmark, S., A. C. Bianco, J. D. Kieffer, and J. E. Silva. "Transcriptional and posttranscriptional mechanisms in uncoupling protein mRNA response to cold." American Journal of Physiology-Endocrinology and Metabolism 262, no. 1 (January 1, 1992): E58—E67. http://dx.doi.org/10.1152/ajpendo.1992.262.1.e58.
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Three mechanisms account for the rapid elevation and maintenance of uncoupling protein (UCP) mRNA levels in cold-exposed rats, namely, an increase in the rate of transcription initiation, an increase in the fraction of nascent UCP transcripts undergoing elongation, and stabilization of the mature UCP mRNA. The second mechanism precedes and outlasts the increase in the rate of UCP gene transcription, which is brisk but short lived. After 48 h of cold exposure, mature UCP mRNA levels are maintained elevated solely on the basis of stabilization, since the levels of both transcription initiation and fifth intron-containing transcripts (precursors) have returned to basal. Results in hypothyroid rats given 3,5,3'-triiodothyronine (T3) and in dispersed brown adipocytes show that T3 is involved both in the increase in UCP mRNA precursor level and stabilization of mature UCP mRNA. These mechanisms are rapidly reversed when the rats are returned to thermoneutrality. These coordinated transcriptional and post-transcriptional mechanisms modulating UCP gene expression ensure a rapid increase in the concentration of UCP and prevent further accumulation of the protein as physiologically adequate levels are attained.
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Rao, Arpit, Howard I. Scher, Peter De Porre, Margaret K. Yu, Anil Londhe, Keqin Qi, Michael J. Morris, and Charles Ryan. "Impact of clinical versus radiographic progression on clinical outcomes in metastatic castration-resistant prostate cancer." ESMO Open 5, no. 6 (November 2020): e000943. http://dx.doi.org/10.1136/esmoopen-2020-000943.
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ObjectivesUnequivocal clinical progression (UCP)—a worsening of clinical status with or without radiographic progression (RAD)—represents a distinct mode of disease progression in metastatic prostate cancer. We evaluated the prevalence, risk factors and the impact of UCP on survival outcomes.MethodsA post-hoc analysis of the COU-AA-302, a randomised phase 3 study of abiraterone plus prednisone (AAP) versus prednisone was performed. Baseline characteristics were summarised. Cox proportional-hazards model and Kaplan-Meier method were used for survival and time to event analyses, respectively. Iterative multiple imputation method was used for correlation between clinicoradiographic progression-free survival (crPFS) and overall survival (OS).ResultsOf 736 patients with disease progression, 280 (38%) had UCP-only and 124 (17%) had UCP plus RAD. Prognostic index model high-risk group was associated with increased likelihood of UCP (p<0.0001). Median OS was 25.7 months in UCP-only and 33.0 months for RAD-only (HR 1.39; 95% CI 1.16 to 1.66; p=0.0003). UCP adversely impacted OS in both treatment groups. Lowest OS was seen in patients with prostate specific antigen (PSA)-non-response plus UCP-only progression (median OS 22.6 months (95% CI 20.7 to 24.4)). Including UCP events lowered estimates of treatment benefit—median crPFS was 13.3 months (95% CI 11.1 to 13.8) versus median rPFS of 16.5 months (95% CI 13.8 to 16.8) in AAP group. Finally, crPFS showed high correlation with OS (r=0.67; 95% CI 0.63 to 0.71).ConclusionsUCP is a common and clinically relevant phenomenon in patients with metastatic castration-resistant prostate cancer (mCRPC) treated with AAP or prednisone. UCP is prognostic and associated with inferior OS and post-progression survival. A combination of PSA-non-response and UCP identifies patients with poorest survival. When included in PFS analysis, UCP diminishes estimates of treatment benefit. Continued study of UCP in mCRPC is warranted.
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Li, Yunfeng, Kathrin Maedler, Luan Shu, and Leena Haataja. "UCP-2 and UCP-3 Proteins Are Differentially Regulated in Pancreatic Beta-Cells." PLoS ONE 3, no. 1 (January 2, 2008): e1397. http://dx.doi.org/10.1371/journal.pone.0001397.
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Smith, Anna M. O., R. George Ratcliffe, and Lee J. Sweetlove. "Activation and Function of Mitochondrial Uncoupling Protein in Plants." Journal of Biological Chemistry 279, no. 50 (September 29, 2004): 51944–52. http://dx.doi.org/10.1074/jbc.m408920200.
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Plant mitochondrial uncoupling protein (UCP) is activated by superoxide suggesting that it may function to minimize mitochondrial reactive oxygen species (ROS) formation. However, the precise mechanism of superoxide activation and the exact function of UCP in plants are not known. We demonstrate that 4-hydroxy-2-nonenal (HNE), a product of lipid peroxidation, and a structurally related compound,trans-retinal, stimulate a proton conductance in potato mitochondria that is inhibitable by GTP (a characteristic of UCP). Proof that the effects of HNE andtrans-retinal are mediated by UCP is provided by examination of proton conductance in transgenic plants overexpressing UCP. These experiments demonstrate that the mechanism of activation of UCP is conserved between animals and plants and imply a conservation of function. Mitochondria from transgenic plants overexpressing UCP were further studied to provide insight into function. Experimental conditions were designed to mimic a bioenergetic state that might be foundin vivo(mitochondria were supplied with pyruvate as well as tricarboxylic cycle acids atin vivocytosolic concentrations and an exogenous ATP sink was established). Under such conditions, an increase in UCP protein content resulted in a modest but significant decrease in the rate of superoxide production. In addition,13C-labeling experiments revealed an increase in the conversion of pyruvate to citrate as a result of increased UCP protein content. These results demonstrate that under simulatedin vivoconditions, UCP is active and suggest that UCP may influence not only mitochondrial ROS production but also tricarboxylic acid cycle flux.
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Barazzoni, Rocco, and K. Sreekumaran Nair. "Changes in uncoupling protein-2 and -3 expression in aging rat skeletal muscle, liver, and heart." American Journal of Physiology-Endocrinology and Metabolism 280, no. 3 (March 1, 2001): E413—E419. http://dx.doi.org/10.1152/ajpendo.2001.280.3.e413.
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Uncoupling protein (UCP)-2 and -3 mediate mitochondrial (mt) proton leak in vitro and are potential regulators of energy expenditure and ATP production. Aging is associated with alteration of tissue functions, suggesting impaired mtATP production. To determine whether age-related changes in UCP expression occur, we measured the transcript levels of UCP-2 and -3 in skeletal muscle, liver, and heart in 6- and 27-mo-old rats. UCP-2 transcripts were higher in old animals in the white (+100%) and red (+70%, both P < 0.04) gastrocnemius muscle and in the liver (+300%, P < 0.03), whereas they were comparable in the heart in both age groups. UCP-2 transcript levels correlated positively with mitochondrial-encoded cytochrome c oxidase transcripts normalized for mtDNA ( P < 0.01) and negatively with mtDNA copy number ( P < 0.001). UCP-3 transcripts were lower in the less oxidative white (−50%, P < 0.04) and unchanged in the more oxidative red (−15%, P = 0.41) gastrocnemius muscle in old animals. Similar changes at protein level were confirmed by UCP-2 protein in aging liver (+300%, P < 0.01) and UCP-2 (+85%, P < 0.05) and UCP-3 (−30%, P = 0.4) protein in aging mixed gastrocnemius muscle. Aging is thus associated with tissue-specific changes of UCP-2 and -3 gene expression. Increased UCP-2 expression may limit ATP production and is related to mitochondrial gene expression in aging muscles and liver. Different age-related changes may reflect differential regulation of UCP-2 and -3 in skeletal muscle. The current data suggest a potential role of uncoupling proteins to alter energy production in aging tissues.
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Moriscot, A., R. Rabelo, and A. C. Bianco. "Corticosterone inhibits uncoupling protein gene expression in brown adipose tissue." American Journal of Physiology-Endocrinology and Metabolism 265, no. 1 (July 1, 1993): E81—E87. http://dx.doi.org/10.1152/ajpendo.1993.265.1.e81.
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Uncoupling protein (UCP) mRNA levels were studied in the interscapular brown adipose tissue (BAT) of rats undergoing different manipulations of the adrenal function and BAT adrenergic stimulation. Adrenalectomy did not affect UCP mRNA levels for up to 8 days post-surgery. However, adrenalectomized rats underwent a greater increase in UCP mRNA levels (26%) than intact rats after 4 h of cold exposure. Administration of corticosterone (500 micrograms.100 g body wt-1.day-1 sc) to intact or adrenalectomized rats, kept at 28 degrees C, produced a marked decrease of UCP mitochondrial content and cellular mRNA levels in a time-dependent manner (30% by 12 h and 50% by 24 h). Pretreatment of intact rats with corticosterone virtually abolished the UCP mRNA response to cold and norepinephrine (NE). In contrast, when rats had been preexposed to cold for 96 h, the injection of corticosterone did not affect UCP mRNA. These results show that corticosterone is a powerful inhibitor of UCP gene expression in vivo. Corticosterone inhibits both basal gene expression at thermoneutrality and the response to adrenergic stimulation either by cold or exogenous NE, suggesting a direct action on BAT. The data further suggest that corticosterone inhibits the initial accumulation of UCP mRNA mediated by UCP gene transcription, rather than accelerating the degradation of UCP mRNA.
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Dulloo, A. G., S. Samec, and J. Seydoux. "Uncoupling protein 3 and fatty acid metabolism." Biochemical Society Transactions 29, no. 6 (November 1, 2001): 785–91. http://dx.doi.org/10.1042/bst0290785.
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A role for uncoupling protein (UCP) 3 in fatty acid metabolism is reviewed within the context of our proposal, first put forward in 1998, that this homologue of UCP1 may be involved in the regulation of lipids as fuel substrate rather than in the mediation of thermogenesis. Since then, the demonstrations of muscle-type differences in UCP3 gene regulation in response to dietary manipulations (starvation, high-fat feeding) or to pharmacological interferences with the flux of lipid substrates between adipose-tissue stores and skeletal-muscle mitochondrial oxidation are all in accord with this proposed role for UCP3 in regulating lipids as fuel substrate. However, given the current limitations of gene-knockout technology for evaluating/interpreting the functional importance of genes encoding mitochondrial membrane proteins, the transition from ‘associative’ to ‘cause-and-effect’ evidence for a physiological role of UCP3 in regulating fatty acid metabolism will have to await the development of assays that are sensitive to changes in UCP3 activity. Furthermore, in evaluating the physiological regulators of UCP3, the available evidence points to the existence of adipose-derived factor(s) which, independently of circulating levels of free fatty acids, initiates events leading to the transcription of genes encoding UCP3 and key enzymes of lipid oxidation in the fast glycolytic or fast oxidative-glycolytic muscles, i.e. in the bulk of the skeletal-muscle mass. It is proposed that in tissues where UCP3 co-exists with UCP2 (skeletal muscle, brown adipose tissue, heart) they may act in concert in the overall regulation of lipid oxidation, concomitant to the prevention of lipid-induced oxidative damage.
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Hernández, Arturo, and Maria Jesús Obregón. "Triiodothyronine amplifies the adrenergic stimulation of uncoupling protein expression in rat brown adipocytes." American Journal of Physiology-Endocrinology and Metabolism 278, no. 5 (May 1, 2000): E769—E777. http://dx.doi.org/10.1152/ajpendo.2000.278.5.e769.
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Uncoupling protein (UCP), the mitochondrial protein specific to brown adipose tissue, is activated transcriptionally in response to cold and adrenergic agents. We studied the role of triiodothyronine (T3) on the adrenergic stimulation of UCP mRNA expression by use of primary cultures of rat brown adipocytes. Basal UCP mRNA levels are undetectable. Norepinephrine (NE) increases UCP mRNA during differentiation, not during proliferation. In hypothyroid conditions, UCP mRNA response to NE is almost absent. The presence of T3 (0.2–20 nM) greatly increases the adrenergic response (30-fold). The sensitivity of UCP mRNA responses to NE is potentiated ∼100-fold by the presence of T3. The effect is proportional to the dose and time of preexposure to T3. The increases obtained with NE and T3 are prevented by actinomycin and cycloheximide. T3 greatly stabilizes UCP mRNA transcripts. The effects of thyroxine and retinoic acid are weaker than those of T3. In conclusion, in cultured rat brown adipocytes, T3 is required and both synergizes with NE to increase UCP mRNA and stabilizes its mRNA transcripts.
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Klaus, S., A. M. Cassard-Doulcier, and D. Ricquier. "Development of Phodopus sungorus brown preadipocytes in primary cell culture: effect of an atypical beta-adrenergic agonist, insulin, and triiodothyronine on differentiation, mitochondrial development, and expression of the uncoupling protein UCP." Journal of Cell Biology 115, no. 6 (December 15, 1991): 1783–90. http://dx.doi.org/10.1083/jcb.115.6.1783.
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A new cellular model for the study of brown adipocyte development and differentiation in vitro is presented. Preadipocytes isolated from brown adipose tissue (BAT) of the djungarian dwarf hamster Phodopus sungorus are able to proliferate and differentiate in vitro into true brown adipocytes able to express the BAT marker protein the uncoupling protein (UCP). Whereas basal UCP expression is very low, its mRNA levels as well as the UCP detected by immunoblotting are highly increased by beta-adrenergic stimulation. The novel, atypical beta-adrenergic compound D7114 (ICI Pharmaceuticals, Macclesfield, Cheshire, England) was found to increase the number of adipocytes as well as UCP mRNA and UCP content of mitochondria, indicating the involvement of an atypical or beta 3 receptor. Insulin was found to play an important role in brown adipocyte differentiation and mitochondrial development, whereas T3 seemed to be implicated more directly in UCP expression. In a defined, serum-free medium a synergistic stimulatory action of insulin and T3 on UCP expression was found, which seems to involve a pathway different from that of beta-adrenergic UCP stimulation.
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Kelly, Linda J., Pasquale P. Vicario, G. Marie Thompson, Mari R. Candelore, Thomas W. Doebber, John Ventre, Margaret S. Wu, et al. "Peroxisome Proliferator-Activated Receptors γ and α Mediate in Vivo Regulation of Uncoupling Protein (UCP-1, UCP-2, UCP-3) Gene Expression." Endocrinology 139, no. 12 (December 1, 1998): 4920–27. http://dx.doi.org/10.1210/endo.139.12.6384.
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TONKONOGI, Michail, Anna KROOK, Brandon WALSH, and Kent SAHLIN. "Endurance training increases stimulation of uncoupling of skeletal muscle mitochondria in humans by non-esterified fatty acids: an uncoupling-protein-mediated effect?" Biochemical Journal 351, no. 3 (October 24, 2000): 805–10. http://dx.doi.org/10.1042/bj3510805.
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Uncoupled respiration (UCR) is an essential property of muscle mitochondria and has several functions in the cell. We hypothesized that endurance training may alter the magnitude and properties of UCR in human muscle. Isolated mitochondria from muscle biopsies taken before and after 6 weeks of endurance exercise training (n = 8) were analysed for UCR. To investigate the role of uncoupling protein 2 (UCP2) and UCP3 in UCR, the sensitivity of UCR to UCP-regulating ligands (non-esterified fatty acids and purine nucleotides) and UCP2 and UCP3 mRNA expression in muscle were examined. Oleate increased the mitochondrial oxygen consumption rate, an effect that was not attenuated by GDP and/or cyclosporin A. The effect of oleate was significantly greater after compared with before training. Training had no effect on UCP2 or UCP3 mRNA levels, but after training the relative increase in respiration rate induced by oleate was positively correlated with the UCP2 mRNA level. In conclusion, we show that the sensitivity of UCR to non-esterified fatty acids is up-regulated by endurance training. This suggests that endurance training causes intrinsic changes in mitochondrial function, which may enhance the potential for regulation of aerobic energy production, prevent excess free radical generation and contribute to a higher basal metabolic rate.