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Journal articles on the topic 'The UCPD'

Author: Grafiati

Published: 11 March 2023

Last updated: 19 July 2025

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1

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 (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,

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2

Liu, Jing, Ji Li, Wen-Jian Li, and Chun-Ming Wang. "The Role of Uncoupling Proteins in Diabetes Mellitus." Journal of Diabetes Research 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/585897.

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Uncoupling proteins (UCPs) are anion carriers expressed in the mitochondrial inner membrane that uncouple oxygen consumption by the respiratory chain from ATP synthesis. The physiological functions of UCPs have long been debated since the new UCPs (UCP2 to 5) were discovered, and the role of UCPs in the pathogeneses of diabetes mellitus is one of the hottest topics. UCPs are thought to be activated by superoxide and then decrease mitochondrial free radicals generation; this may provide a protective effect on diabetes mellitus that is under the oxidative stress conditions. UCP1 is considered to

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3

Vereecken, Jasper. "Consumer Protection by the ECJ in Unit-Linked Group Contracts: On Transparency, Liability and Nullity under the UCPD." European Review of Private Law 31, Issue 5 (2023): 933–54. http://dx.doi.org/10.54648/erpl2023045.

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This case note addresses the ECJ’s drafting of essential information to be given to a consumer in the event of a unit-linked group contract. This information enables consumers to make an informed decision. The ECJ subsequently qualifies the failure to transfer this information as a misleading omission under Article 7 UCPD, which in turn may result in a violation of the transparency requirement enshrined in the UCTD. Liability of the traders on whom the responsibility rests to furnish this information is also examined in this comment, as the ECJ makes a distinction between the responsibilities

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4

Nikanorova, Alena A., Nikolay A. Barashkov, Vera G. Pshennikova, et al. "The Evaluation of Significance of Uncoupling Protein Genes UCP1, UCP2, UCP3, UCP4, UCP5, and UCP6 in Human Adaptation to Cold Climates." Biology 14, no. 5 (2025): 454. https://doi.org/10.3390/biology14050454.

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Six isoforms of uncoupling proteins (UCPs) exist, spanning from UCP1 to UCP6. A precise physiological function has only been established for UCP1, which is involved in non-shivering thermogenesis, but the functions of other UCPs are still not fully defined. Therefore, the purpose of the present study is to search for indications of the involvement of nine polymorphic variants of UCP1-6 genes in human adaptation to cold climates using four criteria: (1) the presence of associations of polymorphic variants of UCP genes with levels of thyroid-stimulating hormone, free triiodothyronine, and free t

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5

Klingenberg, M., E. Winkler, and K. Echtay. "Uncoupling protein, H+ transport and regulation." Biochemical Society Transactions 29, no. 6 (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 ro

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6

Carrageta, David F., Laís Freire-Brito, Bárbara Guerra-Carvalho, et al. "Inhibition of Mitochondrial Uncoupling Proteins Arrests Human Spermatozoa Motility without Compromising Viability." Antioxidants 12, no. 2 (2023): 409. http://dx.doi.org/10.3390/antiox12020409.

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Mitochondrial uncoupling proteins (UCPs) are central in the regulation of mitochondrial activity and reactive oxygen species (ROS) production. High oxidative stress is a major cause of male infertility; however, UCPs expression and function in human spermatozoa are still unknown. Herein, we aimed to assess the expression and function of the different homologs (UCP1-6) in human spermatozoa. For this purpose, we screened for the mRNA expression of all UCP homologs. Protein expression and immunolocalization of UCP1, UCP2, and UCP3 were also assessed. Highly motile spermatozoa were isolated from h

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7

Borecký, Jirí, Ivan G. Maia, and Paulo Arruda. "Mitochondrial Uncoupling Proteins in Mammals and Plants." Bioscience Reports 21, no. 2 (2001): 201–12. http://dx.doi.org/10.1023/a:1013604526175.

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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

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8

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 (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 (mam

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9

Radović, Katarina, Rade Živković, Jovana Kuzmanovic Pficer, Ljiljana Tihaček Šojić, and Aleksandra Milić Lemić. "Unilateral complex partial denture performance evaluation: 5 years follow up clinical study." Stomatoloski glasnik Srbije 65, no. 3 (2018): 140–47. http://dx.doi.org/10.2478/sdj-2018-0014.

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Summary Introduction Removable partial denture (RPD) is common treatment option for unilateral partially edentulous patients not indicated for implant therapy. Unilateral complex partial denture (UCPD) could be an alternative approach to RPD treatment, but there is lack of evidence about UCPD treatment outcomes during the long-term clinical performance. The aim of this this study was to use periodontal, prosthodontic and participant satisfaction measures to evaluate the long-term clinical performance of UCPD. Material and methods This 5 year follow-up clinical study evaluated pocket probing de

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10

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 (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

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11

RICQUIER, Daniel, and Frédéric BOUILLAUD. "The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP." Biochemical Journal 345, no. 2 (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,

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12

Beckers, Anna. "The regulation of market communication and market behaviour: Corporate social responsibility and the Directives on Unfair Commercial Practices and Unfair Contract Terms." Common Market Law Review 54, Issue 2 (2017): 475–515. http://dx.doi.org/10.54648/cola2017033.

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Despite the frequent insistence in EU policies on corporate social responsibility (CSR) being voluntary, this paper argues that under EU consumer law CSR can be interpreted as legally binding. CSR is a strategic form of market communication as well as an inherent aspect of the market behaviour of companies. Since EU consumer law regulates the market communication and the market behaviour of traders, this area of law can be used to interpret CSR as a legally binding obligation, resulting in remedies available to consumers. This paper uses the Unfair Commercial Practices Directive (UCPD) to show

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13

Skulachev, Vladimir P. "Barbara Cannon's Data on the UCP1-Ablated Mice: “Non-Cannonical” Point of View." Bioscience Reports 21, no. 2 (2001): 189–94. http://dx.doi.org/10.1023/a:1013600325266.

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The data of Cannon and co-workers on UCP1-ablated mice are interpreted assuming that UCP2 and UCP3 are involved in thermoregulation as fatty acid-dependent uncouplers although they are not sufficient, in the absence of UCP1, for long term maintenance of normal body temperature of mice after sudden and strong decrease in the ambient temperature. I would like to suggest that in brown fat of control mice, UCP1 is present in an amount higher than UCP2 and 3 and, therefore, is able to cause (a) some fatty acid-mediated decrease in proton motive force in resting state and, hence, (b) oxidation of Co

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14

Masuda, Yoriko, Satoshi Haramizu, Kasumi Oki, et al. "Upregulation of uncoupling proteins by oral administration of capsiate, a nonpungent capsaicin analog." Journal of Applied Physiology 95, no. 6 (2003): 2408–15. http://dx.doi.org/10.1152/japplphysiol.00828.2002.

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Capsiate is a nonpungent capsaicin analog, a recently identified principle of the nonpungent red pepper cultivar CH-19 Sweet. In the present study, we report that 2-wk treatment of capsiate increased metabolic rate and promoted fat oxidation at rest, suggesting that capsiate may prevent obesity. To explain these effects, at least in part, we examined uncoupling proteins (UCPs) and thyroid hormones. UCPs and thyroid hormones play important roles in energy expenditure, the maintenance of body weight, and thermoregulation. Two-week treatment of capsiate increased the levels of UCP1 protein and mR

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15

Scarpace, PJ, M. Matheny, RL Moore, and MV Kumar. "Modulation of uncoupling protein 2 and uncoupling protein 3: regulation by denervation, leptin and retinoic acid treatment." Journal of Endocrinology 164, no. 3 (2000): 331–37. http://dx.doi.org/10.1677/joe.0.1640331.

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We recently reported that the leptin-induced increase in uncoupling protein 1 (UCP1) mRNA in brown adipose tissue (BAT) is prevented by the denervation of BAT. We also reported that retinoic acid (RA) increases UCP1 mRNA in BAT. To extend these finding to UCP2 and UCP3 in BAT, we examined UCP2 and UCP3 mRNA after unilateral denervation of BAT, as well as after leptin, beta(3)-adrenergic agonist, RA, and glucocorticoid administration to rats. UCP3 mRNA was 20% less in the denervated compared with the intact BAT, whereas UCP2 mRNA was unchanged with denervation. The beta(3)-adrenergic agonist, C

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16

Mozo, Julien, Gilles Ferry, Aurélie Studeny, et al. "Expression of UCP3 in CHO cells does not cause uncoupling, but controls mitochondrial activity in the presence of glucose." Biochemical Journal 393, no. 1 (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

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17

Schebesta, Hanna, and Kai Purnhagen. "Island or Ocean: Empirical Evidence on the Average Consumer Concept in the UCPD." European Review of Private Law 28, Issue 2 (2020): 293–310. http://dx.doi.org/10.54648/erpl2020015.

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This article investigates the codification of the average consumer concept in secondary legislation and its interpretation in the Court of Justice of the European Union(CJEU)’s case law, using doctrinal and empirical methods. We first identify all secondary legislation explicitly using the ‘average consumer’ in its wording and respective case law. We show that only the Unfair Commercial Practices Directive (UCPD) developed significant case law and conducted a software supported systematic qualitative analysis of all UCPD average consumer case law to address five research questions: How is the

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18

Laux, Johann, Sandra Wachter, and Brent Mittelstadt. "Neutralizing online behavioural advertising: Algorithmic targeting with market power as an unfair commercial practice." Common Market Law Review 58, Issue 3 (2021): 719–50. http://dx.doi.org/10.54648/cola2021048.

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Online behavioural advertising (OBA) relies on inferential analytics to target consumers based on data about their online behaviour. While the technology can improve the matching of adverts with consumers’ preferences, it also poses risks to consumer welfare as consumers face offer discrimination and the exploitation of their cognitive errors. The technology’s risks are exacerbated by the market power of ad intermediaries. This article shows how the Unfair Commercial Practices Directive (UCPD) can protect consumers from behavioural exploitation by incorporating market power analysis. Drawing o

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19

Dorsa, Karina Kores, Michelle Venâncio dos Santos, and Magnus R. Dias da Silva. "Enhancing T3 and cAMP responsive gene participation in the thermogenic regulation of fuel oxidation pathways." Arquivos Brasileiros de Endocrinologia & Metabologia 54, no. 4 (2010): 381–89. http://dx.doi.org/10.1590/s0004-27302010000400007.

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OBJECTIVE: We sought to identify glycolysis, glycogenolysis, lipolysis, Krebs cycle, respiratory chain, and oxidative phosphorylation enzymes simultaneously regulated by T3 and cAMP. MATERIALS AND METHODS: We performed in silico analysis of 56 promoters to search for cis-cAMP (CREB) and cis-thyroid (TRE) response elements, considering UCP1, SERCA2 and glyceraldehyde 3-phosphate dehydrogenase as reference. Only regulatory regions with prior in vitro validation were selected. RESULTS: 29/56 enzymes presented potential TREs in their regulatory sequence, and some scored over 0.80 (better predictiv

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20

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 (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 reptil

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21

Čater, Maša, and Lidija Križančić Križančić Bombek. "Protective Role of Mitochondrial Uncoupling Proteins against Age-Related Oxidative Stress in Type 2 Diabetes Mellitus." Antioxidants 11, no. 8 (2022): 1473. http://dx.doi.org/10.3390/antiox11081473.

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The accumulation of oxidative damage to DNA and other biomolecules plays an important role in the etiology of aging and age-related diseases such as type 2 diabetes mellitus (T2D), atherosclerosis, and neurodegenerative disorders. Mitochondrial DNA (mtDNA) is especially sensitive to oxidative stress. Mitochondrial dysfunction resulting from the accumulation of mtDNA damage impairs normal cellular function and leads to a bioenergetic crisis that accelerates aging and associated diseases. Age-related mitochondrial dysfunction decreases ATP production, which directly affects insulin secretion by

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Hirschenson, Jonathan, Emiliano Melgar-Bermudez, and Ryan J. Mailloux. "The Uncoupling Proteins: A Systematic Review on the Mechanism Used in the Prevention of Oxidative Stress." Antioxidants 11, no. 2 (2022): 322. http://dx.doi.org/10.3390/antiox11020322.

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Mitochondrial uncoupling proteins (UCP) 1-3 fulfill many physiological functions, ranging from non-shivering thermogenesis (UCP1) to glucose-stimulated insulin release (GSIS) and satiety signaling (UCP2) and muscle fuel metabolism (UCP3). Several studies have suggested that UCPs mediate these functions by facilitating proton return to the matrix. This would decrease protonic backpressure on the respiratory chain, lowering the production of hydrogen peroxide (H2O2), a second messenger. However, controlling mitochondrial H2O2 production to prevent oxidative stress by activating these leaks throu

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23

Никанорова, А. А., Н. А. Барашков, Е. Е. Дьяконов, et al. "Analysis of polymorphism of SNP markers of genes involved in nonshivering thermogenesis, UCP1 (rs1800592), UCP2 (rs659366) and UCP3 (rs2075577) in Yakuts and Chukchi." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 5(214) (May 29, 2020): 97–98. http://dx.doi.org/10.25557/2073-7998.2020.05.97-98.

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Впервые был проведен анализ частот аллелей полиморфизмов генов UCP1 (rs1800592), UCP2 (rs659366) и UCP3 (rs2075577) в популяциях якутов и чукчей, проживающих в условиях экстремального климата Восточной Сибири. For the first time an analysis of the frequencies of alleles polymorphism of the genes UCP1 (rs1800592), UCP2 (rs659366) and UCP3 (rs2075577) were studied in the Yakut and Chukchi populations, living in the extreme climate of Eastern Siberia.

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Guo, Zhenhua, Lei Lv, Di Liu, et al. "Network Meta-Analysis: Effect of Cold Stress on the Gene Expression of Swine Adipocytes ATGL, CIDEA, UCP2, and UCP3." Current Issues in Molecular Biology 46, no. 5 (2024): 3866–76. http://dx.doi.org/10.3390/cimb46050240.

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Cold stress significantly affects gene expression in adipocytes; studying this phenomenon can help reveal the pathogeneses of conditions such as obesity and insulin resistance. Adipocyte triglyceride lipase (ATGL); cell death-inducing deoxyribonucleic acid (DNA) fragmentation factor subunit alpha (DFFA)-like effector (CIDEA); and uncoupling protein genes UCP1, UCP2, and UCP3 are the most studied genes in pig adipose tissues under cold stress. However, contradictory results have been observed in gene expression changes to UCP3 and UCP2 when adipose tissues under cold stress were examined. There

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Commins, Scott P., Patricia M. Watson, Isabell C. Frampton, and Thomas W. Gettys. "Leptin selectively reduces white adipose tissue in mice via a UCP1-dependent mechanism in brown adipose tissue." American Journal of Physiology-Endocrinology and Metabolism 280, no. 2 (2001): E372—E377. http://dx.doi.org/10.1152/ajpendo.2001.280.2.e372.

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We tested the hypothesis that leptin, in addition to reducing body fat by restraining food intake, reduces body fat through a peripheral mechanism requiring uncoupling protein 1 (UCP1). Leptin was administered to wild-type (WT) mice and mice with a targeted disruption of the UCP1 gene (UCP1 deficient), while vehicle-injected control animals of each genotype were pair-fed to each leptin-treated group. Leptin reduced the size of white adipose tissue (WAT) depots in WT mice but not in UCP1-deficient animals. This was accompanied by a threefold increase in the amount of UCP1 protein and mRNA in th

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PEDRAZA, Neus, Gemma SOLANES, Roser IGLESIAS, Manuel VÁZQUEZ, Marta GIRALT, and Francesc VILLARROYA. "Differential regulation of expression of genes encoding uncoupling proteins 2 and 3 in brown adipose tissue during lactation in mice." Biochemical Journal 355, no. 1 (2001): 105–11. http://dx.doi.org/10.1042/bj3550105.

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Thermogenic activity in brown adipose tissue (BAT) decreases during lactation; the down-regulation of the gene encoding uncoupling protein 1 (UCP1) is involved in this process. Our studies show that UCP2 mRNA expression does not change during the breeding cycle in mice. In contrast, UCP3 mRNA is down-regulated in lactation but it recovers after weaning, in parallel with UCP1 mRNA. This leads to a decrease in the content of UCP3 in BAT mitochondria during lactation. Lowering the energy-sparing necessities of lactating dams by decreasing litter size or feeding with a high-fat diet prevented the

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27

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 musc

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Bouillaud, Frédéric, Elodie Couplan, Claire Pecqueur, and Daniel Ricquier. "Homologues of the uncoupling protein from brown adipose tissue (UCP1): UCP2, UCP3, BMCP1 and UCP4." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1504, no. 1 (2001): 107–19. http://dx.doi.org/10.1016/s0005-2728(00)00241-3.

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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 (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 concen

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Schrauwen, Patrick, and Matthijs Hesselink. "UCP2 and UCP3 in muscle controlling body metabolism." Journal of Experimental Biology 205, no. 15 (2002): 2275–85. http://dx.doi.org/10.1242/jeb.205.15.2275.

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SUMMARY The uncoupling protein-1 (UCP1) homologues UCP2 and UCP3 are able to uncouple ATP production from mitochondrial respiration, thereby dissipating energy as heat and affecting energy metabolism efficiency. In contrast to UCP1, which plays an important role in adaptive thermogenesis, UCP2 and UCP3 do not have a primary role in the regulation of energy metabolism. UCP2, which is expressed in a wide variety of tissues, including white adipose tissue,skeletal muscle and tissues of the immune system, has been suggested to affect the production of reactive oxygen species. UCP2 has also been su

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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 (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 p

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Azzu, Vian, Shona A. Mookerjee, and Martin D. Brand. "Rapid turnover of mitochondrial uncoupling protein 3." Biochemical Journal 426, no. 1 (2010): 13–17. http://dx.doi.org/10.1042/bj20091321.

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UCP3 (uncoupling protein 3) and its homologues UCP2 and UCP1 are regulators of mitochondrial function. UCP2 is known to have a short half-life of approx. 1 h, owing to its rapid degradation by the cytosolic 26S proteasome, whereas UCP1 is turned over much more slowly by mitochondrial autophagy. In the present study we investigate whether UCP3 also has a short half-life, and whether the proteasome is involved in UCP3 degradation. UCP3 half-life was examined in the mouse C2C12 myoblast cell line by inhibiting protein synthesis with cycloheximide and monitoring UCP3 protein levels by immunoblot a

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Žáčkova, Markéta, and Petr Ježek. "Reconstitution of Novel Mitochondrial Uncoupling Proteins UCP2 and UCP3." Bioscience Reports 22, no. 1 (2002): 33–46. http://dx.doi.org/10.1023/a:1016009022186.

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Reconstitution of novel mitochondrial uncoupling proteins, human UCP2 and UCP3, expressed in yeast, was performed to characterize fatty acid (FA)-induced H+ efflux in the resulted proteoliposomes. We now demonstrate for the first time that representatives of physiologically abundant long chain FAs, saturated or unsaturated, activate H+ translocation in UCP2- and UCP3-proteoliposomes. Efficiency of lauric, palmitic or linoleic acid was roughly the same, but oleic acid induced faster H+ uniport. We have confirmed that ATP and GTP inhibit such FA-induced H+ uniport mediated by UCP2 and UCP3. Coen

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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 (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 skelet

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Schonfeld-Warden, N. A., and C. H. Warden. "Physiological effects of variants in human uncoupling proteins: UCP2 influences body-mass index." Biochemical Society Transactions 29, no. 6 (2001): 777–84. http://dx.doi.org/10.1042/bst0290777.

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The purpose of this review is to summarize the evidence from more than 40 studies that naturally occurring variants of uncoupling proteins 1–3 (UCP1–3) have detectable physiological effects in humans. Although UCP1 is known to influence mitochondrial proton leak in vitro and core body temperature in mice, genetic studies in humans have produced only weak evidence for association of naturally occurring variants with body-mass index (BMI); the best-reported P value is 0.01. In contrast, current evidence is consistent with the hypothesis that UCP2 and 3 influence BMI, since the best reported P va

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Jastroch, Martin, Kerry Withers, and Martin Klingenspor. "Uncoupling protein 2 and 3 in marsupials: identification, phylogeny, and gene expression in response to cold and fasting in Antechinus flavipes." Physiological Genomics 17, no. 2 (2004): 130–39. http://dx.doi.org/10.1152/physiolgenomics.00165.2003.

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We searched for the presence of uncoupling protein genes so far unknown in marsupials and monotremes and identified uncoupling protein 2 (UCP2) and UCP3 full-length cDNAs in libraries constructed from the marsupials Antechinus flavipes and Sminthopsis macroura. Marsupial UCP2 is 89–90% identical to rodent UCP2, whereas UCP3 exhibits 80% identity to mouse UCP3. A phylogenetic tree including all known UCPs positions the novel marsupial UCP2 and UCP3 at the base of the mammalian orthologs. In the 5′-untranslated region of UCP2 a second open reading frame encoding for a 36-amino acid peptide was i

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Tajima, Daisuke, Takayuki Masaki, Shuji Hidaka, Tetsuya Kakuma, Toshiie Sakata, and Hironobu Yoshimatsu. "Acute Central Infusion of Leptin Modulates Fatty Acid Mobilization by Affecting Lipolysis and mRNA Expression for Uncoupling Proteins." Experimental Biology and Medicine 230, no. 3 (2005): 200–206. http://dx.doi.org/10.1177/153537020523000306.

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Chronic administration of leptin has been shown to reduce adiposity through energy intake and expenditure. The present study alms to examine how acute central infusion of leptin regulates peripheral lipid metabolism, as assessed by markers indicative of their mobilization and utilization. A bolus infusion of 1 μg/rat leptin into the third cerebroventricle increased the expression of mRNA for hormone-sensitive lipase (HSL), an indicator of lipolysis, in white adipose tissue (WAT). This was accompanied by elevation of plasma levels of glycerol, but not of free fatty acids, as compared to the sal

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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 (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-

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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 (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

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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 (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 fo

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Fink, Brian D., Krzysztof J. Reszka, Judy A. Herlein, Mary M. Mathahs, and William I. Sivitz. "Respiratory uncoupling by UCP1 and UCP2 and superoxide generation in endothelial cell mitochondria." American Journal of Physiology-Endocrinology and Metabolism 288, no. 1 (2005): E71—E79. http://dx.doi.org/10.1152/ajpendo.00332.2004.

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Mitochondria represent a major source of reactive oxygen species (ROS), particularly during resting or state 4 respiration wherein ATP is not generated. One proposed role for respiratory mitochondrial uncoupling proteins (UCPs) is to decrease mitochondrial membrane potential and thereby protect cells from damage due to ROS. This work was designed to examine superoxide production during state 4 (no ATP production) and state 3 (active ATP synthesis) respiration and to determine whether uncoupling reduced the specific production of this radical species, whether this occurred in endothelial mitoch

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Fuller, Patrick M., Craig H. Warden, Sean J. Barry, and Charles A. Fuller. "Effects of 2-G exposure on temperature regulation, circadian rhythms, and adiposity in UCP2/3 transgenic mice." Journal of Applied Physiology 89, no. 4 (2000): 1491–98. http://dx.doi.org/10.1152/jappl.2000.89.4.1491.

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Altered ambient force environments affect energy expenditure via changes in thermoregulation, metabolism, and body composition. Uncoupling proteins (UCPs) have been implicated as potential enhancers of energy expenditure and may participate in some of the adaptations to a hyperdynamic environment. To test this hypothesis, this study examined the homeostatic and circadian profiles of body temperature (Tb) and activity and adiposity in wild-type and UCP2/3 transgenic mice exposed to 1 and 2 G. There were no significant differences between the groups in the means, amplitudes, or phases of Tb and

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RICQUIER, Daniel, and Frédéric BOUILLAUD. "The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP." Biochemical Journal 345, no. 2 (2000): 161. http://dx.doi.org/10.1042/0264-6021:3450161.

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Bouillaud, F. "UCP1, UCP2 and UCP3: Are they true uncouplers of respiration?" International Journal of Obesity 23, S6 (1999): S19—S23. http://dx.doi.org/10.1038/sj.ijo.0800938.

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Pratiwi, Yuni Susanti, Melisa Siannoto, Hanna Goenawan, et al. "Effect of nutmeg extract on the white adipose tissue (WAT) browning process of aging rats." Nutrition and Healthy Aging 6, no. 4 (2022): 285–91. http://dx.doi.org/10.3233/nha-200111.

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The white adipose tissue (WAT) browning process has become one of the promising methods for managing obesity. During this process, WAT is transformed into brown-like adipose tissue, which is also known as beige adipose tissue. The browning process can be activated by several inducers. One of the best candidates is peroxisome proliferator-activated receptor γ (PPARγ) agonist. Nutmeg (Myristica fragrans Houtt) is a natural PPARα/γ partial agonist that is known to contribute to the browning effect. This study aimed to explore the potential effect of nutmeg seed extract (NuSE) on body weight reduc

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Keirsbilck, Bert. "The UCPDs notion of commercial practice: UPC Magyarország." Common Market Law Review 53, Issue 2 (2016): 527–42. http://dx.doi.org/10.54648/cola2016040.

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Goshovska, Yu V., N. A. Strutynska, and V. F. Sagach. "EFFECT OF CALCIUM LOAD ON HEART FUNCTION, MPTP OPENING IN SITU AND UCP2/3 MRNA EXPRESSION IN THE HEART OF TRAINED RATS." Fiziolohichnyĭ zhurnal 66, no. 6 (2020): 3–12. http://dx.doi.org/10.15407/fz66.06.003.

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We have studied the effect of calcium load (1.7 to 15 mmol/l in perfusate) on isolated heart function, mitochondrial factor release (as a marker of mitochondrial permeability transition pore, MPTP), and cardiac uncoupling proteins (UCP2/3) mRNA expression in untrained and trained rats (swimming for 4 weeks). It was found that the improvement in the isolated heart function of trained rats was accompanied by an increase in the expression of UCP3, but not UCP2. A gradual increase of the calcium content in the perfusate led to an increase in contractile function, more pronounced in trained rats. H

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Brauner, P., P. Flachs, and J. Kopecký. "Immunodetection of UCP1, UCP2, and UCP3 in human and mouse tissues." Biochemical Society Transactions 28, no. 5 (2000): A187. http://dx.doi.org/10.1042/bst028a187b.

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Inokuma, Ken-ichi, Yuko Okamatsu-Ogura, Asako Omachi та ін. "Indispensable role of mitochondrial UCP1 for antiobesity effect of β3-adrenergic stimulation". American Journal of Physiology-Endocrinology and Metabolism 290, № 5 (2006): E1014—E1021. http://dx.doi.org/10.1152/ajpendo.00105.2005.

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Mitochondrial uncoupling protein-1 (UCP1) has been thought to be a key molecule for thermogenesis during cold exposure and spontaneous hyperphagia and thereby in the autonomic regulation of energy expenditure and adiposity. However, UCP1 knockout (KO) mice were reported to be cold intolerant but unexpectedly did not get obese even after hyperphagia, implying that UCP1 may not be involved in the regulation of adiposity. Treatment of obese animals with β3-adrenergic agonists is known to increase lipid mobilization, induce UCP1, and, finally, reduce body fat content. To obtain direct evidence for

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Dulloo, Abdul G., and Sonia Samec. "Uncoupling Proteins: Do They Have a Role in Body Weight Regulation?" Physiology 15, no. 6 (2000): 313–18. http://dx.doi.org/10.1152/physiologyonline.2000.15.6.313.

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Several members of the mitochondrial carrier protein family are classified as uncoupling proteins. In contrast to the uncoupling protein specific to brown adipose tissue (UCP1), the physiological role of skeletal muscle uncoupling proteins (UCP2 and UCP3) in weight regulation seems more closely associated with the regulation of lipids as fuel substrate than as mediators of adaptive thermogenesis.

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