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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, 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.
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 be a candidate gene for diabetes because of its role in thermogenesis and energy expenditure. UCP2 is expressed in several tissues and acts in the negative regulation of insulin secretion byβ-cells and in fatty acid metabolism. UCP3 plays a role in fatty acid metabolism and energy homeostasis and modulates insulin sensitivity. Several gene polymorphisms of UCP1, UCP2, and UCP3 were reported to be associated with diabetes. The progress in the role of UCP1, UCP2, and UCP3 on diabetes mellitus is summarized in this review.
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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 of traders and intermediaries. The Polish action for annulment when the traders infringe the UCPD was lastly deemed compliant with the UCPD and proportionate by the ECJ, thereby using a cross-reference to its case law in the field of consumer credits on the requirement that national sanctions have to be effective, proportionate and dissuasive. The possible consequences of this cross-reference method are discussed afterwards.
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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 thyroxine; (2) the presence of associations of polymorphic variants of UCP genes with changes in thyroid homeostasis (SPINA); (3) the presence of associations of polymorphic variants of UCP genes with body surface area; (4) the presence of signals of directional selection to cold climate for polymorphic variants of UCP genes. As a result of the evaluation, the highest scores for cold adaptation traits were recorded for polymorphic variants rs3811787 of the UCP1 gene and rs1800849 of the UCP3 gene. We suggest that the results obtained indicate the importance of uncoupling proteins UCP1 and UCP3 in human adaptation to cold through processes of non-shivering and shivering thermogenesis.
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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 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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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 human normozoospermic seminal samples (n = 16) and incubated with genipin, an inhibitor of UCPs (0, 0.5, 5, and 50 µM) for 3 h at 37 °C. Viability and total motility were assessed. Mitochondrial membrane potential and ROS production were evaluated. Media were collected and the metabolic profile and antioxidant potential were analyzed by 1H-NMR and FRAP, respectively. The expression of all UCP homologs (UCP1-6) mRNA by human spermatozoa is herein reported for the first time. UCP1-3 are predominant at the head equatorial segment, whereas UCP1 and UCP2 are also expressed at the spermatozoa midpiece, where mitochondria are located. The inhibition of UCPs by 50 µM genipin, resulting in the UCP3 inhibition, did not compromise sperm cell viability but resulted in irreversible total motility loss that persisted despite washing or incubation with theophylline, a cAMP activator. These effects were associated with decreased mitochondrial membrane potential and lactate production. No differences concerning UCP3 expression, however, were observed in spermatozoa from normozoospermic versus asthenozoospermic men (n = 6). The inhibition of UCPs did not increase ROS production, possibly due to the decreased mitochondrial activity and genipin antioxidant properties. In sum, UCPs are major regulators of human spermatozoa motility and metabolism. The discovery and characterization of UCPs’ role in human spermatozoa can shed new light on spermatozoa ROS-related pathways and bioenergetics physiology.
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 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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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 (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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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 depth (PPD) and vertical clinical attachment loss (CAL-V) of direct abutment (DA), indirect abutment (IA) and control teeth (CT). Also complications and failures of UCPD were analysed using questionnaire of participant satisfaction with UCPD (stability, comfort and manipulation). Results Evaluation of data showed that CAL-V and PPD significantly increased over time for DA, IA and CT (p<0.0001), but the tooth function (DA, IA and CT) did not significantly influence changes in PPD and CAL-V. The fracture of one abutment tooth and increase of the number of artificial teeth deformations (p=0.039) were observed after 5 years. Participant satisfaction with denture after 1 year and 5 years vs. 7 days was significantly improved. Conclusion Despite limitations of this clinical study and assuming regular oral maintenance with proper indication, UCPD might be considered as good treatment option for Kennedy II rehabilitation in patients not indicated for implant therapy or who cannot tolerate extensive RPD design.
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 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.
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, 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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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 how the ECJ could, in a suitable case, consider the breach of a CSR policy either as a form of misleading market communication or as unfair trading behaviour. This interpretation would allow for the additional regulation of CSR by the UCTD, which overlaps with the UCPD in terms of scope, interpretation and remedies. Once CSR is subject to EU market regulation laws, it can result additionally in contract regulation through EU consumer sales law.
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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 CoQH2 to CoQ which is shown by Klingenberg and coworkers to be cofactor for UCPs. This results in strong uncoupling and thermogenesis mediated by UCP1, 2 and 3. In the UCP1-ablated mice, activity of UCP2 and 3 appears to be insufficient to induce CoQH2 oxidation in resting brown fat mitochondria, which results in hypothermia.
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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 mRNA in brown adipose tissue and UCP2 mRNA in white adipose tissue. This dose of capsiate did not change serum triiodothyronine or thyroxine levels. A single dose of capsiate temporarily raised both UCP1 mRNA in brown adipose tissue and UCP3 mRNA in skeletal muscle. These results suggest that UCP1 and UCP2 may contribute to the promotion of energy metabolism by capsiate, but that thyroid hormones do not.
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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, CGP-12177 (0.75 mg/kg), increased UPC3 mRNA by 40% in the innervated and by 85% in the denervated BAT. Leptin (0.9 mg/day for 3 days) increased both UCP2 and UCP3 mRNA by 30% in the innervated and, surprisingly, in the denervated BAT. RA (7.5 mg/kg) increased UCP1 mRNA but decreased UCP2 and UCP3 mRNA by 50%, whereas methylprednisolone (65 mg/kg, two doses 24 h apart) suppressed all three uncoupling proteins by greater than 60%. The present findings indicate that: sympathetic innervation is necessary to maintain basal levels of UCP3 mRNA; beta(3)-adrenergic agonist stimulation induces UCP3 mRNA; leptin induces UCP2 and UCP3 mRNA and this induction is not dependent on sympathetic innervation; RA increases UCP1 but decreases UCP2 and UCP3 mRNA; and methylprednisolone suppresses UCP1, UCP2, and UCP3 mRNA equally. These data suggest that there are distinct patterns of regulation between UCP1, UCP2, and UCP3, and there may be at least two modes by which leptin could modulate thermogenesis in BAT; first, by increasing sympathetic stimulation of BAT and induction of UCP1 mRNA and, secondly, by increasing UCP2 and UCP3 mRNA by a mechanism independent of sympathetic stimulation.
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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 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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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 average consumer test applied? How does the CJEU test the average consumer? How is the average consumer characterized? Who decides who the average consumer is (institutional dimension?) Is the ‘average consumer’ in the UCPD case law the same ‘average consumer’ as elsewhere? The results show that the ‘average consumer’ concept performs a distinct function in UCPD adjudication and has matured to a selfreferential ‘average consumer’ interpretation isolated from case law rendered in other areas. We argue that when the ‘average consumer’ serves as a constitutive feature in order to define what constitutes a misleading practice, a stronger mandate for the CJEU to interpret the concept can be warranted.
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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 on current research in economic theory, it argues for applying a stricter average consumer test if the market for ad intermediaries is highly concentrated. This stricter test should neutralize negative effects of behavioural targeting on consumer welfare. The article shows how OBA can amount to a misleading action and/or a misleading omission under Articles 6 and 7 UCPD, as well as an aggressive practice under Article 8 UCPD. It further considers how the recent legislative proposals by the European Commission to enact a Digital Markets Act (DMA) and a Digital Services Act (DSA) may interact with the UCPD and the suggested stricter average consumer test.
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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 predictive value 1): citrate synthase, phosphoglucose isomerase, succinate dehydrogenases A/C, UCP3, UCP2, UCP4, UCP5, phosphoglycerate mutase, glyceraldehyde 3-P dehydrogenase, glucokinase, malate dehydrogenase, acyl-CoA transferase (thiolase), cytochrome a3, and lactate dehydrogenase. Moreover, some enzymes have not yet been described in the literature as genomically regulated by T3. CONCLUSION: Our results point to other enzymes which may possibly be regulated by T3 and CREB, and speculate their joint roles in contributing to the optimal thermogenic acclimation.
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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 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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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 pancreatic beta cells and triggers the gradual development of the chronic metabolic dysfunction that characterizes T2D. At the same time, decreased glucose oxidation in skeletal muscle due to mitochondrial damage leads to prolonged postprandial blood glucose rise, which further worsens glucose homeostasis. ROS are not only highly reactive by-products of mitochondrial respiration capable of oxidizing DNA, proteins, and lipids but can also function as signaling and effector molecules in cell membranes mediating signal transduction and inflammation. Mitochondrial uncoupling proteins (UCPs) located in the inner mitochondrial membrane of various tissues can be activated by ROS to protect cells from mitochondrial damage. Mitochondrial UCPs facilitate the reflux of protons from the mitochondrial intermembrane space into the matrix, thereby dissipating the proton gradient required for oxidative phosphorylation. There are five known isoforms (UCP1-UCP5) of mitochondrial UCPs. UCP1 can indirectly reduce ROS formation by increasing glutathione levels, thermogenesis, and energy expenditure. In contrast, UCP2 and UCP3 regulate fatty acid metabolism and insulin secretion by beta cells and modulate insulin sensitivity. Understanding the functions of UCPs may play a critical role in developing pharmacological strategies to combat T2D. This review summarizes the current knowledge on the protective role of various UCP homologs against age-related oxidative stress in T2D.
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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 through these proteins is still enthusiastically debated. This is due to compelling evidence that UCP2/3 fulfill other function(s) and the inability to reproduce findings that UCP1-3 use inducible leaks to control reactive oxygen species (ROS) production. Further, other studies have found that UCP2/3 may serve as Ca2+. Therefore, we performed a systematic review aiming to summarize the results collected on the topic. A literature search using a list of curated keywords in Pubmed, BIOSIS Citation Index and Scopus was conducted. Potentially relevant references were screened, duplicate references eliminated, and then literature titles and abstracts were evaluated using Rayyan software. A total of 1101 eligible studies were identified for the review. From this total, 416 studies were evaluated based on our inclusion criteria. In general, most studies identified a role for UCPs in preventing oxidative stress, and in some cases, this may be related to the induction of leaks and lowering protonic backpressure on the respiratory chain. However, some studies also generated evidence that UCP2/3 may mitigate oxidative stress by transporting Ca2+ into the matrix, exporting lipid hydroperoxides, or by transporting C-4 metabolites. Additionally, some showed that activating UCP1 or 3 can increase mitochondrial ROS production, even though there is still augmented protection from oxidative stress. Conclusion: Overall, most available studies demonstrate that UCPs, particularly UCP2/3, prevent oxidative stress. However, the mechanism utilized to do so remains elusive and raises the question that UCP2/3 should be renamed, since they may still not be true “uncoupling proteins”.
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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. Therefore, we conducted a meta-analysis of 32 publications in total on the effect of cold stress on the expression of ATGL, CIDEA, UCP2, and UCP3. Our results showed that cold stress affected the expression of swine adipocyte genes; specifically, it was positively correlated with the expression of UCP3 in swine adipocytes. Conversely, expression of ATGL was negatively affected under cold stress conditions. In addition, the loss of functional UCP1 in pigs likely triggered a compensatory increase in UCP3 activity. We also simulated the docking results of UCP2 and UCP3. Our results showed that UCP2 could strongly bind to adenosine triphosphate (ATP), meaning that UCP3 played a more significant role in pig adipocytes.
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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 the brown adipose tissue (BAT) of WT mice. Leptin also increased UCP2 mRNA in WAT of both WT and UCP1-deficient mice but increased UCP2 and UCP3 mRNA only in BAT from UCP1-deficient mice. These results indicate that leptin reduces WAT through a peripheral mechanism requiring the presence of UCP1, with little or no involvement of UCP2 or UCP3.
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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 down-regulation of UCP1 mRNA and UCP3 mRNA. In most cases this resulted in a less marked decrease in UCP1 and UCP3 protein in BAT mitochondria owing to lactation. Fasting for 24h caused a different response in UCP1 and UCP3 mRNA expression: it decreased UCP1 mRNA levels but had no effect on UCP3 mRNA abundance in virgin mice; it even increased UCP3 mRNA expression in lactating dams. These changes did not lead to modifications in UCP1 or UCP3 protein abundance. Whereas acute treatment with peroxisome-proliferator-activated receptor (PPAR)α and PPARγ agonists increased UCP1 mRNA levels only in lactating dams, UCP3 mRNA expression was induced by both kinds of PPAR activator in lactating dams and by PPARα agonists in virgin mice. It is concluded that modifications of UCP2 mRNA levels are not part of the physiological adaptations taking place in BAT during lactation. In contrast, the down-regulation of UCP3 mRNA expression and mitochondrial UCP3 content is consistent with a role for the gene encoding UCP3 in the decrease in metabolic fuel oxidation and thermogenesis in BAT during lactation.
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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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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 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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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 suggested to regulate the [ATP]/[ADP] ratio and was recently shown to influence insulin secretion in the β-cells of the pancreas. UCP3, in contrast, is expressed predominantly in skeletal muscle and has been associated with whole-body energy metabolism. However, the primary function of UCP3 is not the regulation of energy metabolism. For example, fasting, a condition attenuating energy expenditure, upregulates UCP3 expression. Moreover, UCP3-knockout mice have a normal metabolic rate. The exact function of UCP3 therefore remains to be elucidated, but putative roles for UCP3 include involvement in the regulation of ROS, in mitochondrial fatty acid transport and in the regulation of glucose metabolism in skeletal muscle. Whatever the primary function of these novel uncoupling proteins, a secondary effect via uncoupling might allow them to influence (but not to regulate) energy metabolism, which would be consistent with the observations from linkage and association studies. Therefore, UCP2 and UCP3 remain interesting targets for pharmacological upregulation in the treatment of obesity and diabetes.
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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 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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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 analysis. We show that UCP3 has a short half-life of 0.5–4 h. Rapid degradation was prevented by a cocktail of proteasome inhibitors, supporting a proteasomal mechanism for turnover. In addition, this phenotype is recapitulated in vitro: UCP3 was degraded in mitochondria isolated from rat skeletal muscle or brown adipose tissue with a half-life of 0.5–4 h, but only in the presence of a purified 26S proteasomal fraction. This in vitro proteolysis was also sensitive to proteasome inhibition. This phenotype is in direct contrast with the related proteins UCP1 and the adenine nucleotide translocase, which have long half-lives. Therefore UCP3 is turned over rapidly in multiple cell types in a proteasome-dependent manner.
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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. Coenzyme Q10 did not further significantly activate the observed H+ efflux. In conclusion, careful instant reconstitution yields intact functional recombinant proteins, UCP2 and UCP3, the activity of which is comparable with UCP1.
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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 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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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 values are better: four studies report associations of 0.001 (2 studies) to 0.002 (1 study) and 0.005 (1 study) for a UCP2 insertion/deletion variant, while the best P values for association of UCP3 with BMI are 0.003 (1 study) and 0.0037 (1 study). UCP2 and 3 are adjacent to each other on chromosome 11 and variants in each are in linkage disequilibrium. Thus, variants in UCP2 or 3 may influence results from association studies of variants in the other. Since UCP2 has a greater influence on BMI in humans than UCP3, then the two most likely hypotheses are that only UCP2 affects BMI, and positive results for UCP3 result from linkage disequilibrium to UCP2, or both UCP2 and 3 affect BMI. It is unlikely that only UCP3 influences BMI. UCP2 associations have been observed in a variety of ethnic groups, including Caucasians, African Americans, South Indians and Chinese. Consistent results from diverse ethnic groups are concordant with the hypothesis that the UCP2 insertion/deletion variant itself underlies the association with BMI.
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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 identified which is highly conserved in all vertebrate UCP2 transcripts. Analysis of tissue specificity in A. flavipes with homologous cDNA probes revealed ubiquitous presence of UCP2 mRNA and striated muscle specificity of UCP3 mRNA resembling the known expression pattern in rodents. Neither UCP2 nor UCP3 gene expression was stimulated in adipose tissue and skeletal muscle of cold exposed A. flavipes. However, UCP3 mRNA expression was upregulated 6-fold in heart and 2.5-fold in skeletal muscle as reported for rodents in response to fasting. Furthermore, UCP3 mRNA seems to be coregulated with PDK4 mRNA, indicating a relation to enhanced lipid metabolism. In contrast, UCP2 gene expression was not regulated in response to fasting in adipose tissue and skeletal muscle but was diminished in the lung and increased in adipose tissue. Taken together, the sequence analysis, tissue specificity and physiological regulation suggest a conserved function of UCP2 and UCP3 during 130 million years of mammalian evolution.
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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 saline control (P < 0.03). The same treatment with leptin decreased plasma insulin levels but did not affect the plasma glucose level (P < 0.05 for insulin). Among the major regulators of the transportation or utilization of energy substrates, leptin treatment increased expression of mRNA for uncoupling protein 1 (UCP1) in brown adipose tissue (BAT), UCP2 in WAT, and UCP3 in quadriceps skeletal muscle, but not those for fatty acid–binding protein in WAT, carnitine phosphate transferase-1, a marker for β oxidation of fatty acids in muscle, nor glucose transporter 4 in WAT and muscle (P < 0.01 for HSL, P < 0.05 for UCP1, and P < 0.005 for UCP2 and UCP3). These results indicate that, even in a single bolus, leptin may regulate the mobilization and/or utilization of energy substrates such as fatty acids by affecting lipolytic activity in WAT and by increasing the expression of UCPs in BAT, WAT, and muscle.
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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- 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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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 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.
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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 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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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 mitochondria per se, and whether this could be modulated by UCPs. Superoxide formation by isolated bovine aortic endothelial cell (BAE) mitochondria, determined using electron paramagnetic resonance spectroscopy, was approximately fourfold greater during state 4 compared with state 3 respiration. UCP1 and UCP2 overexpression both increased the proton conductance of endothelial cell mitochondria, as rigorously determined by the kinetic relationship of respiration to inner membrane potential. However, despite uncoupling, neither UCP1 nor UCP2 altered superoxide formation. Antimycin, known to increase mitochondrial superoxide, was studied as a positive control and markedly enhanced the superoxide spin adduct in our mitochondrial preparations, whereas the signal was markedly impaired by the powerful chemical uncoupler p-(trifluoromethoxyl)-phenyl-hydrazone. In summary, we show that UCPs do have uncoupling properties when expressed in BAE mitochondria but that uncoupling by UCP1 or UCP2 does not prevent acute substrate-driven endothelial cell superoxide as effluxed from mitochondria respiring in vitro.
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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 activity rhythms at either the 1- or 2-G level. Percent body fat was significantly lower in transgenic (5.2 ± 0.2%) relative to the wild-type mice (6.2 ± 0.1%) after 2-G exposure; mass-adjusted mesenteric and epididymal fat pads in transgenic mice were also significantly lower ( P < 0.05). The data suggest that 1) the actions of two UCPs (UCP2 and UCP3) do not contribute to an altered energy balance at 2 G, although 2) UCP2 and UCP3 do contribute to the utilization of lipids as a fuel substrate at 2 G.
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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 reduction and uncoupling protein (UCP)1, UCP2, UCP3, and peroxisome proliferator-activated receptor gamma coactivator-1 PGC-1α levels in aging rats. Eight male Wistar rats (80 weeks old) were divided into control and treatment groups. Both groups were fed a standard diet, and the treatment group was given 8.1 mg/kg body weight/day of NuSE via oral gavage for 12 weeks. After 12 weeks, the levels of UCP1, UCP2, UCP3, and PGC-1α from both inguinal WAT (iWAT) and interscapular brown adipose tissue (BAT) were examined. We observed that the administration of NuSE has no significant effect to the decreasement of rats body weights (p = 0.464), levels of UCP1 (p = 0.686), UCP2 (p = 0.360), UCP3 (p = 0.076), and PGC-1α (p = 0.200).
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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. However, 10 mmol/l and higher concentration of calcium led to arrhythmia and drastic decrease in contractility of isolated heart more obvious in untrained rats. Swimming course prevented the calcium-induced release of mitochondrial factor exerting a stabilizing effect on mitochondrial membranes which was, however, diminished by a nitric oxide synthesis blocker (L-NAME). We have found that UCPs genes expression is calcium-sensitive: an increase in UCP3 mRNA at 5 mmol of calcium and a sharp decrease in UCP2/3 expression at 12.5 mmol/l of calcium in perfusate in both trained and untrained rats indicating the participation of UCPs in the regulation of calcium homeostasis. Our data suggest that the calcium load may serve as a test for in situ MPTP titration. Activation of UCPs together with up-regulated nitric oxide may play a protective role against increasing extracellular calcium inhibiting MPTP formation during physical trainings.
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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 the role of UCP1 in the anti-obesity effect of β3-adrenergic stimulation, in the present study, UCP1-KO and wild-type (WT) mice were fed on cafeteria diets for 8 wk and then given a β3-adrenergic agonist, CL-316,243 (CL), or saline for 2 wk. A single injection of CL increased whole body oxygen consumption and brown fat temperature in WT mice but not in KO mice, and it elicited almost the same plasma free fatty acid response in WT and KO mice. WT and KO mice increased similarly their body and white fat pad weights on cafeteria diets compared with those on laboratory chow. Daily treatment with CL resulted in a marked reduction of white fat pad weight and the size of adipocytes in WT mice, but not in KO mice. Compared with WT mice, KO mice expressed increased levels of UCP2 in brown fat but decreased levels in white fat and comparable levels of UCP3. It was concluded that the anti-obesity effect of β3-adrenergic stimulation is largely attributable to UCP1, but less to UCP2 and UCP3, and thereby to UCP1-dependent degradation of fatty acids released from white adipose tissue.
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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.
Full textAbstract:
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.