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The Uncoupling Protein 1 Gene (UCP1) Is Disrupted in the Pig Lineage: A Genetic Explanation for Poor Thermoregulation in Piglets  [PDF]
Frida Berg,Ulla Gustafson,Leif Andersson
PLOS Genetics , 2006, DOI: 10.1371/journal.pgen.0020129
Abstract: Piglets appear to lack brown adipose tissue, a specific type of fat that is essential for nonshivering thermogenesis in mammals, and they rely on shivering as the main mechanism for thermoregulation. Here we provide a genetic explanation for the poor thermoregulation in pigs as we demonstrate that the gene for uncoupling protein 1 (UCP1) was disrupted in the pig lineage. UCP1 is exclusively expressed in brown adipose tissue and plays a crucial role for thermogenesis by uncoupling oxidative phosphorylation. We used long-range PCR and genome walking to determine the complete genome sequence of pig UCP1. An alignment with human UCP1 revealed that exons 3 to 5 were eliminated by a deletion in the pig sequence. The presence of this deletion was confirmed in all tested domestic pigs, as well as in European wild boars, Bornean bearded pigs, wart hogs, and red river hogs. Three additional disrupting mutations were detected in the remaining exons. Furthermore, the rate of nonsynonymous substitutions was clearly elevated in the pig sequence compared with the corresponding sequences in humans, cattle, and mice, and we used this increased rate to estimate that UCP1 was disrupted about 20 million years ago.
The role of the uncoupling protein 1 (UCP1) on the development of obesity and type 2 diabetes mellitus
Brondani, Letícia de Almeida;Assmann, Taís Silveira;Duarte, Guilherme Coutinho Kullmann;Gross, Jorge Luiz;Canani, Luís Henrique;Crispim, Daisy;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2012, DOI: 10.1590/S0004-27302012000400001
Abstract: it is well established that genetic factors play an important role in the development of both type 2 diabetes mellitus (dm2) and obesity, and that genetically susceptible subjects can develop these metabolic diseases after being exposed to environmental risk factors. therefore, great efforts have been made to identify genes associated with dm2 and/or obesity. uncoupling protein 1 (ucp1) is mainly expressed in brown adipose tissue, and acts in thermogenesis, regulation of energy expenditure, and protection against oxidative stress. all these mechanisms are associated with the pathogenesis of dm2 and obesity. hence, ucp1 is a candidate gene for the development of these disorders. indeed, several studies have reported that polymorphisms -3826a/g, -1766a/g and -112a/c in the promoter region, ala64thr in exon 2 and met299leu in exon 5 of ucp1 gene are possibly associated with obesity and/or dm2. however, results are still controversial in different populations. thus, the aim of this study was to review the role of ucp1 in the development of these metabolic diseases.
The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study
Michèle M Sale, Fang-Chi Hsu, Nicholette D Palmer, Candace J Gordon, Keith L Keene, Hermina M Borgerink, Arun J Sharma, Richard N Bergman, Kent D Taylor, Mohammed F Saad, Jill M Norris
BMC Endocrine Disorders , 2007, DOI: 10.1186/1472-6823-7-1
Abstract: We genotyped five promoter or coding single nucleotide polymorphisms (SNPs) in 239 African American (AA) participants and 583 Hispanic participants from San Antonio (SA) and San Luis Valley. Generalized estimating equations using a sandwich estimator of the variance and exchangeable correlation to account for familial correlation were computed for the test of genotypic association, and dominant, additive and recessive models. Tests were adjusted for age, gender and BMI (glucose homeostasis and lipid traits), or age and gender (obesity traits), and empirical P-values estimated using a gene dropping approach.UCP1 A-3826G was associated with AIRg in AA (P = 0.006) and approached significance in Hispanic families (P = 0.054); and with HDL-C levels in SA families (P = 0.0004). Although UCP1 expression is reported to be restricted to adipose tissue, RT-PCR indicated that UCP1 is expressed in human pancreas and MIN-6 cells, and immunohistochemistry demonstrated co-localization of UCP1 protein with insulin in human islets. UCP2 A55V was associated with waist circumference (P = 0.045) in AA, and BMI in SA (P = 0.018); and UCP2 G-866A with waist-to-hip ratio in AA (P = 0.016).This study suggests a functional variant of UCP1 contributes to the variance of AIRg in an AA population; the plausibility of this unexpected association is supported by the novel finding that UCP1 is expressed in islets.Uncoupling proteins are mitochondrial inner membrane electron carriers [1]. Uncoupling protein 2 (UCP2) inhibits glucose stimulated insulin secretion, and models of type 2 diabetes are associated with increased expression in islets [2]. Polymorphisms in the uncoupling protein genes UCP1 (4q31.21) and UCP2 (11q13.4) have been associated with a number of measures of glucose homeostasis and adiposity. These include associations between UCP2 G866A and A55V and glucose-induced insulin secretion [3-5], as well as obesity and metabolism [6-8]. Associations with obesity, weight gain and metaboli
UCP1 Induction during Recruitment of Brown Adipocytes in White Adipose Tissue Is Dependent on Cyclooxygenase Activity  [PDF]
Lise Madsen,Lone M. Pedersen,Haldis Haukaas Lillefosse,Even Fj?re,Ingeborg Bronstad,Qin Hao,Rasmus K. Petersen,Philip Hallenborg,Tao Ma,Rita De Matteis,Pedro Araujo,Josep Mercader,M. Luisa Bonet,Jacob B. Hansen,Barbara Cannon,Jan Nedergaard,Jun Wang,Saverio Cinti,Peter Voshol,Stein Ove D?skeland,Karsten Kristiansen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011391
Abstract: The uncoupling protein 1 (UCP1) is a hallmark of brown adipocytes and pivotal for cold- and diet-induced thermogenesis.
Rol de las proteinas desacoplantes UCP1, UCP2 y UCP3 en el gasto energetico, diabetes tipo 2 y obesidad: Sinergismo con la tiroides Role of uncoupling proteins UCP1, UCP2 and UCP3 in energy balance, type 2 diabetes and obesity: Synergism with the thyroid  [cached]
ángel A. Zaninovich
Medicina (Buenos Aires) , 2005,
Abstract: La formación de tejido graso resulta del balance entre la ingestión y el consumo de energía, lo cual destaca la importancia del estudio de los factores que controlan el gasto energético. La hormona tiroidea es conocida desde hace tiempo como el principal regulador del metabolismo basal, a través de la estimulación del consumo de oxígeno en las células. El descubrimiento de la grasa parda y de la proteína desacoplante-1 (UCP1) demostró la importancia de este tejido para la regulación del consumo energético en mamíferos. La proteína desacoplante-2 (UCP2) se expresa en muchos tejidos y tendría una acción protectora de la función celular, al preservar el potencial de membrana afectado por el superóxido. La proteína desacoplante-3 (UCP3) estaría vinculada a la producción de calor, facilitando la combustión de ácidos grasos en la cadena respiratoria mitocondrial, pero no parece participar en el control del gasto energético. El exceso de UCP3 en ratones transgénicos disminuyó la grasa corporal y aumentó la sensibilidad a la insulina seguido de hipoglucemia, sugiriendo así un futuro, hipotético uso de esta proteína en la diabetes 2 y en la obesidad. Los estudios que se realizan sobre estas proteínas y sobre hormonas del tejido adiposo blanco como la leptina, adiponectina, resistina, de péptidos hipotalámicos como neuropéptido Y, CRF, hormona alfa-melanocítica y péptidos regulados por cocaína y anfetamina (CART), muestran resultados promisorios para una futura aplicación en el control del gasto energético en humanos y con ello en la prevención o el tratamiento de la obesidad y la diabetes tipo 2. Accumulation of fat in the tissues results from the balance between energy intake and expenditure. The thyroid hormones have long been known to be the main regulators of basal metabolism through its stimulation of oxygen consumption in cells. The discovery of brown adipose tissue (BAT) and its unique activity of heat production and dissipation through the action of uncoupling protein-1 (UCP1) during cold stress, showed the relevance of this tissue for energy expenditure in lower mammals. UCP1 is only expressed in BAT through the synergistic action of norepinephrine (NE) and thyroid hormones in animals exposed to cold and to a lesser degree after meals. The uncoupling protein-2 (UCP2) is found in many tissues and exerts dual effects: it protects cells function from damage caused by reactive oxygen species (ROS). On the other hand, the uncoupling induced by UCP2 in mitochondria of pancreatic cells decreases ATP síntesis and impairs insulin secretion in response to gluco
Uncoupling Protein 1 of Brown Adipocytes, the Only Uncoupler: A Historical Perspective  [PDF]
Daniel Ricquier
Frontiers in Endocrinology , 2011, DOI: 10.3389/fendo.2011.00085
Abstract: Uncoupling protein 1 (UCP1), is a unique mitochondrial membranous protein devoted to adaptive thermogenesis, a specialized function performed by brown adipocytes. Whereas the family of mitochondrial metabolite carriers comprises ~40 members, UCP1 is the only memberable to translocate protons through the inner membrane of brown adipocyte mitochondria. By this process, UCP1 uncouples respiration from ATP synthesis and therefore provokes energy dissipation in the form of heat while, also stimulating high levels of fatty acid oxidation. UCP1 homologs were identified but they are biochemically and physiologically different from UCP1. Thirty five years after its identification, UCP1 still appears as a fascinating component. The recent renewal of the interest in human brown adipose tissue makes UCP1 as a potential target for strategies of treatment of metabolic disorders.
Role of IL-6 in Exercise Training- and Cold-Induced UCP1 Expression in Subcutaneous White Adipose Tissue  [PDF]
Jakob G. Knudsen, Maria Murholm, Andrew L. Carey, Rasmus S. Biens?, Astrid L. Basse, Tamara L. Allen, Juan Hidalgo, Bronwyn A. Kingwell, Mark A. Febbraio, Jacob B. Hansen, Henriette Pilegaard
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0084910
Abstract: Expression of brown adipose tissue (BAT) associated proteins like uncoupling protein 1 (UCP1) in inguinal WAT (iWAT) has been suggested to alter iWAT metabolism. The aim of this study was to investigate the role of interleukin-6 (IL-6) in exercise training and cold exposure-induced iWAT UCP1 expression. The effect of daily intraperitoneal injections of IL-6 (3 ng/g) in C57BL/6 mice for 7 days on iWAT UCP1 expression was examined. In addition, the expression of UCP1 in iWAT was determined in response to 3 days of cold exposure (4°C) and 5 weeks of exercise training in wild type (WT) and whole body IL-6 knockout (KO) mice. Repeated injections of IL-6 in C57BL/6 mice increased UCP1 mRNA but not UCP1 protein content in iWAT. Cold exposure increased iWAT UCP1 mRNA content similarly in IL-6 KO and WT mice, while exercise training increased iWAT UCP1 mRNA in WT mice but not in IL-6 KO mice. Additionally, a cold exposure-induced increase in iWAT UCP1 protein content was blunted in IL-6 KO mice, while UCP1 protein content in iWAT was lower in both untrained and exercise trained IL-6 KO mice than in WT mice. In conclusion, repeated daily increases in plasma IL-6 can increase iWAT UCP1 mRNA content and IL-6 is required for an exercise training-induced increase in iWAT UCP1 mRNA content. In addition IL-6 is required for a full induction of UCP1 protein expression in response to cold exposure and influences the UCP1 protein content iWAT of both untrained and exercise trained animals.
中?之??蛋化石  [PDF]
地质论评 , 1937,
Abstract: (一)?去研究中?北方各地新生代後期各地?中,常有易?的一?化石,就是鸵?蛋。他的骨格?也有??,但至今所知尚少。?其蛋皮,差不多每次旅行,都可以?得若干,但完全的究?少?。安特生在他的中?北部之新生界一?中,有一篇文章,??????
Synergism between cAMP and PPAR Signalling in the Initiation of UCP1 Gene Expression in HIB1B Brown Adipocytes  [PDF]
H. Y. Chen,Q. Liu,A. M. Salter,M. A. Lomax
PPAR Research , 2013, DOI: 10.1155/2013/476049
Abstract: Expression of the brown adipocyte-specific gene, uncoupling protein 1 (UCP1), is increased by both PPAR stimulation and cAMP activation through their ability to stimulate the expression of the PPAR coactivator PGC1 . In HIB1B brown preadipocytes, combination of the PPAR agonist, rosiglitazone, and the cAMP stimulator forskolin synergistically increased UCP1 mRNA expression, but PGC1 expression was only increased additively by the two drugs. The PPAR antagonist, GW9662, and the PKA inhibitor, H89, both inhibited UCP1 expression stimulated by rosiglitazone and forskolin but PGC1 expression was not altered to the same extent. Reporter studies demonstrated that combined rosiglitazone and forskolin synergistically activated transcription from a full length 3.1?kbp UCP1 luciferase promoter construct, but the response was only additive and much reduced when a minimal 260?bp proximal UCP1 promoter was examined. Rosiglitazone and forskolin in combination were able to synergistically stimulate promoters comprising of tandem repeats of either PPREs or CREs. We conclude that rosiglitazone and forskolin act together to synergistically activate the UCP1 promoter directly rather than by increasing PGC1 expression and by a mechanism involving cross-talk between the signalling systems regulating the CRE and PPRE on the promoters. 1. Introduction Nonshivering thermogenesis in brown adipose tissue (BAT) in response to a cold environment is initiated by sympathetic neural stimulation of -adrenergic receptors on brown adipocytes which elevate intracellular cyclic AMP (cAMP) and, via the protein kinase A (PKA) pathway, increase the expression and thermogenic activity of uncoupling protein 1 (UCP1) [1]. UCP1 is BAT specific and responsible for uncoupling oxidative phosphorylation by enabling protons to return to the mitochondrial matrix without ATP synthesis, thereby producing heat. UCP1 expressing BAT has recently been identified in humans and has been proposed as a target for activation to increase energy expenditure and prevent or treat obesity [2]. UCP1 expression has been suggested to be regulated by the cAMP-inducible peroxisome proliferator activated coactivator 1 (PGC1 ) which interacts with a BAT determination factor, PRDM16, to increase the expression of a number of BAT-selective genes including Cidea [3]. We have also shown that the cAMP-inducible transcription factor C/EBP stimulates PGC1 expression in white and brown adipocytes by binding to the cAMP response element (CRE) on the PGC1 proximal promoter [4, 5] while others have demonstrated that PKA activation of
Molecular evolution of UCP1 and the evolutionary history of mammalian non-shivering thermogenesis
David A Hughes, Martin Jastroch, Mark Stoneking, Martin Klingenspor
BMC Evolutionary Biology , 2009, DOI: 10.1186/1471-2148-9-4
Abstract: Models of adaptive evolution through phylogenetic analysis of amino acid sequences by maximum likelihood were implemented to determine the mode of UCP1 protein evolution in Eutherians. An increase in the rate of amino acid substitutions on the branch leading to Eutherians is observed, but is best explained by relaxed constraints, not positive selection. Further, evidence for branch and site heterogeneity in selection pressures, as well as divergent selection pressures between UCP1 and its paralogs (UCP2-3) is observed.We propose that the unique thermogenic function of UCP1 in Eutherians may be best explained by neutral processes. Along with other evidence, this suggests that the primary biochemical properties of UCP1 may not differ between Eutherians and non-Eutherians.Uncoupling protein 1 (UCP1) is a mitochondrial protein carrier which, until recently, was thought to be found only in endothermic placental (Eutherian) mammals [1,2]. In Eutherians, UCP1 is the only gene known to be exclusively expressed in brown adipose tissue (BAT), accounting for up to 5% of the total mitochondrial protein in BAT [3]; UCP1 (also known as thermogenin) provides Eutherians, particularly small mammals, hibernators and newborns, with a unique mechanism of non-shivering thermogenesis (NST) [4]. UCP1-dependent NST is probably a feature of most Eutherian mammals, as it has been found recently in the rock elephant shrew, a member of the Afrotherian mammalian lineage which separated early during the evolution of the Eutherians [5]. NST is produced by increasing the proton conductance in the inner membrane of brown adipocyte mitochondria. This increased proton conductance uncouples mitochondrial respiration from ATP synthesis and thereby dissipates the proton motive force as heat [6-9]. It is the high oxidative capacity of mitochondria in BAT and the cellular composition of BAT that allows heat dissipation rates at a power of 300 – 400 W/kg [10-12]. It is these properties of BAT, their mitoch
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