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Leite, Celso Vieira de Souza
[PMID]:28977211
[Au] Autor:Schnor NPP; Verlengia R; Novais PFS; Crisp AH; Leite CVS; Rasera-Junior I; Oliveira MRM
[Ad] Endereço:Universidade Estadual Paulista Júlio de Mesquita Filho (Unesp), Programa de Pós-Graduação em Alimentos e Nutrição, Araraquara, SP, Brasil.
[Ti] Título:Association of 5-HT2C (rs3813929) and UCP3 (rs1800849) gene polymorphisms with type 2 diabetes in obese women candidates for bariatric surgery.
[So] Source:Arch Endocrinol Metab;61(4):326-331, 2017 Jul-Aug.
[Is] ISSN:2359-4292
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Obesity can cause systemic arterial hypertension (SAH) and type 2 diabetes mellitus (DM2) factor that is also influenced by genetic variability. The present study aims to investigate the association between gene polymorphisms related with obesity on the prevalence of SAH and DM2 in the preoperative period and 1 year after Roux-en-Y gastric bypass surgery. SUBJECTS AND METHODS: In total, 351 obese women in a Brazilian cohort completed the study. The clinical diagnosis of SAH and DM2 was monitored from medical records. Twelve gene polymorphisms (rs26802; rs572169; rs7799039; rs1137101; rs3813929; rs659366; rs660339; rs1800849; rs7498665; rs35874116; rs9701796; and rs9939609) were determined using real-time polymerase chain reaction and TaqMan assay. RESULTS: In the preoperative period, prevalence of SAH and DM2 was 57% and 22%, respectively. One year postoperatively, 86.8% subjects had remission of DM2 and 99.5% had control of SAH. Subjects with T allele from the serotonin receptor gene (5-HT2C, rs3813929) had five times greater chance of DM2, and the CC genotype from uncoupling protein 3 gene (UCP3, rs1800849) had three times greater chance in the preoperative period. CONCLUSION: These findings indicate that polymorphisms rs3813929 and rs1800849 from 5-HT2C and UCP3 genes were related to DM2 prevalence among the Brazilian obese women candidates for bariatric surgery.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/epidemiologia
Diabetes Mellitus Tipo 2/genética
Hipertensão/epidemiologia
Hipertensão/genética
Obesidade/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Adulto
Feminino
Derivação Gástrica
Seres Humanos
Meia-Idade
Obesidade/complicações
Obesidade/cirurgia
Período Pós-Operatório
Período Pré-Operatório
Prevalência
Estudos Prospectivos
Proteína Desacopladora 3/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (UCP3 protein, human); 0 (Uncoupling Protein 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE


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[PMID]:28336113
[Au] Autor:Duan Y; Zeng L; Li F; Wang W; Li Y; Guo Q; Ji Y; Tan B; Yin Y
[Ad] Endereço:Key Laboratory of Agro-ecological Processes in Subtropical Region, Institute of Subtropical Agriculture, Chinese Academy of Sciences, National Engineering Laboratory for Pollution Control and Waste Utilization in Livestock and Poultry Production; Hunan Provincial Engineering Research Center for Heal
[Ti] Título:Effect of branched-chain amino acid ratio on the proliferation, differentiation, and expression levels of key regulators involved in protein metabolism of myocytes.
[So] Source:Nutrition;36:8-16, 2017 Apr.
[Is] ISSN:1873-1244
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Branched-chain amino acids (BCAAs), including leucine (Leu), isoleucine (Ile), and valine (Val), are key regulators of protein synthesis in muscle. The aim of this study was to investigate the effect of different BCAA ratios (Leu:Ile:Val) on the proliferation, differentiation, and expression levels of the regulators related to protein metabolism of C2 C12 myocytes. METHODS: Studies were conducted in C2C12 myocytes exposed to different BCAA ratios (Leu: Ile: Val = 0, 1:0.25:0.25, 1:1:1). RESULTS: The ratio of 1:0.25:0.25 increased cell viability and promoted cell cycle progression from G0/G1 phase to S phase, which was an indicator of proliferation enhancement (P < 0.05). Moreover, this optimal ratio (1:0.25:0.25) promoted the differentiation of myocytes into myotubes by upregulating myogenin and interleukin-15 gene expression, and differently regulated the expression of L-type amino acid transporter 1 and 4 and system ASC amino acid transporters 2. Furthermore, the ratio stimulated mTOR expression at the mRNA and phosphorylated protein levels, as well as ribosomal protein S6 kinase and regulatory-associated protein of mTOR (raptor). In contrast, the optimal ratio decreased the amount of ubiquitin ligase muscle-specific RING finger 1 and muscle atrophy F-box during proliferation and differentiation (P < 0.05). No change was observed in the expression of key genes related to energy metabolism except for uncoupling protein 3 (P > 0.05). CONCLUSIONS: The results suggested that appropriate BCAA ratios could enhance proliferation and differentiation of the C2 C12 myocytes, also mediate the key regulators related to protein metabolism including the mTORC1 pathway. A proper utilization of balanced BCAA ratio in food would be beneficial to human and animal nutrition.
[Mh] Termos MeSH primário: Aminoácidos de Cadeia Ramificada/farmacologia
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Musculares/efeitos dos fármacos
Biossíntese de Proteínas
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Regulação para Baixo
Alvo Mecanístico do Complexo 1 de Rapamicina
Camundongos
Complexos Multiproteicos/genética
Complexos Multiproteicos/metabolismo
Células Musculares/metabolismo
Fibras Musculares Esqueléticas/citologia
Fibras Musculares Esqueléticas/efeitos dos fármacos
Fibras Musculares Esqueléticas/metabolismo
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Proteínas Ligases SKP Culina F-Box/genética
Proteínas Ligases SKP Culina F-Box/metabolismo
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/metabolismo
Proteínas com Motivo Tripartido/genética
Proteínas com Motivo Tripartido/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Proteína Desacopladora 3/genética
Proteína Desacopladora 3/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids, Branched-Chain); 0 (Multiprotein Complexes); 0 (Muscle Proteins); 0 (RNA, Messenger); 0 (Tripartite Motif Proteins); 0 (Ucp3 protein, mouse); 0 (Uncoupling Protein 3); EC 2.3.2.27 (Fbxo32 protein, mouse); EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases); EC 2.3.2.27 (Trim63 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE


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[PMID]:28236433
[Au] Autor:Kavanagh K; Davis AT; Peters DE; LeGrand AC; Bharadwaj MS; Molina AJ
[Ad] Endereço:Department of Pathology, Wake Forest School of Medicine, Wake Forest University Health Sciences, Winston-Salem, North Carolina, USA.
[Ti] Título:Regulators of mitochondrial quality control differ in subcutaneous fat of metabolically healthy and unhealthy obese monkeys.
[So] Source:Obesity (Silver Spring);25(4):689-696, 2017 Apr.
[Is] ISSN:1930-739X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Obesity exists with and without accompanying cardiometabolic disease, termed metabolically unhealthy obesity (MUO) and healthy obesity (MHO), respectively. Underlying differences in the ability of subcutaneous (SQ) fat to respond to nutrient excess are emerging as a key pathway. This study aimed to document the first spontaneous animal model of MHO and MUO and differences in SQ adipose tissue. METHODS: Vervet monkeys (Chlorocebus aethiops; N = 171) were screened for metabolic syndrome. A subset of MHO and MUO monkeys (n = 6/group) had SQ fat biopsies collected for histological evaluations and examination of key mitochondrial proteins. RESULTS: Obesity was seen in 20% of monkeys, and within this population, 31% were healthy, which mirrors human prevalence estimates. MUO monkeys had more than 60% lower adiponectin concentrations despite similar fat cell size, uncoupling protein 3, and activated macrophage abundance. However, alternatively activated/anti-inflammatory macrophages were 70% lower. Deficiencies of 50% or more in mitochondrial quality control regulators and selected mitochondrial fission and fusion markers were observed in the SQ fat of MUO monkeys despite comparable mitochondrial content. CONCLUSIONS: A novel and translatable spontaneously obese animal model of MHO and MUO, occurring independently of dietary factors, was characterized. Differences in mitochondrial quality and inflammatory cell populations of subcutaneous fat may underpin divergent metabolic health.
[Mh] Termos MeSH primário: Síndrome Metabólica/fisiopatologia
Mitocôndrias/metabolismo
Obesidade/fisiopatologia
Gordura Subcutânea/metabolismo
[Mh] Termos MeSH secundário: Adiponectina/análise
Animais
Biomarcadores/análise
Cercopithecus aethiops
Modelos Animais de Doenças
Ativação de Macrófagos
Macrófagos/metabolismo
Gordura Subcutânea/citologia
Proteína Desacopladora 3/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Biomarkers); 0 (Uncoupling Protein 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170226
[St] Status:MEDLINE
[do] DOI:10.1002/oby.21762


  4 / 910 MEDLINE  
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[PMID]:27919820
[Au] Autor:Patel HJ; Patel BM
[Ad] Endereço:Apex Pharmacy, Arroyo Grand, California, USA.
[Ti] Título:TNF-α and cancer cachexia: Molecular insights and clinical implications.
[So] Source:Life Sci;170:56-63, 2017 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cancer cachexia characterized by a chronic wasting syndrome, involves skeletal muscle loss and adipose tissue loss and resistance to conventional nutritional support. Cachexia is responsible for the reduction in quality and length of life of cancer patients. It also decreases the muscle strength of the patients. The pro-inflammatory and pro-cachectic factors produced by the tumor cells have important role in genesis of cachexia. A number of pro-inflammatory cytokines, like interleukin-1 (IL-1), IL-6, tumor necrosis factor- alpha (TNF-α) may have important role in the pathological mechanisms of cachexia in cancer. Particularly, TNF-α has a direct catabolic effect on skeletal muscle and causes wasting of muscle by the induction of the ubiquitin-proteasome system (UPS). In cancer cachexia condition, there is alteration in carbohydrate, protein and fat metabolism. TNF-α is responsible for the increase in gluconeogenesis, loss of adipose tissue and proteolysis, while causing decrease in protein, lipid and glycogen synthesis. It has been associated with the formation of IL-1 and increases the uncoupling protein-2 (UCP2) and UCP3 expression in skeletal muscle in cachectic state. The main aim of the present review is to evaluate and discuss the role of TNF-α in different metabolic alterations and muscle wasting in cancer cachexia.
[Mh] Termos MeSH primário: Caquexia/metabolismo
Neoplasias/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo/metabolismo
Animais
Anorexia/metabolismo
Carboidratos/química
Gluconeogênese
Seres Humanos
Inflamação
Resistência à Insulina
Interleucina-6/metabolismo
Lipídeos/química
Metabolismo
Músculo Esquelético/metabolismo
Atrofia Muscular/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Ubiquitina/química
Proteína Desacopladora 2/metabolismo
Proteína Desacopladora 3/metabolismo
Perda de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Carbohydrates); 0 (Interleukin-6); 0 (Lipids); 0 (Tumor Necrosis Factor-alpha); 0 (UCP2 protein, human); 0 (UCP3 protein, human); 0 (Ubiquitin); 0 (Uncoupling Protein 2); 0 (Uncoupling Protein 3); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170302
[Lr] Data última revisão:
170302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161207
[St] Status:MEDLINE


  5 / 910 MEDLINE  
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[PMID]:27871066
[Au] Autor:Aguer C; Piccolo BD; Fiehn O; Adams SH; Harper ME
[Ad] Endereço:Department of Biochemistry, Microbiology, and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada.
[Ti] Título:A novel amino acid and metabolomics signature in mice overexpressing muscle uncoupling protein 3.
[So] Source:FASEB J;31(2):814-827, 2017 Feb.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uncoupling protein 3 (UCP3) is highly selectively expressed in skeletal muscle and is known to lower mitochondrial reactive oxygen species and promote fatty acid oxidation; however, the global impact of UCP3 activity on skeletal muscle and whole-body metabolism have not been extensively studied. We utilized untargeted metabolomics to identify novel metabolites that distinguish mice overexpressing UCP3 in muscle, both at rest and after exercise regimens that challenged muscle metabolism, to potentially unmask subtle phenotypes. Male wild-type (WT) and muscle-specific UCP3-overexpressing transgenic (UCP3 Tg) C57BL/6J mice were compared with or without a 5 wk endurance training protocol at rest or after an acute exercise bout (EB). Skeletal muscle, liver, and plasma samples were analyzed by gas chromatography time-of-flight mass spectrometry. Discriminant metabolites were considered if within the top 99th percentile of variable importance measurements obtained from partial least-squares discriminant analysis models. A total of 80 metabolites accurately discriminated UCP3 Tg mice from WT when modeled within a specific exercise condition (i.e., untrained/rested, endurance trained/rested, untrained/EB, and endurance trained/EB). Results revealed that several amino acids and amino acid derivatives in skeletal muscle and plasma of UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced after an EB; that metabolites associated with skeletal muscle glutathione/Met/Cys metabolism (2-hydroxybutanoic acid, oxoproline, Gly, and Glu) were altered in UCP3 Tg mice across all training and exercise conditions; and that muscle metabolite indices of dehydrogenase activity were increased in UCP3 Tg mice, suggestive of a shift in tissue NADH/NAD ratio. The results indicate that mitochondrial UCP3 activity affects metabolism well beyond fatty acid oxidation, regulating biochemical pathways associated with amino acid metabolism and redox status. That select metabolites were altered in liver of UCP3 Tg mice highlights that changes in muscle UCP3 activity can also affect other organ systems, presumably through changes in systemic metabolite trafficking.-Aguer, C., Piccolo, B. D., Fiehn, O., Adams, S. H., Harper, M.-E. A novel amino acid and metabolomics signature in mice overexpressing muscle uncoupling protein 3.
[Mh] Termos MeSH primário: Aminoácidos/metabolismo
Regulação da Expressão Gênica/fisiologia
Metabolômica
Proteína Desacopladora 3/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Ciclo do Ácido Cítrico/fisiologia
Ácidos Graxos/sangue
Ácidos Graxos/metabolismo
Masculino
Camundongos
Músculo Esquelético
Oxirredução
Condicionamento Físico Animal
Proteína Desacopladora 3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Fatty Acids); 0 (Ucp3 protein, mouse); 0 (Uncoupling Protein 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161122
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201600914R


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[PMID]:27494693
[Au] Autor:Tekin S; Erden Y; Sandal S; Etem Onalan E; Ozyalin F; Ozen H; Yilmaz B
[Ad] Endereço:a Department of Physiology , Faculty of Medicine, Inonu University , Malatya , Turkey.
[Ti] Título:Effects of apelin on reproductive functions: relationship with feeding behavior and energy metabolism.
[So] Source:Arch Physiol Biochem;123(1):9-15, 2017 Feb.
[Is] ISSN:1744-4160
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Apelin is an adipose tissue derived peptidergic hormone. In this study, 40 male Sprague-Dawley rats were used (four groups; n = 10). Apelin-13 at three different dosages (1, 5 and 50 µg/kg) was given intraperitoneally while the control group received vehicle the same route for a period of 14 days. In results, apelin-13 caused significant decreases in serum testosterone, luteinizing hormone and follicle-stimulating hormone levels (p < 0.05). Administration of apelin-13 significantly increased body weights, food intake, serum low-density lipoprotein and total cholesterol levels (p < 0.05), but caused significant decreases in high-density lipoprotein levels (p < 0.05). Serum glucose and triglyceride levels were not significantly altered by apelin-13 administration. Significant decreases in both uncoupling protein (UCP)-1 levels in the white and brown adipose tissues and UCP-3 levels in the biceps muscle (p < 0.05) were noted. The findings of the study suggest that apelin-13 may not only lead to obesity by increasing body weight but also cause infertility by suppressing reproductive hormones.
[Mh] Termos MeSH primário: Ingestão de Energia/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Comportamento Alimentar/efeitos dos fármacos
Hipercolesterolemia/induzido quimicamente
Infertilidade Masculina/induzido quimicamente
Peptídeos e Proteínas de Sinalização Intercelular/toxicidade
Sobrepeso/induzido quimicamente
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/efeitos dos fármacos
Tecido Adiposo Marrom/metabolismo
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Animais
Relação Dose-Resposta a Droga
Gonadotropinas Hipofisárias/antagonistas & inibidores
Gonadotropinas Hipofisárias/sangue
Hipercolesterolemia/sangue
Hipercolesterolemia/metabolismo
Infertilidade Masculina/sangue
Infertilidade Masculina/metabolismo
Injeções Intraperitoneais
Masculino
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Sobrepeso/sangue
Sobrepeso/metabolismo
Distribuição Aleatória
Ratos Sprague-Dawley
Testosterona/antagonistas & inibidores
Testosterona/sangue
Testes de Toxicidade Crônica
Proteína Desacopladora 1/antagonistas & inibidores
Proteína Desacopladora 1/genética
Proteína Desacopladora 1/metabolismo
Proteína Desacopladora 3/antagonistas & inibidores
Proteína Desacopladora 3/genética
Proteína Desacopladora 3/metabolismo
Ganho de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gonadotropins, Pituitary); 0 (Intercellular Signaling Peptides and Proteins); 0 (Ucp1 protein, rat); 0 (Ucp3 protein, rat); 0 (Uncoupling Protein 1); 0 (Uncoupling Protein 3); 0 (apelin-13 peptide); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160806
[St] Status:MEDLINE
[do] DOI:10.1080/13813455.2016.1211709


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[PMID]:27994193
[Au] Autor:Wang Y; Yang W; Gui L; Wang H; Zan L
[Ad] Endereço:College of Animal Science and Technology, Northwest A and F University, Yangling, Shaanxi 712100, People's Republic of China. zanlinsen@163.com.
[Ti] Título:Association and expression analyses of the Ucp2 and Ucp3 gene polymorphisms with body measurement and meat quality traits in Qinchuan cattle.
[So] Source:J Genet;95(4):939-946, 2016 Dec.
[Is] ISSN:0973-7731
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:The uncoupling proteins (UCPs) belong to the mitochondrial inner membrane anion carrier superfamily and play an important role in energy homeostasis. Genetic studies have demonstrated that Ucp2 and Ucp3 gene variants are involved in obesity and metabolic syndrome. The aim of this study was to identify associations between polymorphisms of Ucp2 and Ucp3 genes and economically-important traits in Qinchuan cattle. In the present study, one single-nucleotide polymorphism (SNP) in the 5'UTR region (SNP1:g.C-754G) of the Ucp2 gene was identified by direct sequencing of 441 Qinchuan cattle. Two SNPs in exon 3 (SNP2: g.G4877A: SNP3: g.C4902T) of the Ucp3 gene were identified by sequencing and polymerase chain reactionrestriction fragment length polymorphism (PCR-RFLP) among 441 Qinchuan cattle. Association analysis showed that SNP1 and SNP2 were associated with the meat quality traits (MQTs) including back fat thickness, loin muscle area and intramuscular fat content. SNP3 was found to be associated with part of the body measurement traits (BMTs) which referred to withers height and chest depth. In addition, QTL pyramiding analysis showed that individuals with diplotype P3P3 (GG-GG-CC) exhibited the best performance in terms of back fat thickness, loin muscle area, intramuscular fat content, rump length, hip width, chest depth and chest circumference. With regard to the G4877A mutation, real time PCR analysis revealed that individuals with AA genotype of the Ucp3 gene expressed higher mRNA levels than those with GG genotype. These results suggest that the diplotype P3P3 (GG-GG-CC) could be used as a molecular marker of the combined genotypes for future selection of body measurement traits and meat quality traits in Qinchuan cattle.
[Mh] Termos MeSH primário: Pesos e Medidas Corporais
Estudos de Associação Genética
Carne/normas
Polimorfismo de Nucleotídeo Único
Proteína Desacopladora 2/genética
Proteína Desacopladora 3/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Bovinos
Feminino
Qualidade dos Alimentos
Expressão Gênica
Frequência do Gene
Genótipo
Haplótipos
Desequilíbrio de Ligação
Locos de Características Quantitativas
Característica Quantitativa Herdável
RNA Mensageiro/genética
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Uncoupling Protein 2); 0 (Uncoupling Protein 3)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


  8 / 910 MEDLINE  
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[PMID]:27983991
[Au] Autor:Nagai S; Ikeda K; Horie-Inoue K; Shiba S; Nagasawa S; Takeda S; Inoue S
[Ad] Endereço:Division of Gene Regulation and Signal Transduction, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan; Department of Obstetrics and Gynecology, Juntendo University, School of Medicine, Tokyo, Japan.
[Ti] Título:Estrogen modulates exercise endurance along with mitochondrial uncoupling protein 3 downregulation in skeletal muscle of female mice.
[So] Source:Biochem Biophys Res Commun;480(4):758-764, 2016 Nov 25.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Estrogen is a hormone that regulates physiological processes and its dysregulation may relate to muscle disorders particularly in female, although the mechanism remains to be elucidated. We here show that estrogen deficiency repressed exercise endurance in female mice whereas the administration of estrogen to ovariectomized mice recovered it. Microarray analysis of mouse muscles showed that mitochondrial uncoupling protein 3 (UCP3) is upregulated by ovariectomy and downregulated by estrogen administration. Intriguingly, ectopic expression of constitutively active estrogen receptor α decreased UCP3 level and increased cellular ATP content in differentiated myoblastic C2C12 cells. Overall, the present study suggests that estrogen plays a critical role in the regulation of energy expenditure and exercise endurance in female.
[Mh] Termos MeSH primário: Regulação para Baixo/fisiologia
Estrogênios/metabolismo
Músculo Esquelético/fisiologia
Condicionamento Físico Animal
Resistência Física/fisiologia
Proteína Desacopladora 3/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo/efeitos dos fármacos
Estrogênios/farmacologia
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Músculo Esquelético/efeitos dos fármacos
Ovariectomia
Resistência Física/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogens); 0 (Uncoupling Protein 3)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170529
[Lr] Data última revisão:
170529
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


  9 / 910 MEDLINE  
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[PMID]:27647490
[Au] Autor:Riley CL; Dao C; Kenaston MA; Muto L; Kohno S; Nowinski SM; Solmonson AD; Pfeiffer M; Sack MN; Lu Z; Fiermonte G; Sprague JE; Mills EM
[Ad] Endereço:Department of Molecular Biosciences, College of Natural Sciences, The University of Texas at Austin, Austin, TX, 78712, USA.
[Ti] Título:The complementary and divergent roles of uncoupling proteins 1 and 3 in thermoregulation.
[So] Source:J Physiol;594(24):7455-7464, 2016 Dec 15.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:KEY POINTS: Both uncoupling protein 1 (UCP1) and UCP3 are important for mammalian thermoregulation. UCP1 and UCP3 in brown adipose tissue mediate early and late phases of sympathomimetic thermogenesis, respectively. Lipopolysaccharide thermogenesis requires skeletal muscle UCP3 but not UCP1. Acute noradrenaline-induced hyperthermia requires UCP1 but not UCP3. Loss of both UCP1 and UCP3 accelerate the loss of body temperature compared to UCP1KO alone during acute cold exposure. ABSTRACT: Uncoupling protein 1 (UCP1) is the established mediator of brown adipose tissue-dependent thermogenesis. In contrast, the role of UCP3, expressed in both skeletal muscle and brown adipose tissue, in thermoregulatory physiology is less well understood. Here, we show that mice lacking UCP3 (UCP3KO) have impaired sympathomimetic (methamphetamine) and completely abrogated lipopolysaccharide (LPS) thermogenesis, but a normal response to noradrenaline. By comparison, UCP1 knockout (UCP1KO) mice exhibit blunted methamphetamine and fully inhibited noradrenaline thermogenesis, but an increased febrile response to LPS. We further establish that mice lacking both UCP1 and 3 (UCPDK) fail to show methamphetamine-induced hyperthermia, and have a markedly accelerated loss of body temperature and survival after cold exposure compared to UCP1KO mice. Finally, we show that skeletal muscle-specific human UCP3 expression is able to significantly rescue LPS, but not sympathomimetic thermogenesis blunted in UCP3KO mice. These studies identify UCP3 as an important mediator of physiological thermogenesis and support a renewed focus on targeting UCP3 in metabolic physiology.
[Mh] Termos MeSH primário: Regulação da Temperatura Corporal/fisiologia
Proteína Desacopladora 1/fisiologia
Proteína Desacopladora 3/fisiologia
[Mh] Termos MeSH secundário: Animais
Temperatura Baixa
Hipertermia Induzida
Lipopolissacarídeos/farmacologia
Masculino
Metanfetamina/farmacologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Norepinefrina/farmacologia
Proteína Desacopladora 1/genética
Proteína Desacopladora 3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (UCP3 protein, human); 0 (Ucp1 protein, mouse); 0 (Ucp3 protein, mouse); 0 (Uncoupling Protein 1); 0 (Uncoupling Protein 3); 44RAL3456C (Methamphetamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160921
[St] Status:MEDLINE
[do] DOI:10.1113/JP272971


  10 / 910 MEDLINE  
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[PMID]:27473111
[Au] Autor:Fan Y; Futawaka K; Koyama R; Fukuda Y; Hayashi M; Imamoto M; Miyawaki T; Kasahara M; Tagami T; Moriyama K
[Ad] Endereço:Department of Medicine & Clinical Science, Faculty of Pharmaceutical Sciences, Mukogawa Women's University, Hyogo, 663-8179, Japan.
[Ti] Título:Vitamin D3/VDR resists diet-induced obesity by modulating UCP3 expression in muscles.
[So] Source:J Biomed Sci;23(1):56, 2016 Jul 29.
[Is] ISSN:1423-0127
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The impact of vitamin D3 (VD3) on obesity has been reported in the past. Our study was aimed at investigating the possible mechanisms by which VD3 affects obesity induced by a high fat diet. METHODS: Eight-week-old C57BL/6 J male mice were fed a normal- or high-fat diet for 9 weeks and were treated with a gavage of vehicle (corn oil) or cholecalciferol (50 µg/kg, daily). Body weight, white adipose tissue weight, blood lipid and glucose levels were measured. In addition, we investigated the expression of 1,25(OH)2D3 (calcitriol)/VDR-regulated genes involved in energy and lipid metabolism, such as of uncoupling protein 3 (UCP3), by using qRT-PCR in the liver, adipose tissue, skeletal muscle and C2C12, L6, and H-EMC-SS cells. We also measured UCP3 promoter transcription in the same cell lines using a Dual Luciferase Assay. Furthermore, we analyzed the binding site consensus sequences of VDR on the UCP3 promoter. RESULTS: Mice consuming a high-fat diet treated with cholecalciferol had lower body weight and adipose tissue weight and higher expression of UCP3 compared to the other treatment groups. Changes in the expression of genes correlated with calcitriol/VDR. Luciferase activity was dose-dependently associated with calcitriol/VDR levels. We confirmed the functional VDR binding site consensus sequences at -2200, -1561, -634, and +314 bp in the UCP3 promoter region. CONCLUSION: We suggest that VD3/VDR inhibits weight gain by activating UCP3 in the muscles.
[Mh] Termos MeSH primário: Calcitriol/farmacologia
Colecalciferol/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas Musculares/biossíntese
Músculo Esquelético/metabolismo
Obesidade/metabolismo
Receptores de Calcitriol/metabolismo
Proteína Desacopladora 3/biossíntese
[Mh] Termos MeSH secundário: Animais
Gorduras na Dieta/efeitos adversos
Gorduras na Dieta/farmacologia
Masculino
Camundongos
Proteínas Musculares/genética
Músculo Esquelético/patologia
Obesidade/induzido quimicamente
Obesidade/genética
Obesidade/patologia
Receptores de Calcitriol/genética
Proteína Desacopladora 3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Muscle Proteins); 0 (Receptors, Calcitriol); 0 (Ucp3 protein, mouse); 0 (Uncoupling Protein 3); 1C6V77QF41 (Cholecalciferol); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160731
[St] Status:MEDLINE
[do] DOI:10.1186/s12929-016-0271-2



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