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[PMID]:29339530
[Au] Autor:Kasuki L; Wildemberg LE; Gadelha MR
[Ad] Endereço:Neuroendocrinology Research Center/Endocrine Section and Medical SchoolHospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Título:MANAGEMENT OF ENDOCRINE DISEASE: Personalized medicine in the treatment of acromegaly.
[So] Source:Eur J Endocrinol;178(3):R89-R100, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acromegaly is associated with high morbidity and elevated mortality when not adequately treated. Surgery is the first-line treatment for most patients as it is the only one that can lead to immediate cure. In patients who are not cured by surgery, treatment is currently based on a trial-and-error approach. First-generation somatostatin receptor ligands (fg-SRL) are initiated for most patients, although approximately 25% of patients present resistance to this drug class. Some biomarkers of treatment outcome are described in the literature, with the aim of categorizing patients into different groups to individualize their treatments using a personalized approach. In this review, we will discuss the current status of precision medicine for the treatment of acromegaly and future perspectives on the use of personalized medicine for this purpose.
[Mh] Termos MeSH primário: Acromegalia/tratamento farmacológico
Adenoma/tratamento farmacológico
Agonistas de Dopamina/uso terapêutico
Adenoma Hipofisário Secretor de Hormônio do Crescimento/tratamento farmacológico
Medicina de Precisão
Receptores da Somatotropina/antagonistas & inibidores
Somatostatina/análogos & derivados
[Mh] Termos MeSH secundário: Seres Humanos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Dopamine Agonists); 0 (Receptors, Somatotropin); 51110-01-1 (Somatostatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-1006


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[PMID]:28977606
[Au] Autor:Liu Y; Jiang J; Lepik B; Zhang Y; Zinn KR; Frank SJ
[Ad] Endereço:Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Alabama at Birmingham, Birmingham, Alabama 35294.
[Ti] Título:Subdomain 2, Not the Transmembrane Domain, Determines the Dimerization Partner of Growth Hormone Receptor and Prolactin Receptor.
[So] Source:Endocrinology;158(10):3235-3248, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growth hormone receptor (GHR) and prolactin (PRL) receptor (PRLR) are homologous transmembrane class I cytokine receptors. In humans, GH interacts with GHR homodimers or PRLR homodimers and PRL interacts with only PRLR homodimers to promote signaling. In human breast cancer cells endogenously expressing both receptors, GHR and PRLR specifically coimmunoprecipitate. We previously devised a split luciferase complementation assay to study GHR and PRLR assemblages. In this technique, firefly luciferase is split into two fragments (N- and C-terminal fragments of the luciferase), each without enzyme activity and tethered to the tails of two receptors. The fragments restore luciferase activity when brought close to each other by the receptors. Real-time ligand-induced complementation changes reflect the arrangement of receptors and indicate that GHR/PRLR is arranged as a heteromultimer comprised of GHR-GHR homodimers and PRLR-PRLR homodimers. We now dissect determinants for GHR and PRLR homodimerization versus heteroassociation. GHR and PRLR have extracellular domains comprised of the ligand-binding N-terminal subdomain 1 and a membrane-proximal subdomain 2 (S2), which fosters receptor-receptor contact. Based on previous studies of S2 versus the transmembrane domain (TMD) in GHR dimerization, we constructed GHR(PRLRS2), GHR(PRLRS2-TMD), and GHR(PRLRTMD), replacing GHR's S2 alone, S2 plus TMD, and TMD alone with PRLR's counterpart. We tested by complementation the ability of these chimeras and GHR or PRLR to homodimerize or heteroassociate. Comparing various combinations, we found GHR(PRLRS2) and GHR(PRLRS2-TMD) behaved as PRLR, whereas GHR(PRLRTMD) behaved as GHR regarding their dimerization partners. We conclude that S2 of GHR and PRLR, rather than their TMDs, determines their dimerization partner.
[Mh] Termos MeSH primário: Multimerização Proteica
Receptores da Prolactina/química
Receptores da Somatotropina/química
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/farmacologia
Neoplasias da Mama/química
Linhagem Celular Tumoral
Membrana Celular/química
Hormônio do Crescimento/metabolismo
Seres Humanos
Ligantes
Luciferases
Medições Luminescentes
Receptores da Prolactina/imunologia
Receptores da Prolactina/metabolismo
Receptores da Somatotropina/imunologia
Receptores da Somatotropina/metabolismo
Proteínas Recombinantes de Fusão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Ligands); 0 (Receptors, Prolactin); 0 (Receptors, Somatotropin); 0 (Recombinant Fusion Proteins); 9002-72-6 (Growth Hormone); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00469


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Boguszewski, Cesar L
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[PMID]:28904008
[Au] Autor:Boguszewski CL; Barbosa EJL; Svensson PA; Johannsson G; Glad CAM
[Ad] Endereço:SEMPREndocrine Division, Department of Internal Medicine, Federal University of Parana, Curitiba, Brazil clbogus@uol.com.br.
[Ti] Título:MECHANISMS IN ENDOCRINOLOGY: Clinical and pharmacogenetic aspects of the growth hormone receptor polymorphism.
[So] Source:Eur J Endocrinol;177(6):R309-R321, 2017 Dec.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pharmacogenetics aims to maximize the beneficial effects of a medical therapy by identifying genetic finger prints from responders and non-responders and, thereby improving safety and efficacy profile of the drug. Most subjects who are deficient in growth hormone (GHD) are candidates for recombinant human GH (rhGH) therapy. To date, it is well established that even after adjustments for several clinical variables, such as age, gender, body composition and the age at onset of the GHD, response to rhGH treatment is highly variable among individuals, part of which is believed to be due to genetic factors within the GH system. As the first genetic variant to potentially influence the individual response to rhGH therapy in children with growth disorders, polymorphism in the GH receptor (GHR) has attracted a great interest as a target for pharmacogenetics. Studies have been conducted to compare the functional and molecular effects of the full-length GHR (fl-GHR) isoform with the exon 3 deleted (d3-GHR) isoform in children and adults treated with rhGH therapy. Additionally, the impact of the GHR polymorphism has been investigated in relation to the clinical status and response to medical treatment in acromegaly, especially to the GHR antagonist drug pegvisomant. We have performed a narrative review of the studies performed to date on the association of GHR polymorphism with rhGH response in children and adults, and its potential influence in the medical management of acromegaly. In addition, data from studies on the general population and in other chronic diseases examining a role of this genetic variant in the regulation of growth and metabolism are summarized.
[Mh] Termos MeSH primário: Transtornos do Crescimento/tratamento farmacológico
Terapia de Reposição Hormonal/efeitos adversos
Hormônio do Crescimento Humano/deficiência
Hormônio do Crescimento Humano/uso terapêutico
Variantes Farmacogenômicos
Polimorfismo Genético
Receptores da Somatotropina/genética
[Mh] Termos MeSH secundário: Acromegalia/induzido quimicamente
Acromegalia/genética
Acromegalia/metabolismo
Acromegalia/terapia
Adulto
Criança
Resistência a Medicamentos
Éxons
Deleção de Genes
Transtornos do Crescimento/etiologia
Transtornos do Crescimento/genética
Transtornos do Crescimento/metabolismo
Hormônio do Crescimento Humano/efeitos adversos
Hormônio do Crescimento Humano/análogos & derivados
Hormônio do Crescimento Humano/genética
Seres Humanos
Fragmentos de Peptídeos/efeitos adversos
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Fragmentos de Peptídeos/uso terapêutico
Isoformas de Proteínas/efeitos adversos
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Isoformas de Proteínas/uso terapêutico
Receptores da Somatotropina/agonistas
Receptores da Somatotropina/antagonistas & inibidores
Receptores da Somatotropina/metabolismo
Proteínas Recombinantes/efeitos adversos
Proteínas Recombinantes/metabolismo
Proteínas Recombinantes/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Peptide Fragments); 0 (Protein Isoforms); 0 (Receptors, Somatotropin); 0 (Recombinant Proteins); 12629-01-5 (Human Growth Hormone); N824AOU5XV (pegvisomant)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0549


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[PMID]:28791847
[Au] Autor:Topsakal S; Akin F; Turgut S; Yerlikaya E; Yaylali GF
[Ad] Endereço:Department of Endocrinology and Metabolism, Pamukkale University, Denizli, Turkey.
[Ti] Título:Serum leptin levels and GHR-d3/fl gene polymorphism in acromegalic patients with thyroid nodules.
[So] Source:Adv Clin Exp Med;26(2):281-286, 2017 Mar-Apr.
[Is] ISSN:1899-5276
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acromegaly is a rare and serious syndrome that is commonly associated with pituitary neoplasms. Thyroid multinodular disease is a common finding in acromegaly. Leptin is a polypeptide hormone, and studies have shown that it can increase cell proliferation and inhibit apoptosis. OBJECTIVES: The aim of the study was to determine the relationship of serum leptin levels with certain blood parameters and determine if growth hormone receptor (GHR)-d3/fl gene polymorphism is associated with thyroid nodules in acromegalic patients. MATERIAL AND METHODS: A total of 24 acromegalic patients with or without thyroid nodules were included in the study. Gene polymorphisms and blood parameters were examined. RESULTS: A marked increase was observed in serum leptin concentration in acromegalic patients with thyroid nodules compared to patients without them (p < 0.05). GH levels were lower in patients without nodules than in patients with nodules (p < 0.05). Blood glucose levels were higher in patients with nodules compared to those without them (p < 0.05), and the presence of thyroid nodules was associated with decreased blood low-density lipoprotein (LDL) levels compared to patients without nodules (p < 0.05). A significant relationship was observed between growth hormone receptor (GHR)-d3/fl gene polymorphism and leptin levels in acromegalic patients with thyroid nodules (p < 0.001). CONCLUSIONS: These data from acromegalic patients indicate that thyroid nodules are associated with increased serum leptin, GH and blood glucose levels and with decreased LDL levels. GHR-d3/fl gene polymorphism status was strongly related to higher leptin levels.
[Mh] Termos MeSH primário: Acromegalia/genética
Leptina/sangue
Polimorfismo Genético
Receptores da Somatotropina/genética
Nódulo da Glândula Tireoide/complicações
[Mh] Termos MeSH secundário: Acromegalia/sangue
Acromegalia/complicações
Adulto
Idoso
Idoso de 80 Anos ou mais
Glicemia/metabolismo
Éxons/genética
Feminino
Deleção de Genes
Frequência do Gene
Genótipo
Hormônio do Crescimento Humano/sangue
Seres Humanos
Lipoproteínas LDL/sangue
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Leptin); 0 (Lipoproteins, LDL); 0 (Receptors, Somatotropin); 12629-01-5 (Human Growth Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.17219/acem/34793


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[PMID]:28686668
[Au] Autor:Sawada T; Arai D; Jing X; Miyajima M; Frank SJ; Sakaguchi K
[Ad] Endereço:Department of Molecular Cell Biology and Molecular Medicine, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.
[Ti] Título:Molecular interactions of EphA4, growth hormone receptor, Janus kinase 2, and signal transducer and activator of transcription 5B.
[So] Source:PLoS One;12(7):e0180785, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that EphA4, a member of the Eph family of receptor tyrosine kinases, is an important modulator of growth hormone (GH) signaling, leading to augmented synthesis of insulin-like growth factor 1 (IGF1) for postnatal body growth. In the present study, we report the molecular interactions of EphA4, GH receptor (GHR), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 5B (STAT5B). EphA4 binds to GHR at both its extracellular and intracellular domains and phosphorylates GHR when stimulated with a ligand. The cytoplasmic domain of EphA4 binds to the carboxy-terminus of JAK2 in contrast to the known binding of GHR to the amino-terminus. STAT5B binds to the amino-terminal kinase domain of EphA4. Ligand-activated EphA4 and JAK2 phosphorylate each other and STAT5B, but JAK2 does not appear to phosphorylate EphA4-bound STAT5B. Ligand-activated EphA4 induces the nuclear translocation of STAT5B in a JAK2-independent manner. GHR expression is required for the activation of STAT5B signaling, even via the JAK2-independent pathway. Various ephrins that have affinity for EphA4 induce STAT5B phosphorylation. These findings suggest the molecular mechanisms by which ephrin/EphA4 signaling enhances the canonical GH-IGF1 axis.
[Mh] Termos MeSH primário: Janus Quinase 2/genética
Receptor EphA4/genética
Receptores da Somatotropina/genética
Fator de Transcrição STAT5/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação
Linhagem Celular
Fibroblastos/citologia
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Fator de Crescimento Insulin-Like I/genética
Fator de Crescimento Insulin-Like I/metabolismo
Janus Quinase 2/metabolismo
Camundongos
Fosforilação
Ligação Proteica
Domínios Proteicos
Receptor EphA4/metabolismo
Receptores da Somatotropina/metabolismo
Fator de Transcrição STAT5/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IGF1 protein, human); 0 (Receptors, Somatotropin); 0 (STAT5 Transcription Factor); 0 (STAT5B protein, human); 67763-96-6 (Insulin-Like Growth Factor I); EC 2.7.10.1 (Receptor, EphA4); EC 2.7.10.2 (Janus Kinase 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180785


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[PMID]:28528685
[Au] Autor:Laron Z; Kauli R; Lapkina L; Werner H
[Ad] Endereço:Endocrinology and Diabetes Research Unit, Schneider Children's Medical Center, Israel. Electronic address: Laronz@clalit.org.il.
[Ti] Título:IGF-I deficiency, longevity and cancer protection of patients with Laron syndrome.
[So] Source:Mutat Res Rev Mutat Res;772:123-133, 2017 Apr - Jun.
[Is] ISSN:1388-2139
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Laron syndrome (LS) is a unique model of congenital IGF-I deficiency. It is characterized by dwarfism and obesity, and is caused by deletion or mutations of the growth hormone receptor (GH-R) gene. It is hypothesized that LS is an old disease originating in Indonesia and that the mutated gene spread to South Asia, the Middle East, the Mediterranean region and South America.
[Mh] Termos MeSH primário: Fator de Crescimento Insulin-Like I/deficiência
Síndrome de Laron/genética
Longevidade
Neoplasias/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Estudos de Coortes
Éxons
Feminino
Deleção de Genes
Seres Humanos
Fator de Crescimento Insulin-Like I/genética
Fator de Crescimento Insulin-Like I/farmacologia
Israel
Síndrome de Laron/complicações
Masculino
Meia-Idade
Mutação
Obesidade/complicações
Obesidade/genética
Linhagem
Receptores da Somatotropina/genética
Receptores da Somatotropina/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Somatotropin); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE


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[PMID]:28502327
[Au] Autor:Castilla-Cortazar I; de Ita JR; Aguirre GA; Castorena-Torres F; Ortiz-Urbina J; García-Magariño M; de la Garza RG; Diaz Olachea C; Elizondo Leal MI
[Ad] Endereço:Escuela de Medicina, Tecnologico de Monterrey, Monterrey, Nuevo Leon, Mexico; Fundación de Investigación HM Hospitales, Madrid, Spain. Electronic address: iccortazar@itesm.mx.
[Ti] Título:Fanconi Anemia and Laron Syndrome.
[So] Source:Am J Med Sci;353(5):425-432, 2017 May.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fanconi anemia (FA) is a condition characterized by genetic instability and short stature, which is due to growth hormone (GH) deficiency in most cases. However, no apparent relationships have been identified between FA complementation group genes and GH. In this study, we thereby considered an association between FA and Laron syndrome (LS) (insulin-like growth factor 1 [IGF-1] deficiency). METHODS: A 21-year-old female Mexican patient with a genetic diagnosis of FA was referred to our research department for an evaluation of her short stature. Upon admission to our facility, her phenotype led to a suspicion of LS; accordingly, serum levels of IGF-1 and IGF binding protein 3 were analyzed and a GH stimulation test was performed. In addition, we used a next-generation sequencing approach for a molecular evaluation of FA disease-causing mutations and genes involved in the GH-IGF signaling pathway. RESULTS: Tests revealed low levels of IGF-1 and IGF binding protein 3 that remained within normal ranges, as well as a lack of response to GH stimulation. Sequencing confirmed a defect in the GH receptor signaling pathway. CONCLUSIONS: To the best of our knowledge, this study is the first to suggest an association between FA and LS. We propose that IGF-1 administration might improve some FA complications and functions based upon IGF-1 beneficial actions observed in animal, cell and indirect clinical models: erythropoiesis modulation, immune function improvement and metabolic regulation.
[Mh] Termos MeSH primário: Anemia de Fanconi/complicações
Anemia de Fanconi/genética
Síndrome de Laron/complicações
Síndrome de Laron/genética
[Mh] Termos MeSH secundário: Estatura
Feminino
Hormônio do Crescimento Humano/sangue
Seres Humanos
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/sangue
Fator de Crescimento Insulin-Like I/metabolismo
Síndrome de Laron/patologia
México
Receptores da Somatotropina/sangue
Transdução de Sinais
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IGF1 protein, human); 0 (IGFBP3 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (Receptors, Somatotropin); 12629-01-5 (Human Growth Hormone); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE


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[PMID]:28498917
[Au] Autor:Rotwein P
[Ad] Endereço:Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech Health University Health Sciences Center, El Paso, Texas 79905.
[Ti] Título:The New Genomics: What Molecular Databases Can Tell Us About Human Population Variation and Endocrine Disease.
[So] Source:Endocrinology;158(7):2035-2042, 2017 Jul 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Major recent advances in genetics and genomics present unique opportunities for enhancing our understanding of human physiology and disease predisposition. Here I demonstrate how analysis of genomic information can provide new insights into endocrine systems, using the human growth hormone (GH) signaling pathway as an illustrative example. GH is essential for normal postnatal growth in children, and plays important roles in other biological processes throughout life. GH actions are mediated by the GH receptor, primarily via the JAK2 protein tyrosine kinase and the STAT5B transcription factor, and inactivating mutations in this pathway all lead to impaired somatic growth. Variation in GH signaling genes has been evaluated using DNA sequence data from the Exome Aggregation Consortium, a compendium of information from >60,000 individuals. Results reveal many potential missense and other alterations in the coding regions of GH1, GHR, JAK2, and STAT5B, with most changes being uncommon. The total number of different alleles per gene varied by ~threefold, from 101 for GH1 to 338 for JAK2. Several known disease-linked mutations in GH1, GHR, and JAK2 were present but infrequent in the population; however, three amino acid changes in GHR were sufficiently prevalent (~4% to 44% of chromosomes) to suggest that they are not disease causing. Collectively, these data provide new opportunities to understand how genetically driven variability in GH signaling and action may modify human physiology and disease.
[Mh] Termos MeSH primário: Bases de Dados de Compostos Químicos
Doenças do Sistema Endócrino/genética
Variação Genética/fisiologia
Genômica/tendências
[Mh] Termos MeSH secundário: Genômica/métodos
Hormônio do Crescimento Humano/genética
Hormônio do Crescimento Humano/fisiologia
Seres Humanos
Polimorfismo Genético
Receptores da Somatotropina/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Somatotropin); 12629-01-5 (Human Growth Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00338


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[PMID]:28425851
[Au] Autor:Darcy J; McFadden S; Bartke A
[Ad] Endereço:a Department of Internal Medicine , Southern Illinois University School of Medicine , Springfield , Illinois , USA.
[Ti] Título:Altered structure and function of adipose tissue in long-lived mice with growth hormone-related mutations.
[So] Source:Adipocyte;6(2):69-75, 2017 Apr 03.
[Is] ISSN:2162-397X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major focus of biogerontology is elucidating the role(s) of the endocrine system in aging and the accumulation of age-related diseases. Endocrine control of mammalian longevity was first reported in Ames dwarf (Prop1 ) mice, which are long-lived due to a recessive Prop1 loss-of-function mutation resulting in deficiency of growth hormone (GH), thyroid-stimulating hormone, and prolactin. Following this report, several other GH-related mutants with altered longevity have been described including long-lived Snell dwarf and growth hormone receptor knockout mice, and short-lived GH overexpressing transgenic mice. One of the emerging areas of interest in these mutant mice is the role of adipose tissue in their altered healthspan and lifespan. Here, we provide an overview of the alterations in body composition of GH-related mutants, as well as the altered thermogenic potential of their brown adipose tissue and the altered cellular senescence and adipokine production of their white adipose tissue.
[Mh] Termos MeSH primário: Tecido Adiposo/metabolismo
Hormônio do Crescimento/genética
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/metabolismo
Tecido Adiposo Branco/metabolismo
Envelhecimento/genética
Animais
Composição Corporal/fisiologia
Proteínas de Transporte/metabolismo
Hormônio do Crescimento/metabolismo
Resistência à Insulina
Fator de Crescimento Insulin-Like I/genética
Longevidade/genética
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Mutação
Prolactina/genética
Receptores da Somatotropina/genética
Relação Estrutura-Atividade
Termogênese
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Receptors, Somatotropin); 0 (somatotropin-binding protein); 67763-96-6 (Insulin-Like Growth Factor I); 9002-62-4 (Prolactin); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1080/21623945.2017.1308990


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[PMID]:28323915
[Au] Autor:Hjortebjerg R; Berryman DE; Comisford R; Frank SJ; List EO; Bjerre M; Frystyk J; Kopchick JJ
[Ad] Endereço:Medical Research Laboratory, Department of Clinical Medicine, Faculty of Health, Aarhus University, 8000 Aarhus, Denmark.
[Ti] Título:Insulin, IGF-1, and GH Receptors Are Altered in an Adipose Tissue Depot-Specific Manner in Male Mice With Modified GH Action.
[So] Source:Endocrinology;158(5):1406-1418, 2017 May 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growth hormone (GH) is a determinant of glucose homeostasis and adipose tissue (AT) function. Using 7-month-old transgenic mice expressing the bovine growth hormone (bGH) gene and growth hormone receptor knockout (GHR-/-) mice, we examined whether changes in GH action affect glucose, insulin, and pyruvate tolerance and AT expression of proteins involved in the interrelated signaling pathways of GH, insulinlike growth factor 1 (IGF-1), and insulin. Furthermore, we searched for AT depot-specific differences in control mice. Glycated hemoglobin levels were reduced in bGH and GHR-/- mice, and bGH mice displayed impaired gluconeogenesis as judged by pyruvate tolerance testing. Serum IGF-1 was elevated by 90% in bGH mice, whereas IGF-1 and insulin were reduced by 97% and 61% in GHR-/- mice, respectively. Igf1 RNA was increased in subcutaneous, epididymal, retroperitoneal, and brown adipose tissue (BAT) depots in bGH mice (mean increase ± standard error of the mean in all five depots, 153% ± 27%) and decreased in all depots in GHR-/- mice (mean decrease, 62% ± 4%). IGF-1 receptor expression was decreased in all AT depots of bGH mice (mean decrease, 49% ± 6%) and increased in all AT depots of GHR-/- mice (mean increase, 94% ± 8%). Insulin receptor expression was reduced in retroperitoneal, mesenteric, and BAT depots in bGH mice (mean decrease in all depots, 56% ± 4%) and augmented in subcutaneous, retroperitoneal, mesenteric, and BAT depots in GHR-/- mice (mean increase: 51% ± 1%). Collectively, our findings indicate a role for GH in influencing hormone signaling in AT in a depot-dependent manner.
[Mh] Termos MeSH primário: Tecido Adiposo/efeitos dos fármacos
Tecido Adiposo/metabolismo
Hormônio do Crescimento/farmacologia
Fator de Crescimento Insulin-Like I/genética
Insulina/genética
Receptores da Somatotropina/genética
[Mh] Termos MeSH secundário: Animais
Bovinos
Regulação da Expressão Gênica/efeitos dos fármacos
Insulina/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Especificidade de Órgãos/efeitos dos fármacos
Especificidade de Órgãos/genética
Receptores da Somatotropina/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Receptors, Somatotropin); 47V0IB0717 (growth hormone, bovine); 67763-96-6 (Insulin-Like Growth Factor I); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00084



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