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[PMID]:29293570
[Au] Autor:Yang Y; Niu T
[Ad] Endereço:Department of Global Biostatistics and Data Science, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, United States of America.
[Ti] Título:A meta-analysis of associations of LEPR Q223R and K109R polymorphisms with Type 2 diabetes risk.
[So] Source:PLoS One;13(1):e0189366, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Leptin receptor (LEPR) plays a pivotal role in the control of body weight, energy metabolism, and insulin sensitivity. Various genetic association studies were performed to evaluate associations of LEPR genetic variants with type 2 diabetes (T2D) susceptibility. METHODS: A comprehensive search was conducted to identify all eligible case-control studies for examining the associations of LEPR single nucleotide polymorphisms (SNPs) Q223R (rs1137101) and K109R (rs1137100) with T2D risk. Odds ratios (OR) and corresponding 95% confidence intervals (CIs) were used to measure the magnitudes of association. RESULTS: For Q223R, 13 studies (11 articles) consisting of a total of 4030 cases and 2844 controls, and for K109R 7 studies (7 articles) consisting of 3319 cases and 2465 controls were available. Under an allele model, Q223R was not significantly associated with T2D risk (OR = 1.09, 95% CI: 0.80-1.48, P-value = 0.5989), which was consistent with results obtained under four genotypic models (ranges: ORs 1.08-1.20, 95% CIs: 0.58-2.02 to 0.64-2.26; P-values, 0.3650-0.8177, which all exceeded multiplicity-adjusted α = 0.05/5 = 0.01). In addition, no significant association was found between K109R and T2D risk based on either an allele model (OR = 0.93, 95% CI: 0.85-1.03, P-value = 0.1868) or four genotypic models (ranges: ORs 0.81-0.99, 95% CIs: 0.67-0.86 to 0.97-1.26, P-values, 0.0207-0.8804 which all exceeded multiplicity-adjusted α of 0.01). The magnitudes of association for these two SNPs were not dramatically changed in subgroup analyses by ethnicity or sensitivity analyses. Funnel plot inspections as well as Begg and Mazumdar adjusted rank correlation test and Egger linear regression test did not reveal significant publication biases in main and subgroup analyses. Bioinformatics analysis predicted that both missense SNPs were functionally neutral and benign. CONCLUSIONS: The present meta-analysis did not detect significant genetic associations between LEPR Q223R and K109R polymorphisms and T2D risk.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/genética
Predisposição Genética para Doença
Polimorfismo de Nucleotídeo Único
Receptores para Leptina/genética
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Leptin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189366


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[PMID]:29211902
[Au] Autor:Simonds SE; Cowley MA
[Ad] Endereço:Department of Physiology, Monash Biomedicine Discovery Institute, Monash University, Australia.
[Ti] Título:Leptin Effects on DAT Neurons To Control Energy Homeostasis.
[So] Source:Endocrinology;158(12):4126-4128, 2017 12 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Homeostase
Leptina
[Mh] Termos MeSH secundário: Metabolismo Energético
Seres Humanos
Neurônios
Receptores para Leptina
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Leptin); 0 (Receptors, Leptin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00820


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[PMID]:28461456
[Au] Autor:Zhao H; Matsuzaka T; Nakano Y; Motomura K; Tang N; Yokoo T; Okajima Y; Han SI; Takeuchi Y; Aita Y; Iwasaki H; Yatoh S; Suzuki H; Sekiya M; Yahagi N; Nakagawa Y; Sone H; Yamada N; Shimano H
[Ad] Endereço:Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
[Ti] Título:Elovl6 Deficiency Improves Glycemic Control in Diabetic / Mice by Expanding ß-Cell Mass and Increasing Insulin Secretory Capacity.
[So] Source:Diabetes;66(7):1833-1846, 2017 07.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dysfunctional fatty acid (FA) metabolism plays an important role in the pathogenesis of ß-cell dysfunction and loss of ß-cell mass in type 2 diabetes (T2D). Elovl6 is a microsomal enzyme that is responsible for converting C16 saturated and monounsaturated FAs into C18 species. We previously showed that Elovl6 played a critical role in the development of obesity-induced insulin resistance by modifying FA composition. To further define its role in T2D development, we assessed the effects of deletion in leptin receptor-deficient C57BL/KsJ / mice, a model of T2D. The / ; mice had a markedly increased ß-cell mass with increased proliferation and decreased apoptosis, an adaptive increase in insulin, and improved glycemic control. / islets were characterized by a prominent elevation of oleate (C18:1n-9), cell stress, and inflammation, which was completely suppressed by Elovl6 deletion. As a mechanistic ex vivo experiment, isolated islets from mice exhibited reduced susceptibility to palmitate-induced inflammation, endoplasmic reticulum stress, and ß-cell apoptosis. In contrast, oleate-treated islets resulted in impaired glucose-stimulated insulin secretion with suppressed related genes irrespective of the Elovl6 gene. Taken together, Elovl6 is a fundamental factor linking dysregulated lipid metabolism to ß-cell dysfunction, islet inflammation, and ß-cell apoptosis in T2D, highlighting oleate as the potential culprit of ß-cell lipotoxicity.
[Mh] Termos MeSH primário: Acetiltransferases/deficiência
Acetiltransferases/genética
Diabetes Mellitus Experimental/genética
Diabetes Mellitus Tipo 2/genética
Células Secretoras de Insulina/secreção
Insulina/secreção
[Mh] Termos MeSH secundário: Acetiltransferases/fisiologia
Animais
Apoptose/genética
Glicemia/metabolismo
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Estresse do Retículo Endoplasmático
Ácidos Graxos não Esterificados/metabolismo
Feminino
Imuno-Histoquímica
Técnicas In Vitro
Inflamação/induzido quimicamente
Inflamação/genética
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/patologia
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/patologia
Ilhotas Pancreáticas/secreção
Metabolismo dos Lipídeos/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ácido Oleico/farmacologia
Tamanho do Órgão
Palmitatos/efeitos adversos
Reação em Cadeia da Polimerase em Tempo Real
Receptores para Leptina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Fatty Acids, Nonesterified); 0 (Insulin); 0 (Palmitates); 0 (Receptors, Leptin); 0 (leptin receptor, mouse); 2UMI9U37CP (Oleic Acid); EC 2.3.1.- (Acetyltransferases); EC 2.3.1.- (fatty acid elongases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1277


  4 / 3605 MEDLINE  
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[PMID]:28450417
[Au] Autor:Li H; Li Y; Xiang L; Zhang J; Zhu B; Xiang L; Dong J; Liu M; Xiang G
[Ad] Endereço:Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuhan, Hubei Province, China.
[Ti] Título:GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet ß-Cell Function and Survival.
[So] Source:Diabetes;66(7):1914-1927, 2017 07.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growth differentiation factor 11 (GDF11) has been implicated in the regulation of islet development and a variety of aging conditions, but little is known about the physiological functions of GDF11 in adult pancreatic islets. Here, we showed that systematic replenishment of GDF11 not only preserved insulin secretion but also improved the survival and morphology of ß-cells and improved glucose metabolism in both nongenetic and genetic mouse models of type 2 diabetes (T2D). Conversely, anti-GDF11 monoclonal antibody treatment caused ß-cell failure and lethal T2D. In vitro treatment of isolated murine islets and MIN6 cells with recombinant GDF11 attenuated glucotoxicity-induced ß-cell dysfunction and apoptosis. Mechanistically, the GDF11-mediated protective effects could be attributed to the activation of transforming growth factor-ß/Smad2 and phosphatidylinositol-4,5-bisphosphate 3-kinase-AKT-FoxO1 signaling. These findings suggest that GDF11 repletion may improve ß-cell function and mass and thus may lead to a new therapeutic approach for T2D.
[Mh] Termos MeSH primário: Glicemia/efeitos dos fármacos
Proteínas Morfogenéticas Ósseas/farmacologia
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Fatores de Diferenciação de Crescimento/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Insulina/secreção
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Apoptose
Glicemia/metabolismo
Western Blotting
Proteínas Morfogenéticas Ósseas/antagonistas & inibidores
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Dieta Hiperlipídica
Modelos Animais de Doenças
Proteína Forkhead Box O1/efeitos dos fármacos
Proteína Forkhead Box O1/metabolismo
Teste de Tolerância a Glucose
Fatores de Diferenciação de Crescimento/antagonistas & inibidores
Células Secretoras de Insulina/secreção
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/secreção
Camundongos
Fosfotransferases (Aceptor do Grupo Álcool)/efeitos dos fármacos
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores para Leptina/genética
Transdução de Sinais/efeitos dos fármacos
Proteína Smad2/efeitos dos fármacos
Proteína Smad2/metabolismo
Fator de Crescimento Transformador beta/efeitos dos fármacos
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Blood Glucose); 0 (Bone Morphogenetic Proteins); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Gdf11 protein, mouse); 0 (Growth Differentiation Factors); 0 (Insulin); 0 (Receptors, Leptin); 0 (Smad2 Protein); 0 (Smad2 protein, mouse); 0 (Transforming Growth Factor beta); 0 (leptin receptor, mouse); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (phosphatidylinositol 4,5-biphosphate kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0086


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[PMID]:28407241
[Au] Autor:Jiang H; Chen Y; Chen G; Tian X; Tang J; Luo L; Huang M; Yan B; Ao X; Zhou W; Wang L; Bai X; Zhang Z; Wang L; Xian CJ
[Ad] Endereço:Department of Orthopedics, The Third Affiliated Hospital of Southern Medical University, Guangzhou, Guangdong, China.
[Ti] Título:Leptin accelerates the pathogenesis of heterotopic ossification in rat tendon tissues via mTORC1 signaling.
[So] Source:J Cell Physiol;233(2):1017-1028, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Leptin, an adipocyte-derived cytokine associated with bone metabolism, is believed to play a critical role in the pathogenesis of heterotopic ossification (HO). The effect and underlying action mechanism of leptin were investigated on osteogenic differentiation of tendon-derived stem cells (TDSCs) in vitro and the HO formation in rat tendons. Isolated rat TDSCs were treated with various concentrations of leptin in the presence or absence of mTORC1 signaling specific inhibitor rapamycin in vitro. A rat model with Achilles tenotomy was employed to evaluate the effect of leptin on HO formation together with or without rapamycin treatment. In vitro studies with TDSCs showed that leptin increased the expression of osteogenic biomarkers (alkaline phosphatase, runt-related transcription factor 2, osterix, osteocalcin) and enhanced mineralization of TDSCs via activating the mTORC1 signal pathway (as indicated by phosphorylation of p70 ribosomal S6 kinase 1 and p70 ribosomal S6). However, mTORC1 signaling blockade with rapamycin treatment suppressed leptin-induced osteogenic differentiation and mineralization. In vivo studies showed that leptin promoted HO formation in the Achilles tendon after tenotomy, and rapamycin treatment blocked leptin-induced HO formation. In conclusion, leptin can promote TDSC osteogenic differentiation and heterotopic bone formation via mTORC1 signaling in both vitro and vivo model, which provides a new potential therapeutic target for HO prevention.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Leptina/toxicidade
Alvo Mecanístico do Complexo 1 de Rapamicina/metabolismo
Ossificação Heterotópica/induzido quimicamente
Osteoblastos/efeitos dos fármacos
Osteogênese/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Células-Tronco/efeitos dos fármacos
Tendões/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Masculino
Ossificação Heterotópica/enzimologia
Ossificação Heterotópica/patologia
Osteoblastos/enzimologia
Osteoblastos/patologia
Fenótipo
Ratos Sprague-Dawley
Receptores para Leptina/metabolismo
Células-Tronco/enzimologia
Células-Tronco/patologia
Tendões/enzimologia
Tendões/patologia
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 1 Subunit); 0 (Leptin); 0 (Osterix protein, rat); 0 (Receptors, Leptin); 0 (Runx2 protein, rat); 0 (Transcription Factors); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25955


  6 / 3605 MEDLINE  
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[PMID]:28938461
[Au] Autor:Sarmento-Cabral A; L-López F; Luque RM
[Ad] Endereço:Maimonides Institute of Biomedical Research of Cordoba, 14004 Cordoba, Spain.
[Ti] Título:Adipokines and Their Receptors Are Widely Expressed and Distinctly Regulated by the Metabolic Environment in the Prostate of Male Mice: Direct Role Under Normal and Tumoral Conditions.
[So] Source:Endocrinology;158(10):3540-3552, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adipose tissue-derived adipokines (i.e., leptin/adiponectin/resistin) play important roles in the regulation of several pathophysiologic processes through the activation of specific receptors. However, although adipokines and their receptors are widely distributed in many tissues and exhibit a clear modulation according to particular metabolic conditions (e.g., obesity and/or fasting), their expression, regulation, and putative action on normal prostate glands (PGs; a hormone-dependent organ tightly regulated by the endocrine-metabolic milieu) are still to be defined. Different in vivo/in vitro models were used to comprehensively characterize the expression pattern and actions of different adipokine systems (i.e., leptin/adiponectin/resistin/receptors) in mouse PGs. Adiponectin, resistin, and adiponectin receptors (1 and 2) and leptin receptor are coexpressed at different levels in PG cells, wherein they are finely regulated under fasting and/or obesity conditions. Furthermore, treatment with different adipokines exerted both homologous and heterologous regulation of specific adipokines/receptor-synthesis and altered the expression of key proliferation and oncogenesis markers (i.e., Ki67/c-Myc/p53) in mouse PG cell cultures, wherein some of these actions might be elicited through extracellular signal-regulated kinase (ERK) activation. Moreover, treatment with leptin, adiponectin, and resistin differentially regulated key functional parameters [i.e., proliferation and migration capacity and/or prostate-specific antigen (PSA) secretion] in human normal and/or tumoral prostate cell lines. Altogether, our data show that various adipokine and receptor systems are differentially expressed in normal PG cells; that their expression is under a complex ligand- and receptor-selective regulation under extreme metabolic conditions; and that they mediate distinctive and common direct actions in normal and tumoral PG cells (i.e., homologous and heterologous regulation of ligand and receptor synthesis, ERK signaling activation, modulation of proliferation markers, proliferation and migration capacity, and PSA secretion), suggesting a relevant role of these systems in the regulation of PG pathophysiology.
[Mh] Termos MeSH primário: Adipocinas/metabolismo
Jejum/metabolismo
Obesidade/metabolismo
Próstata/metabolismo
Neoplasias da Próstata/metabolismo
Receptores de Adiponectina/metabolismo
Receptores para Leptina/metabolismo
[Mh] Termos MeSH secundário: Adipocinas/farmacologia
Adiponectina/metabolismo
Animais
Western Blotting
Linhagem Celular
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Antígeno Ki-67/efeitos dos fármacos
Antígeno Ki-67/metabolismo
Leptina/metabolismo
Sistema de Sinalização das MAP Quinases
Masculino
Camundongos
Antígeno Prostático Específico/efeitos dos fármacos
Antígeno Prostático Específico/secreção
Proteínas Proto-Oncogênicas c-myc/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-myc/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Resistina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Proteína Supressora de Tumor p53/efeitos dos fármacos
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adipokines); 0 (Adiponectin); 0 (Adipoq protein, mouse); 0 (Ki-67 Antigen); 0 (Leptin); 0 (Proto-Oncogene Proteins c-myc); 0 (Receptors, Adiponectin); 0 (Receptors, Leptin); 0 (Resistin); 0 (Retn protein, mouse); 0 (Tumor Suppressor Protein p53); 0 (adiponectin receptor 1, mouse); 0 (adiponectin receptor 2, mouse); EC 3.4.21.77 (Prostate-Specific Antigen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00370


  7 / 3605 MEDLINE  
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[PMID]:28935755
[Au] Autor:Xie Y; Potter CMF; Le Bras A; Nowak WN; Gu W; Bhaloo SI; Zhang Z; Hu Y; Zhang L; Xu Q
[Ad] Endereço:From the Cardiovascular Division, King's College London BHF Centre, United Kingdom (Y.X., C.M.F.P., W.N.N., A.L.B., W.G., S.I.B., Z.Z., Y.H., Q.X.); and Department of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, China (L.Z.).
[Ti] Título:Leptin Induces Sca-1 Progenitor Cell Migration Enhancing Neointimal Lesions in Vessel-Injury Mouse Models.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2114-2127, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Leptin is an adipokine initially thought to be a metabolic factor. Recent publications have shown its roles in inflammation and vascular disease, to which Sca-1 vascular progenitor cells within the vessel wall may contribute. We sought to elucidate the effects of leptin on Sca-1 progenitor cells migration and neointimal formation and to understand the underlying mechanisms. APPROACH AND RESULTS: Sca-1 progenitor cells from the vessel wall of Lepr and Lepr mice were cultured and purified. The migration of Lepr Sca-1 progenitor cells in vitro was markedly induced by leptin. Western blotting and kinase assays revealed that leptin induced the activation of phosphorylated signal transducer and activator of transcription 3, phosphorylated extracellular signal-regulated kinases 1/2, pFAK (phosphorylated focal adhesion kinase), and Rac1 (ras-related C3 botulinum toxin substrate 1)/Cdc42 (cell division control protein 42 homolog). In a mouse femoral artery guidewire injury model, an increased expression of leptin in both injured vessels and serum was observed 24 hours post-surgery. RFP (red fluorescent protein)-Sca-1 progenitor cells in Matrigel were applied to the adventitia of the injured femoral artery. RFP cells were observed in the intima 24 hours post-surgery, subsequently increasing neointimal lesions at 2 weeks when compared with the arteries without seeded cells. This increase was reduced by pre-treatment of Sca-1 cells with a leptin antagonist. Guidewire injury could only induce minor neointima in Lepr mice 2 weeks post-surgery. However, transplantation of Lepr Sca-1 progenitor cells into the adventitial side of injured artery in Lepr mice significantly enhanced neointimal formation. CONCLUSIONS: Upregulation of leptin levels in both the vessel wall and the circulation after vessel injury promoted the migration of Sca-1 progenitor cells via leptin receptor-dependent signal transducer and activator of transcription 3- Rac1/Cdc42-ERK (extracellular signal-regulated kinase)-FAK pathways, which enhanced neointimal formation.
[Mh] Termos MeSH primário: Antígenos Ly/metabolismo
Movimento Celular
Leptina/metabolismo
Proteínas de Membrana/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Neointima
Células-Tronco/metabolismo
Lesões do Sistema Vascular/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Modelos Animais de Doenças
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Artéria Femoral/lesões
Artéria Femoral/metabolismo
Artéria Femoral/patologia
Quinase 1 de Adesão Focal/metabolismo
Predisposição Genética para Doença
Masculino
Camundongos Knockout
Músculo Liso Vascular/lesões
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Miócitos de Músculo Liso/transplante
Neuropeptídeos/metabolismo
Fenótipo
Fosforilação
Receptores para Leptina/deficiência
Receptores para Leptina/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Transplante de Células-Tronco
Células-Tronco/patologia
Fatores de Tempo
Regulação para Cima
Lesões do Sistema Vascular/genética
Lesões do Sistema Vascular/patologia
Proteína cdc42 de Ligação ao GTP/metabolismo
Proteínas rac1 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Cdc42 protein, mouse); 0 (Leptin); 0 (Ly6a protein, mouse); 0 (Membrane Proteins); 0 (Neuropeptides); 0 (Rac1 protein, mouse); 0 (Receptors, Leptin); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (leptin receptor, mouse); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (Ptk2 protein, mouse); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309852


  8 / 3605 MEDLINE  
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[PMID]:28714970
[Au] Autor:Zhou BO; Yu H; Yue R; Zhao Z; Rios JJ; Naveiras O; Morrison SJ
[Ad] Endereço:State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China.
[Ti] Título:Bone marrow adipocytes promote the regeneration of stem cells and haematopoiesis by secreting SCF.
[So] Source:Nat Cell Biol;19(8):891-903, 2017 Aug.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Endothelial cells and leptin receptor (LepR ) stromal cells are critical sources of haematopoietic stem cell (HSC) niche factors, including stem cell factor (SCF), in bone marrow. After irradiation or chemotherapy, these cells are depleted while adipocytes become abundant. We discovered that bone marrow adipocytes synthesize SCF. They arise from Adipoq-Cre/ER progenitors, which represent ∼5% of LepR cells, and proliferate after irradiation. Scf deletion using Adipoq-Cre/ER inhibited haematopoietic regeneration after irradiation or 5-fluorouracil treatment, depleting HSCs and reducing mouse survival. Scf from LepR cells, but not endothelial, haematopoietic or osteoblastic cells, also promoted regeneration. In non-irradiated mice, Scf deletion using Adipoq-Cre/ER did not affect HSC frequency in long bones, which have few adipocytes, but depleted HSCs in tail vertebrae, which have abundant adipocytes. A-ZIP/F1 'fatless' mice exhibited delayed haematopoietic regeneration in long bones but not in tail vertebrae, where adipocytes inhibited vascularization. Adipocytes are a niche component that promotes haematopoietic regeneration.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Células da Medula Óssea/metabolismo
Proliferação Celular
Hematopoese
Células-Tronco Hematopoéticas/metabolismo
Comunicação Parácrina
Regeneração
Fator de Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Adipócitos/efeitos da radiação
Adipócitos/secreção
Adiponectina/genética
Adolescente
Animais
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/efeitos da radiação
Células da Medula Óssea/secreção
Transplante de Medula Óssea
Linhagem da Célula
Células Cultivadas
Criança
Fluoruracila/farmacologia
Genótipo
Células-Tronco Hematopoéticas/efeitos dos fármacos
Células-Tronco Hematopoéticas/efeitos da radiação
Seres Humanos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Receptores para Leptina/genética
Receptores para Leptina/metabolismo
Transdução de Sinais
Fator de Células-Tronco/secreção
Nicho de Células-Tronco
Fatores de Tempo
Irradiação Corporal Total
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Adipoq protein, mouse); 0 (Receptors, Leptin); 0 (Stem Cell Factor); 0 (leptin receptor, mouse); U3P01618RT (Fluorouracil)
[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:170718
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3570


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[PMID]:28714862
[Au] Autor:Flak JN; Arble D; Pan W; Patterson C; Lanigan T; Goforth PB; Sacksner J; Joosten M; Morgan DA; Allison MB; Hayes J; Feldman E; Seeley RJ; Olson DP; Rahmouni K; Myers MG
[Ad] Endereço:Department of Internal Medicine.
[Ti] Título:A leptin-regulated circuit controls glucose mobilization during noxious stimuli.
[So] Source:J Clin Invest;127(8):3103-3113, 2017 Aug 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adipocytes secrete the hormone leptin to signal the sufficiency of energy stores. Reductions in circulating leptin concentrations reflect a negative energy balance, which augments sympathetic nervous system (SNS) activation in response to metabolically demanding emergencies. This process ensures adequate glucose mobilization despite low energy stores. We report that leptin receptor-expressing neurons (LepRb neurons) in the periaqueductal gray (PAG), the largest population of LepRb neurons in the brain stem, mediate this process. Application of noxious stimuli, which often signal the need to mobilize glucose to support an appropriate response, activated PAG LepRb neurons, which project to and activate parabrachial nucleus (PBN) neurons that control SNS activation and glucose mobilization. Furthermore, activating PAG LepRb neurons increased SNS activity and blood glucose concentrations, while ablating LepRb in PAG neurons augmented glucose mobilization in response to noxious stimuli. Thus, decreased leptin action on PAG LepRb neurons augments the autonomic response to noxious stimuli, ensuring sufficient glucose mobilization during periods of acute demand in the face of diminished energy stores.
[Mh] Termos MeSH primário: Glucose/metabolismo
Leptina/fisiologia
Neurônios/fisiologia
Sistema Nervoso Simpático
[Mh] Termos MeSH secundário: Adipócitos/fisiologia
Animais
Comportamento Animal
Glicemia/metabolismo
Encéfalo/fisiologia
Feminino
Teste de Tolerância a Glucose
Hiperglicemia/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Dor
Fenótipo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores para Leptina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Leptin); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Leptin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


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[PMID]:28705795
[Au] Autor:Hubert A; Bochenek ML; Schütz E; Gogiraju R; Münzel T; Schäfer K
[Ad] Endereço:From the Center for Cardiology, Cardiology I (A.H., M.L.B., E.S., R.G., T.M., K.S.) and Center for Thrombosis and Hemostasis (M.L.B.), University Medical Center Mainz, Germany.
[Ti] Título:Selective Deletion of Leptin Signaling in Endothelial Cells Enhances Neointima Formation and Phenocopies the Vascular Effects of Diet-Induced Obesity in Mice.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1683-1697, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Obesity is associated with elevated circulating leptin levels and hypothalamic leptin resistance. Leptin receptors (LepRs) are expressed on endothelial cells, and leptin promotes neointima formation in a receptor-dependent manner. Our aim was to examine the importance of endothelial LepR (End.LepR) signaling during vascular remodeling and to determine whether the cardiovascular consequences of obesity are because of hyperleptinemia or endothelial leptin resistance. APPROACH AND RESULTS: Mice with loxP-flanked LepR alleles were mated with mice expressing Cre recombinase controlled by the inducible endothelial receptor tyrosine kinase promoter. Obesity was induced with high-fat diet. Neointima formation was examined after chemical carotid artery injury. Morphometric quantification revealed significantly greater intimal hyperplasia, neointimal cellularity, and proliferation in End.LepR knockout mice, and similar findings were obtained in obese, hyperleptinemic End.LepR wild-type animals. Analysis of primary endothelial cells confirmed abrogated signal transducer and activator of transcription-3 phosphorylation in response to leptin in LepR knockout and obese LepR wild-type mice. Quantitative PCR, ELISA, and immunofluorescence analyses revealed increased expression and release of endothelin-1 in End.LepR-deficient and LepR-resistant cells, and ET receptor A/B antagonists abrogated their paracrine effects on murine aortic smooth muscle cell proliferation. Reduced expression of peroxisome proliferator-activated receptor-γ and increased nuclear activator protein-1 staining was observed in End.LepR-deficient and LepR-resistant cells, and peroxisome proliferator-activated receptor-γ antagonization increased endothelial endothelin-1 expression. CONCLUSIONS: Our findings suggest that intact endothelial leptin signaling limits neointima formation and that obesity represents a state of endothelial leptin resistance. These observations and the identification of endothelin-1 as soluble mediator of the cardiovascular risk factor obesity may have relevant therapeutic implications.
[Mh] Termos MeSH primário: Lesões das Artérias Carótidas/complicações
Dieta Hiperlipídica
Células Endoteliais/metabolismo
Leptina/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Neointima
Obesidade/complicações
Receptores para Leptina/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Artérias Carótidas/metabolismo
Artérias Carótidas/patologia
Lesões das Artérias Carótidas/genética
Lesões das Artérias Carótidas/metabolismo
Lesões das Artérias Carótidas/patologia
Movimento Celular
Proliferação Celular
Células Cultivadas
Modelos Animais de Doenças
Células Endoteliais/patologia
Endotelina-1/metabolismo
Feminino
Genótipo
Integrases
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/patologia
Obesidade/genética
Obesidade/metabolismo
Obesidade/patologia
PPAR gama/metabolismo
Comunicação Parácrina
Fenótipo
Fosforilação
Regiões Promotoras Genéticas
Receptor TIE-2/genética
Receptores de Endotelina/metabolismo
Receptores para Leptina/deficiência
Receptores para Leptina/genética
Fator de Transcrição STAT3/metabolismo
Remodelação Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Leptin); 0 (PPAR gamma); 0 (Receptors, Endothelin); 0 (Receptors, Leptin); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (leptin receptor, mouse); EC 2.7.10.1 (Receptor, TIE-2); EC 2.7.10.1 (Tek protein, mouse); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309798



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