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[PMID]:29429161
[Au] Autor:Li L; Duan XJ; Sun Y; Lu Y; Xu HY; Wang QZ; Wang HY
[Ad] Endereço:Department of Pathology, Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing 100037, China.
[Ti] Título:[Classification of cardiac amyloidosis: an immunohistochemical analysis].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):105-109, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To evaluate the sensitivity and specificity of immunohistochemistry (IHC) in the classification of cardiac amyloidosis on endomyocardial biopsy (EMB) and heart allograft. Twenty cardiac tissues from 19 patients at Fuwai Hospital from January, 1990 to April, 2017 with histopathologic features of amyloidosis and Congo red staining positivity were included. IHC was performed with monoclonal antibodies against AA amyloid and polyclonal antibodies against transthyretin (ATTR), λ-light chain (AL-λ), κ-light chain (AL-κ), ApoAⅠ, ApoAⅡ, ApoA Ⅳ and ß(2)-microglobin. The extent of interstitial staining was evaluated by light microscopy, and three patterns were recognized; these included diffuse pericellular pattern, discrete pericellular pattern, and nodular pattern. Two patterns of vascular deposition were also noted, including arterial pattern and venous pattern. Endocardial involvement was also assessed and recorded. Nineteen cases were divided into three groups according to the pattern of proteins expression in specimens. The first group (5 cases) only showed single protein expression on EMB. The second group (6 cases) showed more than one protein expression, but one of them was intensely stained or any staining of any protein together with ApoA Ⅳ co-staining. The third group (8 cases) also showed more than one protein expression and all of them had intense staining. Amyloid deposits were successfully subtyped as AL-λ, ATTR, AL-κ and ApoAⅠby IHC in the former two groups with the sensitivity of 11/19. In the third group, amyloid deposits could not be subtyped by immunohistochemistry due to their poor specificity. The pericellular pattern tended to favor AL over ATTR amyloidosis and vascular deposition tended to favor ATTR. Amyloid deposits can be reliably subtyped in diagnostic cardiac specimens using IHC. The co-deposition of chaperon proteins, the distribution of amyloid proteins and clinical features are also auxiliary to subtype cardiac amyloidosis.
[Mh] Termos MeSH primário: Amiloidose/patologia
Cardiomiopatias/patologia
[Mh] Termos MeSH secundário: Amiloide/análise
Neuropatias Amiloides Familiares/patologia
Anticorpos Monoclonais/análise
Apolipoproteína A-I/análise
Apolipoproteínas A/análise
Biópsia
Seres Humanos
Cadeias kappa de Imunoglobulina/análise
Cadeias lambda de Imunoglobulina/análise
Imuno-Histoquímica
Placa Amiloide/patologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOA1 protein, human); 0 (Amyloid); 0 (Antibodies, Monoclonal); 0 (Apolipoprotein A-I); 0 (Apolipoproteins A); 0 (Immunoglobulin kappa-Chains); 0 (Immunoglobulin lambda-Chains); 0 (apolipoprotein A-IV)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.005


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[PMID]:29025558
[Au] Autor:Dai Y; Shen Y; Li QR; Ding FH; Wang XQ; Liu HJ; Yan XX; Wang LJ; Yang K; Wang HB; Chen QJ; Shen WF; Zhang RY; Lu L
[Ad] Endereço:Department of Cardiology, Rui Jin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China; Institute of Cardiovascular Diseases, Shanghai Jiaotong University School of Medicine, Shanghai, China.
[Ti] Título:Glycated Apolipoprotein A-IV Induces Atherogenesis in Patients With CAD in Type 2 Diabetes.
[So] Source:J Am Coll Cardiol;70(16):2006-2019, 2017 Oct 17.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nonenzymatic glycation of apolipoproteins plays a role in the pathogenesis of the vascular complications of diabetes. OBJECTIVES: This study investigated whether apolipoprotein (apo) A-IV was glycated in patients with type 2 diabetes mellitus (T2DM) and whether apoA-IV glycation was related to coronary artery disease (CAD). The study also determined the biological effects of glycated apoA-IV. METHODS: The authors consecutively enrolled 204 patients with T2DM without CAD (Group I), 515 patients with T2DM with CAD (Group II), and 176 healthy subjects (control group) in this study. ApoA-IV was precipitated from ultracentrifugally isolated high-density lipoprotein, and its glycation level was determined based on Western blotting densitometry (relative intensity of apoA-IV glycation). ApoA-IV NƐ-(carboxylmethyl) lysine (CML) modification sites were identified by mass spectrometry in 37 control subjects, 63 patients in Group I, and 138 patients in Group II. Saline or glycated apoA-IV (g-apoA-IV) generated by glyoxal culture was injected into apoE mice to evaluate atherogenesis, and was also used for the cell experiments. RESULTS: The relative intensity and the abundance of apoA-IV glycation were associated with the presence and severity of CAD in patients with T2DM (all p < 0.05). The experiments showed that g-apoA-IV induced proinflammatory reactions in vitro and promoted atherogenesis in apoE mice through the nuclear receptor NR4A3. G-apoA-IV with mutations (K-A) at high-frequency glycation sites exhibited more weakened proinflammatory and atherogenic effects than did g-apoA-IV both in vitro and in vivo. CONCLUSIONS: ApoA-IV glycation is associated with CAD severity in patients with T2DM, and g-apoA-IV induces atherogenesis through NR4A3 in apoE mice.
[Mh] Termos MeSH primário: Apolipoproteínas A/metabolismo
Aterosclerose/metabolismo
Doença da Artéria Coronariana/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
[Mh] Termos MeSH secundário: Idoso
Animais
Apolipoproteínas A/isolamento & purificação
Aterosclerose/diagnóstico por imagem
Aterosclerose/epidemiologia
Biomarcadores/metabolismo
Angiografia Coronária/métodos
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/epidemiologia
Diabetes Mellitus Tipo 2/diagnóstico por imagem
Diabetes Mellitus Tipo 2/epidemiologia
Feminino
Glicosilação
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (Biomarkers); 0 (apolipoprotein A-IV)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


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[PMID]:28750079
[Au] Autor:Romagnuolo R; Scipione CA; Marcovina SM; Gemin M; Seidah NG; Boffa MB; Koschinsky ML
[Ad] Endereço:Department of Chemistry & Biochemistry, University of Windsor, Windsor, Ontario, Canada.
[Ti] Título:Roles of the low density lipoprotein receptor and related receptors in inhibition of lipoprotein(a) internalization by proprotein convertase subtilisin/kexin type 9.
[So] Source:PLoS One;12(7):e0180869, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated plasma concentrations of lipoprotein(a) (Lp(a)) are a causal risk factor for cardiovascular disease. The mechanisms underlying Lp(a) clearance from plasma remain unclear, which is an obvious barrier to the development of therapies to specifically lower levels of this lipoprotein. Recently, it has been documented that monoclonal antibody inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) can lower plasma Lp(a) levels by 30%. Since PCSK9 acts primarily through the low density lipoprotein receptor (LDLR), this result is in conflict with the prevailing view that the LDLR does not participate in Lp(a) clearance. To support our recent findings in HepG2 cells that the LDLR can act as a bona fide receptor for Lp(a) whose effects are sensitive to PCSK9, we undertook a series of Lp(a) internalization experiments using different hepatic cells, with different variants of PCSK9, and with different members of the LDLR family. We found that PCSK9 decreased Lp(a) and/or apo(a) internalization by Huh7 human hepatoma cells and by primary mouse and human hepatocytes. Overexpression of human LDLR appeared to enhance apo(a)/Lp(a) internalization in both types of primary cells. Importantly, internalization of Lp(a) by LDLR-deficient mouse hepatocytes was not affected by PCSK9, but the effect of PCSK9 was restored upon overexpression of human LDLR. In HepG2 cells, Lp(a) internalization was decreased by gain-of-function mutants of PCSK9 more than by wild-type PCSK9, and a loss-of function variant had a reduced ability to influence Lp(a) internalization. Apo(a) internalization by HepG2 cells was not affected by apo(a) isoform size. Finally, we showed that very low density lipoprotein receptor (VLDLR), LDR-related protein (LRP)-8, and LRP-1 do not play a role in Lp(a) internalization or the effect of PCSK9 on Lp(a) internalization. Our findings are consistent with the idea that PCSK9 inhibits Lp(a) clearance through the LDLR, but do not exclude other effects of PCSK9 such as on Lp(a) biosynthesis.
[Mh] Termos MeSH primário: Endocitose
Lipoproteína(a)/metabolismo
Pró-Proteína Convertase 9/metabolismo
Receptores de LDL/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas A/metabolismo
Células CHO
Cricetinae
Cricetulus
Células HEK293
Células Hep G2
Hepatócitos/metabolismo
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Mutação/genética
Isoformas de Proteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (Lipoprotein(a)); 0 (Protein Isoforms); 0 (Receptors, LDL); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Pcsk9 protein, mouse); EC 3.4.21.- (Proprotein Convertase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180869


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[PMID]:28523576
[Au] Autor:Lee HJ; Kim JH; Kim SW; Joo HA; Lee HW; Kim YS; Park SJ; Hong SP; Kim TI; Kim WH; Kim YH; Cheon JH
[Ad] Endereço:Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Korea.
[Ti] Título:Proteomic Analysis of Serum Amyloid A as a Potential Marker in Intestinal Behçet's Disease.
[So] Source:Dig Dis Sci;62(8):1953-1962, 2017 Aug.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Data regarding biomarkers to understand disease pathogenesis and to assess disease activity of intestinal Behçet's disease (BD) are limited. Therefore, we aimed to investigate the differentially expressed proteins in sera from patients with intestinal BD and to search for biomarkers using mass spectrometry-based proteomic analysis. METHODS: Serum samples were pooled for the screening study, and two-dimensional electrophoresis (2-DE) was performed to characterize the proteins present in intestinal BD patients. Candidate protein spots were identified using matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry (MALDI-TOF/TOF MS) and bioinformatic analysis. To validate the proteomic results, serum samples from an independent cohort were assessed by enzyme-linked immunosorbent assay. RESULTS: Pooled serum samples were used for 2-DE, and approximately 400 protein spots were detected in the sera of intestinal BD patients. Of the 22 differentially expressed proteins, 3 were successfully identified using MALDI-TOF/TOF MS. The three up-regulated proteins identified in the intestinal BD group included fibrin, apolipoprotein A-IV, and serum amyloid A (SAA). Serum SAA in intestinal BD patients (2.76 ± 2.50 ng/ml) was significantly higher than that in controls (1.68 ± 0.90 ng/ml, p = 0.007), which is consistent with the proteomic results. In addition, the level of IL-1ß in patients with intestinal BD (8.96 ± 1.23 pg/ml) was higher than that in controls (5.40 ± 0.15 pg/ml, p = 0.009). SAA released by HT-29 cells was markedly increased by tumor necrosis factor-α (TNF-α) and lipopolysaccharides stimulation. CONCLUSIONS: Our proteomic analysis revealed that SAA was up-regulated in intestinal BD patients.
[Mh] Termos MeSH primário: Síndrome de Behçet/sangue
Enteropatias/sangue
Proteômica/métodos
Proteína Amiloide A Sérica/análise
[Mh] Termos MeSH secundário: Adulto
Apolipoproteínas A/sangue
Biomarcadores/sangue
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Feminino
Fibrina/análise
Células HT29
Seres Humanos
Interleucina-1beta/sangue
Masculino
Espectrometria de Massas
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (Biomarkers); 0 (Interleukin-1beta); 0 (Serum Amyloid A Protein); 0 (apolipoprotein A-IV); 9001-31-4 (Fibrin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4606-y


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[PMID]:28412351
[Au] Autor:Zhang Y; He J; Zhao J; Xu M; Lou D; Tso P; Li Z; Li X
[Ad] Endereço:National Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:Effect of ApoA4 on SERPINA3 mediated by nuclear receptors NR4A1 and NR1D1 in hepatocytes.
[So] Source:Biochem Biophys Res Commun;487(2):327-332, 2017 May 27.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ApoA4 exerts anti-inflammatory effects, but the mechanism remains unclear. SERPINA3 is a member of the serine proteinase inhibitor gene family, and has been shown to be involved in anti-inflammation and associated with a number of human diseases. In this study, we revealed that ApoA4 stimulates the gene expression of SERPINA3 in mouse hepatocytes both in vivo and in vitro, in a dose- and time-dependent manner. The transcriptional response of SERPINA3 to ApoA4 is regulated through the binding of ApoA4 with nuclear receptors NR4A1 and NR1D1 on the SERPINA3 promoter, which was verified with ChIP, Luciferase activity assay and RNA interference-mediated NR4A1 or NR1D1 gene knockdown. These data suggests that ApoA4 transcriptionally induced SERPINA3 expression via NR1D1 and NR4A1. Our findings may throw light on the function of ApoA4 in inflammatory responses and acute-phase reactions, as well as the development of SERPINA3 relative diseases.
[Mh] Termos MeSH primário: Apolipoproteínas A/farmacologia
Hepatócitos/metabolismo
Fígado/metabolismo
Membro 1 do Grupo D da Subfamília 1 de Receptores Nucleares/metabolismo
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Serpinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Hepatócitos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Masculino
Taxa de Depuração Metabólica
Camundongos
Camundongos Endogâmicos C57BL
Especificidade de Órgãos/fisiologia
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (Nr1d1 protein, mouse); 0 (Nr4a1 protein, mouse); 0 (Nuclear Receptor Subfamily 1, Group D, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Serpina3k protein, mouse); 0 (Serpins); 0 (apolipoprotein A-IV)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170417
[St] Status:MEDLINE


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[PMID]:28381424
[Au] Autor:Barbosa S; Carreira S; O'Hare P
[Ad] Endereço:Department of Medicine, Imperial College, London W2 1PG, United Kingdom.
[Ti] Título:GSK-3-mediated phosphorylation couples ER-Golgi transport and nuclear stabilization of the CREB-H transcription factor to mediate apolipoprotein secretion.
[So] Source:Mol Biol Cell;28(11):1565-1579, 2017 Jun 01.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CREB-H, an ER-anchored transcription factor, plays a key role in regulating secretion in metabolic pathways, particularly triglyceride homeostasis. It controls the production both of secretory pathway components and cargoes, including apolipoproteins ApoA-IV and ApoC-II, contributing to VLDL/HDL distribution and lipolysis. The key mechanism controlling CREB-H activity involves its ER retention and forward transport to the Golgi, where it is cleaved by Golgi-resident proteases, releasing the N-terminal product, which traffics to the nucleus to effect transcriptional responses. Here we show that a serine-rich motif termed the P-motif, located in the N-terminus between serines 73 and 90, controls release of the precursor transmembrane form from the ER and its forward transport to the Golgi. This motif is subject to GSK-3 phosphorylation, promoting ER retention, while mutation of target serines and drug inhibition of GSK-3 activity coordinately induce both forward transport of the precursor and cleavage, resulting in nuclear import. We previously showed that for the nuclear product, the P-motif is subject to multiple phosphorylations, which regulate stability by targeting the protein to the SCF E3 ubiquitin ligase. Thus phosphorylation at the P-motif provides integrated control of CREB-H function, coupling intercompartmental transport in the cytoplasm with stabilization of the active form in the nucleus.
[Mh] Termos MeSH primário: Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sequência de Aminoácidos
Animais
Apolipoproteínas/metabolismo
Apolipoproteínas/secreção
Apolipoproteínas A
Células COS
Técnicas de Cultura de Células
Núcleo Celular/metabolismo
Cercopithecus aethiops
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/fisiologia
Citoplasma/metabolismo
Retículo Endoplasmático/metabolismo
Retículo Endoplasmático/fisiologia
Quinase 3 da Glicogênio Sintase/metabolismo
Complexo de Golgi/metabolismo
Complexo de Golgi/fisiologia
Células Hep G2
Seres Humanos
Lipólise
Fosforilação
Via Secretória
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins); 0 (Apolipoproteins A); 0 (Creb3l3 protein, mouse); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Transcription Factors); 0 (apolipoprotein A-IV); EC 2.7.11.26 (Glycogen Synthase Kinase 3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E17-01-0075


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[PMID]:28246167
[Au] Autor:Kang M; Kim J; An HT; Ko J
[Ti] Título:Human leucine zipper protein promotes hepatic steatosis induction of apolipoprotein A-IV.
[So] Source:FASEB J;31(6):2548-2561, 2017 Jun.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular mechanism of stress-induced hepatic steatosis is not well known. Human leucine zipper protein (LZIP) regulates the expression of genes involved in inflammation, cell migration, and stress response. The aim of this study was to determine the regulatory role of LZIP in stress-induced hepatic steatosis. We used a microarray analysis to identify LZIP-induced genes involved in hepatic lipid metabolism. LZIP increased the expression of apolipoprotein A-IV (APOA4) mRNA. In the presence of stress inducer, APOA4 promoter analysis was performed, and LZIP-induced lipid accumulation was monitored in mouse primary cells and human tissues. Under Golgi stress conditions, LZIP underwent proteolytic cleavage and was phosphorylated by AKT to protect against proteasome degradation. The stabilized N-terminal LZIP was translocated to the nucleus, where it directly bound to the APOA4 promoter, leading to APOA4 induction. LZIP-induced APOA4 expression resulted in increased absorption of surrounding free fatty acids. LZIP also promoted hepatic steatosis in mouse liver. Both LZIP and APOA4 were highly expressed in human steatosis samples. Our findings indicate that LZIP is a novel modulator of APOA4 expression and hepatic lipid metabolism. LZIP might be a therapeutic target for developing treatment strategies for hepatic steatosis and related metabolic diseases.-Kang, M., Kim, J., An, H.-T., Ko, J. Human leucine zipper protein promotes hepatic steatosis induction of apolipoprotein A-IV.
[Mh] Termos MeSH primário: Apolipoproteínas A/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Fígado Gorduroso/metabolismo
[Mh] Termos MeSH secundário: Apolipoproteínas A/genética
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Fígado Gorduroso/genética
Regulação da Expressão Gênica/fisiologia
Complexo de Golgi/fisiologia
Células Hep G2
Hepatócitos/metabolismo
Seres Humanos
Metabolismo dos Lipídeos/genética
Metabolismo dos Lipídeos/fisiologia
Mutação
Ácido Oleico/metabolismo
Fosforilação
Plasmídeos
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Estresse Fisiológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (CREB3 protein, human); 0 (Cyclic AMP Response Element-Binding Protein); 0 (RNA, Messenger); 0 (apolipoprotein A-IV); 2UMI9U37CP (Oleic Acid); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201601227R


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[PMID]:28219664
[Au] Autor:Liu A; Abbasi F; Kim SH; Ariel D; Lamendola C; Cardell J; Xu S; Patel S; Tomasso V; Mojaddidi H; Grove K; Tsao PS; Kushida CA; Reaven GM
[Ad] Endereço:Department of Medicine, Stanford University School of Medicine, Stanford, California. Electronic address: aliceliu@stanford.edu.
[Ti] Título:Effect of Pioglitazone on Cardiometabolic Risk in Patients With Obstructive Sleep Apnea.
[So] Source:Am J Cardiol;119(8):1205-1210, 2017 Apr 15.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prevalence of insulin resistance is increased in patients with obstructive sleep apnea (OSA). Because insulin resistance is an independent predictor of cardiovascular disease (CVD), this study was initiated to see if pioglitazone administration would improve insulin sensitivity and thereby decrease risk of CVD in overweight/obese, nondiabetic, insulin-resistant patients with untreated OSA. Patients (n = 30) were administered pioglitazone (45 mg/day) for 8 weeks, and measurements were made before and after intervention of insulin action (insulin-mediated glucose uptake by the insulin suppression test), C-reactive protein, lipid/lipoprotein profile, and gene expression profile of periumbilical subcutaneous fat tissue. Insulin sensitivity increased 31% (p <0.001) among pioglitazone-treated subjects, associated with a decrease in C-reactive protein concentration (p ≤0.001), a decrease in plasma triglyceride, and increase in high-density lipoprotein cholesterol concentrations (p ≤0.001), accompanied by significant changes in apolipoprotein A1 and B concentrations and lipoprotein subclasses known to decrease CVD risk. In addition, subcutaneous adipose tissue gene expression profile showed a 1.6-fold (p <0.01) increase in GLUT4 expression and decreased expression in 5 of 9 inflammatory genes (p <0.05). In conclusion, enhanced insulin sensitivity can significantly decrease multiple cardiometabolic risk factors in patients with untreated OSA, consistent with the view that coexisting insulin resistance plays an important role in the association between OSA and increased risk of CVD.
[Mh] Termos MeSH primário: Hipoglicemiantes/uso terapêutico
Resistência à Insulina/fisiologia
Apneia Obstrutiva do Sono/fisiopatologia
Tiazolidinedionas/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Apolipoproteínas A/sangue
Apolipoproteínas B/sangue
Glicemia/análise
Proteína C-Reativa/análise
HDL-Colesterol/sangue
Feminino
Transportador de Glucose Tipo 4/genética
Transportador de Glucose Tipo 4/metabolismo
Seres Humanos
Masculino
Meia-Idade
Sobrepeso/fisiopatologia
RNA/metabolismo
Gordura Subcutânea/metabolismo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (Apolipoproteins B); 0 (Blood Glucose); 0 (Cholesterol, HDL); 0 (Glucose Transporter Type 4); 0 (Hypoglycemic Agents); 0 (SLC2A4 protein, human); 0 (Thiazolidinediones); 0 (Triglycerides); 63231-63-0 (RNA); 9007-41-4 (C-Reactive Protein); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170525
[Lr] Data última revisão:
170525
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE


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[PMID]:28193513
[Au] Autor:Monteiro MP; Batterham RL
[Ad] Endereço:Clinical and Experimental Endocrinology, Unit for Multidisciplinary Research in Biomedicine, Instituto de Ciências Biomédicas Abel Salazar, University of Porto, Portugal; Centre for Obesity Research, University College London, London, United Kingdom; University College London Hospitals Bariatric Centre for Weight Management and Metabolic Surgery, London, United Kingdom.
[Ti] Título:The Importance of the Gastrointestinal Tract in Controlling Food Intake and Regulating Energy Balance.
[So] Source:Gastroenterology;152(7):1707-1717.e2, 2017 May.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gastrointestinal tract, the key interface between ingested nutrients and the body, plays a critical role in regulating energy homeostasis. Gut-derived signals convey information regarding incoming nutrients to the brain, initiating changes in eating behavior and energy expenditure, to maintain energy balance. Here we review hormonal, neural, and nutrient signals emanating from the gastrointestinal tract and evidence for their role in controlling feeding behavior. Mechanistic studies that have utilized pharmacologic and/or transgenic approaches targeting an individual hormone/mediator have yielded somewhat disappointing body weight changes, often leading to the hormone/mediator in question being dismissed as a potential obesity therapy. However, the recent finding of sustained weight reduction in response to systemic administration of a long-acting analog of the gut-hormone glucagon-like peptide-1 highlights the therapeutic potential of gut-derived signals acting via nonphysiologic mechanisms. Thus, we also review therapeutics strategies being utilized or developed to leverage gastrointestinal signals in order to treat obesity.
[Mh] Termos MeSH primário: Ingestão de Alimentos
Metabolismo Energético
Células Enteroendócrinas/secreção
Trato Gastrointestinal/metabolismo
Obesidade/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas A/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Colecistocinina/metabolismo
Proteínas de Ligação a DNA/metabolismo
Hormônios Gastrointestinais/metabolismo
Trato Gastrointestinal/fisiologia
Grelina/metabolismo
Peptídeo 1 Semelhante ao Glucagon/metabolismo
Homeostase
Seres Humanos
Leptina/metabolismo
Peptídeos Natriuréticos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios Aferentes
Neurotensina/metabolismo
Obesidade/tratamento farmacológico
Obesidade/fisiopatologia
Oxintomodulina/metabolismo
Peptídeo YY/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins A); 0 (Calcium-Binding Proteins); 0 (DNA-Binding Proteins); 0 (Gastrointestinal Hormones); 0 (Ghrelin); 0 (Leptin); 0 (Natriuretic Peptides); 0 (Nerve Tissue Proteins); 0 (Oxyntomodulin); 0 (Receptors, G-Protein-Coupled); 0 (apolipoprotein A-IV); 0 (nucleobindin); 0 (taste receptors, type 1); 0 (taste receptors, type 2); 106388-42-5 (Peptide YY); 140653-38-9 (guanylin); 152175-68-3 (uroguanylin); 39379-15-2 (Neurotensin); 89750-14-1 (Glucagon-Like Peptide 1); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE


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[PMID]:28139293
[Au] Autor:Sethi S; Dasari S; Amin MS; Vrana JA; Theis JD; Alexander MP; Kurtin PJ
[Ad] Endereço:Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA. Electronic address: sethi.sanjeev@mayo.edu.
[Ti] Título:Clinical, biopsy, and mass spectrometry findings of renal gelsolin amyloidosis.
[So] Source:Kidney Int;91(4):964-971, 2017 Apr.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gelsolin amyloidosis is a rare type of amyloidosis typically involving the cranial and peripheral nerves, but rarely the kidney. Here we report the clinical, kidney biopsy, and mass spectrometry findings in 12 cases of renal gelsolin amyloidosis. Of the 12 patients, five were men and seven were women with mean age at diagnosis of 63.8 years. Gelsolin amyloidosis was most common in Caucasians (six patients) and Asians (four patients), and included one each African-American and Hispanic patients. Nephrotic syndrome was the most common cause of biopsy, although most patients also had progressive loss of kidney function. Hematological and serological evaluation was negative in 11 patients, while one patient had a monoclonal gammopathy. The renal biopsy showed large amounts of pale eosinophilic Congo red-positive amyloid deposits typically restricted to the glomeruli. Immunofluorescence studies were negative for immunoglobulins in nine cases with three cases of smudgy glomerular staining for IgG. Electron microscopy showed mostly random arrangement of amyloid fibrils with focally parallel bundles/sheets of amyloid fibrils present. Laser microdissection of the amyloid deposits followed by mass spectrometry showed large spectra numbers for gelsolin, serum amyloid P component, and apolipoproteins E and AIV. Furthermore, the p. Asn211Lys gelsolin mutation on mass spectrometry studies was detected in three patients by mass spectrometry, which appears to represent a renal-limited form of gelsolin amyloidosis. Thus, renal gelsolin amyloidosis is seen in older patients, presents with nephrotic syndrome and progressive chronic kidney disease, and histologically exhibits glomerular involvement. The diagnosis can be confirmed by mass spectrometry studies.
[Mh] Termos MeSH primário: Amiloidose/diagnóstico
Biópsia
Distrofias Hereditárias da Córnea/diagnóstico
Nefropatias/diagnóstico
Rim/química
Rim/patologia
Espectrometria de Massas em Tandem
[Mh] Termos MeSH secundário: Idoso
Amiloidose/complicações
Amiloidose/metabolismo
Amiloidose/patologia
Apolipoproteínas A/análise
Apolipoproteínas E/análise
Biomarcadores/análise
Distrofias Hereditárias da Córnea/complicações
Distrofias Hereditárias da Córnea/metabolismo
Distrofias Hereditárias da Córnea/patologia
Progressão da Doença
Feminino
Gelsolina/análise
Seres Humanos
Imuno-Histoquímica
Rim/ultraestrutura
Nefropatias/complicações
Nefropatias/metabolismo
Nefropatias/patologia
Masculino
Meia-Idade
Síndrome Nefrótica/diagnóstico
Síndrome Nefrótica/etiologia
Valor Preditivo dos Testes
Prognóstico
Insuficiência Renal Crônica/diagnóstico
Insuficiência Renal Crônica/etiologia
Componente Amiloide P Sérico/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ApoE protein, human); 0 (Apolipoproteins A); 0 (Apolipoproteins E); 0 (Biomarkers); 0 (Gelsolin); 0 (Serum Amyloid P-Component); 0 (apolipoprotein A-IV)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE



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