Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea

Detalhes bibliográficos
Ano de defesa: 2005
Autor(a) principal: Oliveira, Joselina Luzia Menezes lattes
Orientador(a): Oliveira, Manuel Hermínio de Aguiar lattes
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Sergipe
Programa de Pós-Graduação: Pós-Graduação em Ciências da Saúde
Departamento: Não Informado pela instituição
País: BR
Palavras-chave em Português:
Palavras-chave em Inglês:
Área do conhecimento CNPq:
Link de acesso: https://ri.ufs.br/handle/riufs/3899
Resumo: Insulin-Like growth factor I (IGF-I) is a peptide that has an important action on cell division, differentiation, migration and apoptosis for vascular smooth muscle cells (VSMCs), may intervene in atherosclerosis. It antiapoptotic factor and it also stimulates. Thus, potential reductions in IGF-I effects might be beneficial in certain pathologic conditions, such as hypertension and the early stages of atherosclerosclerotic plaque formation characterized by hypertrophy/hyperplasia of VSMCs, but detrimental in other conditions in which loss of VSMCs contributes to the disease process, such as destabilization of atherosclerotic plaques. Conversely, it has been suggested that serum IGF-1 levels are low in patients with coronary heart disease. Recently, we have described a GH naïve homogeneous population with a monogenic mutation that inactives the growth hormone-releasing hormone receptor (GHRHR) (IVS1+ 1GA) with extremely low levels of IGF-1. Moreover, they also presented central obesity, higher levels of systolic blood pressure and dyslipidemia unique opportunity to evaluate the impact of extremely low levels of IGF-1 on the myocardial ischemic and carotid atherosclerosisis in high risk cardiovascular population, pertaining to the research object. It has been studied 22 dwarfs with GHD and no past of growth hormone therapy (10M:12F; 44±12 yrs) and compared to 26 age-matched normal subjects, control group[CO]. It has been examined clinical, biochemical data, including insulin-like growth factor 1(IGF-1), rest and exercise echodopplercardiography and, carotid intima-media thickness by a high-resolution carotid ultrasonography. IGF-1 in GHD group was markedly lower (3,3±5,5 vs 228,4±134,7ng/Ml; p<0.001) and fasting insulin (3,37±3,9 vs 3,59±3,0 microU/mL; p=NS) were smaller but not significantly in GHD. In the resting echocardiographic study, we observed normal indices of both systolic and diastolic function. During exercise treadmill (Bruce Protocol), both groups reached similar peak heart rate (162±16,5 vs 168±15,7bpm; p=NS) and peak systolic blood pressure (49±20 vs 59,4±23,6mmHg p=NS). Comparison of exercise wall motion score index in GHD group (1±0.0) vs CO group (1±0.0) did not show differences. Moreover, intima-media thickness measured at the far wall of the distal common carotid artery (0,59 ± 0,10 mm vs 0,60 ± 0,14 mm; p=NS (GHD vs CO group) was not indicative of premature atherosclerosis in GHD population. Only one of the subjects in the population studied presented carotid atherosclerotic plaque. Our data suggest that in a very homogeneous population with isolated GHD is not associated with premature carotid atherosclerosis or a higher prevalence of myocardial ischemia. Extremely low levels of the IGF-1 may be a protective mechanism against premature atherosclerosis in this apparently high risk selected group.
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spelling Oliveira, Joselina Luzia Menezeshttp://lattes.cnpq.br/9237658656139251Oliveira, Manuel Hermínio de Aguiarhttp://lattes.cnpq.br/28010938405752912017-09-26T12:18:48Z2017-09-26T12:18:48Z2005-06-17OLIVEIRA, Joselina Luzia Menezes. Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea. 2005. 108 f. Dissertação (Mestrado em Ciências da Saúde) - Universidade Federal de Sergipe, Aracaju, 2005.https://ri.ufs.br/handle/riufs/3899Insulin-Like growth factor I (IGF-I) is a peptide that has an important action on cell division, differentiation, migration and apoptosis for vascular smooth muscle cells (VSMCs), may intervene in atherosclerosis. It antiapoptotic factor and it also stimulates. Thus, potential reductions in IGF-I effects might be beneficial in certain pathologic conditions, such as hypertension and the early stages of atherosclerosclerotic plaque formation characterized by hypertrophy/hyperplasia of VSMCs, but detrimental in other conditions in which loss of VSMCs contributes to the disease process, such as destabilization of atherosclerotic plaques. Conversely, it has been suggested that serum IGF-1 levels are low in patients with coronary heart disease. Recently, we have described a GH naïve homogeneous population with a monogenic mutation that inactives the growth hormone-releasing hormone receptor (GHRHR) (IVS1+ 1GA) with extremely low levels of IGF-1. Moreover, they also presented central obesity, higher levels of systolic blood pressure and dyslipidemia unique opportunity to evaluate the impact of extremely low levels of IGF-1 on the myocardial ischemic and carotid atherosclerosisis in high risk cardiovascular population, pertaining to the research object. It has been studied 22 dwarfs with GHD and no past of growth hormone therapy (10M:12F; 44±12 yrs) and compared to 26 age-matched normal subjects, control group[CO]. It has been examined clinical, biochemical data, including insulin-like growth factor 1(IGF-1), rest and exercise echodopplercardiography and, carotid intima-media thickness by a high-resolution carotid ultrasonography. IGF-1 in GHD group was markedly lower (3,3±5,5 vs 228,4±134,7ng/Ml; p<0.001) and fasting insulin (3,37±3,9 vs 3,59±3,0 microU/mL; p=NS) were smaller but not significantly in GHD. In the resting echocardiographic study, we observed normal indices of both systolic and diastolic function. During exercise treadmill (Bruce Protocol), both groups reached similar peak heart rate (162±16,5 vs 168±15,7bpm; p=NS) and peak systolic blood pressure (49±20 vs 59,4±23,6mmHg p=NS). Comparison of exercise wall motion score index in GHD group (1±0.0) vs CO group (1±0.0) did not show differences. Moreover, intima-media thickness measured at the far wall of the distal common carotid artery (0,59 ± 0,10 mm vs 0,60 ± 0,14 mm; p=NS (GHD vs CO group) was not indicative of premature atherosclerosis in GHD population. Only one of the subjects in the population studied presented carotid atherosclerotic plaque. Our data suggest that in a very homogeneous population with isolated GHD is not associated with premature carotid atherosclerosis or a higher prevalence of myocardial ischemia. Extremely low levels of the IGF-1 may be a protective mechanism against premature atherosclerosis in this apparently high risk selected group.O fator do crescimento semelhante a insulina (IGF-I) é um peptídeo que tem importante ação sobre a divisão, diferenciação, migração e apoptose das células musculares lisas vasculares (CMLVs) e que pode interferir no mecanismo da aterosclerose. Assim a redução potencial do IGF-I pode ser benéfica em certas condições patológicas, tais como hipertensão e estágios iniciais da formação de placas ateroscleróticas caracterizadas por hipertrofia/hiperplasia das CMLVs, mas danoso em outras condições nas quais a perda de CMLVs contribui para o processo da doença, tais como desestabilização das placas ateroscleróticas. Porém, tem sido sugerido que níveis séricos de IGF-I estão baixos em pacientes com doença arterial coronariana. Recentemente, foi descrita uma população homogênea com uma mutação monogênica no gene receptor do hormônio regulador do hormônio do crescimento (GHRH-R) (IVS1+ 1GA) com deficiência isolada do hormônio do crescimento (DIGH) e níveis extremamente baixos de IGF-1. Apresentavam obesidade central, níveis elevados de pressão arterial sistólica e dislipidemia, oportunidade única para avaliar o impacto de níveis extremamente baixos de IGF-I na isquemia miocárdica e aterosclerose carotídea em população de alto risco, objetivo do nosso trabalho. Foram estudados 22 anões nunca tratados com DIGH (10M:12F; 44±12 anos) e comparados com 26 indivíduos normais de mesma idade e região, grupo controle (CO). Foram analisados: dados clínicos, bioquímicos, eletrocardiograma, ecocardiograma em repouso e exercício e duplex scan das carótidas (DSC) para quantificação da espessura médio-intimal das carótidas e pesquisa de placa aterosclerótica. Os resultados encontrados indicaram que o IGF-1 no grupo DIGH estava marcadamente baixo (3,3±5,5 vs 228,4±134,7ng/Ml; p<0,001) e a insulina de jejum (3,37±3,9 vs 3,59±3,0 microU/mL; p=NS) estava mais baixa, mas não significativa no DIGH. No estudo do ecocardiograma de repouso foi observado funções sistólica e diastólica normais. Durante o exercício na esteira ergométrica, ambos os grupos obtiveram semelhante pico de freqüência cardíaca (162±16,5 vs 168±15,7bpm;p=NS) e delta de pressão sistólica (49±20 vs 59,4±23,6mmHg; p=NS). Comparando-se o índice de escore de motilidade do VE no grupo DIGH (1±0.0) vs grupo (CO) (1±0.0) não demonstrou diferenças. A análise comparativa da espessura médio-intimal das carótidas,entre as populações dos grupos DIGH vs grupo (CO) não demonstrou diferença significativa (0,59 ± 0,10 mm vs 0,60 ± 0,14 mm), não foi demonstrado aterosclerose prematura na população com DIGH. Apenas um portador de DIGH apresentou placas ateroscleróticas. Nossos dados sugerem que a deficiência isolada DIGH associada com baixos níveis do IGF-1 não se associou com aterosclerose prematura e alta prevalência de isquemia miocárdica. Foi especulado que níveis extremamente baixos do fator de crescimento IGF-1 pode ter mecanismos protetores contra aterosclerose prematura, apesar de apresentarem um grupo de fatores de elevado risco cardiovascular.Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorapplication/pdfporUniversidade Federal de SergipePós-Graduação em Ciências da SaúdeUFSBRHormônio de crescimentoEcocardiografia sob estresseAterosclerose de carótidasDoença arterial coronarianaGrowth hormoneStress echodopplercardiographyCarotid atherosclerosisCoronary heart diseaseCNPQ::CIENCIAS DA SAUDE::MEDICINAConseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídeaConsequences of the Isolated and Lifetime Deficiency of the Hormone of the Growth on the Isquemia Miocardic and Aterosclerose Carotideainfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFSinstname:Universidade Federal de Sergipe (UFS)instacron:UFSTEXTJOSELINA_LUZIA_MENEZES_OLIVEIRA.pdf.txtJOSELINA_LUZIA_MENEZES_OLIVEIRA.pdf.txtExtracted texttext/plain168295https://ri.ufs.br/jspui/bitstream/riufs/3899/2/JOSELINA_LUZIA_MENEZES_OLIVEIRA.pdf.txtb70defdbed76a01f9a496d28f85d8186MD52THUMBNAILJOSELINA_LUZIA_MENEZES_OLIVEIRA.pdf.jpgJOSELINA_LUZIA_MENEZES_OLIVEIRA.pdf.jpgGenerated Thumbnailimage/jpeg1282https://ri.ufs.br/jspui/bitstream/riufs/3899/3/JOSELINA_LUZIA_MENEZES_OLIVEIRA.pdf.jpg2e7195a4a0fc4e2c250e4f4e499b2c0bMD53ORIGINALJOSELINA_LUZIA_MENEZES_OLIVEIRA.pdfapplication/pdf5039720https://ri.ufs.br/jspui/bitstream/riufs/3899/1/JOSELINA_LUZIA_MENEZES_OLIVEIRA.pdfe2c615481a739f8584aa1c885f19922aMD51riufs/38992017-11-28 16:23:04.827oai:oai:ri.ufs.br:repo_01:riufs/3899Repositório InstitucionalPUBhttps://ri.ufs.br/oai/requestrepositorio@academico.ufs.bropendoar:2017-11-28T19:23:04Repositório Institucional da UFS - Universidade Federal de Sergipe (UFS)false
dc.title.por.fl_str_mv Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
dc.title.alternative.eng.fl_str_mv Consequences of the Isolated and Lifetime Deficiency of the Hormone of the Growth on the Isquemia Miocardic and Aterosclerose Carotidea
title Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
spellingShingle Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
Oliveira, Joselina Luzia Menezes
Hormônio de crescimento
Ecocardiografia sob estresse
Aterosclerose de carótidas
Doença arterial coronariana
Growth hormone
Stress echodopplercardiography
Carotid atherosclerosis
Coronary heart disease
CNPQ::CIENCIAS DA SAUDE::MEDICINA
title_short Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
title_full Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
title_fullStr Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
title_full_unstemmed Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
title_sort Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea
author Oliveira, Joselina Luzia Menezes
author_facet Oliveira, Joselina Luzia Menezes
author_role author
dc.contributor.author.fl_str_mv Oliveira, Joselina Luzia Menezes
dc.contributor.advisor1Lattes.fl_str_mv http://lattes.cnpq.br/9237658656139251
dc.contributor.advisor1.fl_str_mv Oliveira, Manuel Hermínio de Aguiar
dc.contributor.authorLattes.fl_str_mv http://lattes.cnpq.br/2801093840575291
contributor_str_mv Oliveira, Manuel Hermínio de Aguiar
dc.subject.por.fl_str_mv Hormônio de crescimento
Ecocardiografia sob estresse
Aterosclerose de carótidas
Doença arterial coronariana
topic Hormônio de crescimento
Ecocardiografia sob estresse
Aterosclerose de carótidas
Doença arterial coronariana
Growth hormone
Stress echodopplercardiography
Carotid atherosclerosis
Coronary heart disease
CNPQ::CIENCIAS DA SAUDE::MEDICINA
dc.subject.eng.fl_str_mv Growth hormone
Stress echodopplercardiography
Carotid atherosclerosis
Coronary heart disease
dc.subject.cnpq.fl_str_mv CNPQ::CIENCIAS DA SAUDE::MEDICINA
description Insulin-Like growth factor I (IGF-I) is a peptide that has an important action on cell division, differentiation, migration and apoptosis for vascular smooth muscle cells (VSMCs), may intervene in atherosclerosis. It antiapoptotic factor and it also stimulates. Thus, potential reductions in IGF-I effects might be beneficial in certain pathologic conditions, such as hypertension and the early stages of atherosclerosclerotic plaque formation characterized by hypertrophy/hyperplasia of VSMCs, but detrimental in other conditions in which loss of VSMCs contributes to the disease process, such as destabilization of atherosclerotic plaques. Conversely, it has been suggested that serum IGF-1 levels are low in patients with coronary heart disease. Recently, we have described a GH naïve homogeneous population with a monogenic mutation that inactives the growth hormone-releasing hormone receptor (GHRHR) (IVS1+ 1GA) with extremely low levels of IGF-1. Moreover, they also presented central obesity, higher levels of systolic blood pressure and dyslipidemia unique opportunity to evaluate the impact of extremely low levels of IGF-1 on the myocardial ischemic and carotid atherosclerosisis in high risk cardiovascular population, pertaining to the research object. It has been studied 22 dwarfs with GHD and no past of growth hormone therapy (10M:12F; 44±12 yrs) and compared to 26 age-matched normal subjects, control group[CO]. It has been examined clinical, biochemical data, including insulin-like growth factor 1(IGF-1), rest and exercise echodopplercardiography and, carotid intima-media thickness by a high-resolution carotid ultrasonography. IGF-1 in GHD group was markedly lower (3,3±5,5 vs 228,4±134,7ng/Ml; p<0.001) and fasting insulin (3,37±3,9 vs 3,59±3,0 microU/mL; p=NS) were smaller but not significantly in GHD. In the resting echocardiographic study, we observed normal indices of both systolic and diastolic function. During exercise treadmill (Bruce Protocol), both groups reached similar peak heart rate (162±16,5 vs 168±15,7bpm; p=NS) and peak systolic blood pressure (49±20 vs 59,4±23,6mmHg p=NS). Comparison of exercise wall motion score index in GHD group (1±0.0) vs CO group (1±0.0) did not show differences. Moreover, intima-media thickness measured at the far wall of the distal common carotid artery (0,59 ± 0,10 mm vs 0,60 ± 0,14 mm; p=NS (GHD vs CO group) was not indicative of premature atherosclerosis in GHD population. Only one of the subjects in the population studied presented carotid atherosclerotic plaque. Our data suggest that in a very homogeneous population with isolated GHD is not associated with premature carotid atherosclerosis or a higher prevalence of myocardial ischemia. Extremely low levels of the IGF-1 may be a protective mechanism against premature atherosclerosis in this apparently high risk selected group.
publishDate 2005
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dc.date.accessioned.fl_str_mv 2017-09-26T12:18:48Z
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dc.identifier.citation.fl_str_mv OLIVEIRA, Joselina Luzia Menezes. Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea. 2005. 108 f. Dissertação (Mestrado em Ciências da Saúde) - Universidade Federal de Sergipe, Aracaju, 2005.
dc.identifier.uri.fl_str_mv https://ri.ufs.br/handle/riufs/3899
identifier_str_mv OLIVEIRA, Joselina Luzia Menezes. Conseqüências da deficiência isolada e vitalícia do hormônio do crescimento na isquemia miocárdica e aterosclerose carotídea. 2005. 108 f. Dissertação (Mestrado em Ciências da Saúde) - Universidade Federal de Sergipe, Aracaju, 2005.
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