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| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Zeca, Suelen Guedes | |
| dc.date.accessioned | 2023-12-22T01:52:18Z | - |
| dc.date.available | 2023-12-22T01:52:18Z | - |
| dc.date.issued | 2020-09-18 | |
| dc.identifier.citation | ZECA, Suelen Guedes. Estudo da transmissão inter- e transgeracional de alterações metabólicas, comportamentais e cardíacas na prole de camundongos obesos por duas gerações consecutivas. 2020. 99 F. Tese (Doutorado em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica, 2020. | por |
| dc.identifier.uri | https://rima.ufrrj.br/jspui/handle/20.500.14407/11400 | - |
| dc.description.abstract | Dados epidemiológicos e experimentais demonstram que a obesidade materna é capaz de transmitir distúrbios metabólicos, comportamentais e cardiovasculares na prole, transmitidas potencialmente de forma epigenética. Trabalhos mais recentes indicam a participação da obesidade paterna no desenvolvimento de alterações na composição corporal e distúrbios metabólicos através de alterações epigenéticas no espermatozóide. Pouco ainda é conhecido sobre esse fenômeno em mamíferos, e no dimorfismo da programação metabólica nesses modelos. O objetivo deste trabalho foi compreender se a obesidade materna ou paterna, separadamente, modula o metabolismo, comportamento, e função cardíaca em roedores, por duas gerações consecutivas. Camundongos C57BL/6J fêmeas ou machos alimentaram-se com dieta controle (NC, 6% de lipídeos) ou hiperlipídicas (HF45 e HF60, 45 e 60% de lipídeos, respectivamente) ad libitum por seis semanas antes da avaliação da composição corporal, metabolismo glicídico e comportamental. Os grupos maternos e paternos NC, HF45 e HF60, considerados geração F0, foram acasalados com animais NC do sexo oposto para obtenção da geração F1. Para aumentar a influência da programação, a geração F2 foi obtida pelo cruzamento de camundongos F1 dentro de seu próprio grupo. Excetuando-se F0, todos os animais foram mantidos em NC durante todo o período. Observamos que fêmeas e machos F0-HF45 e F0-HF60 apresentaram maior peso corporal e adiposidade (fêmeas: p<0,01; machos: p<0,001) e prejuízo no metabolismo glicídico (p<0,05). Nas fêmeas, nenhuma diferença significativa foi observada nas taxas de gravidez e número de filhotes ao nascimento; porém fêmeas F0-HF60 apresentaram menor taxa de sobrevivência dos filhotes após o desmame (p< 0,05). A obesidade materna afetou em maior proporção os filhotes machos MHF45, que na F1 apresentaram maior massa corporal (p<0,001), adiposidade (p<0,001) e prejuízo no metabolismo glicídico (p<0,05) e, na F2 apresentaram menor peso corporal (p<0,05) e alterações cardíacas representadas pela redução na fração de ejeção (p<0,05) e aumento no volume sistólico final do ventrículo esquerdo (p<0,05). A obesidade paterna afetou filhotes machos e fêmeas em proporções semelhantes. Observamos maior massa corporal (p<0,05) e adiposidade (p<0,05) em ambos sexos na prole F1-PHF45 e nos machos F1-PHF60. Na F2 observamos menor peso corporal na prole PHF45 (p<0,05), com menor adiposidade nas fêmeas F2-PHF45 (p<0,01), sem alteração no metabolismo glicídico nas duas gerações. A função cardíaca apresentava-se normal na F1, mas uma redução substancial na fração de ejeção e aumento do volume sistólico final do VE foi detectado nas proles F2-PHF45, em machos (p<0,05) e fêmeas (p<0,01). Dessa forma, concluímos que os filhotes machos foram mais afetados pela obesidade materna, enquanto alterações na obesidade paterna foram observadas em ambos os sexos, principalmente em relação aos prejuízos na função cardíaca. Tal dimorfismo mostra a importância do estudo em ambos os sexos, bem como a necessidade de estudos adicionais para a busca de marcadores epigenéticos chaves na manutenção e transmissão destes fenótipos às proles subsequentes. | por |
| dc.description.sponsorship | CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior | por |
| dc.format | application/pdf | * |
| dc.language | por | por |
| dc.publisher | Universidade Federal Rural do Rio de Janeiro | por |
| dc.rights | Acesso Aberto | por |
| dc.subject | ecocardiograma | por |
| dc.subject | epigenética | por |
| dc.subject | obesidade materna e paterna | por |
| dc.subject | echocardiogram | eng |
| dc.subject | epigenetic | eng |
| dc.subject | maternal, and paternal obesity | eng |
| dc.title | Estudo da transmissão inter- e transgeracional de alterações metabólicas, comportamentais e cardíacas na prole de camundongos obesos por duas gerações consecutivas | por |
| dc.title.alternative | Studying inter- and transgenerational transmission of metabolic, behavioral, and heart phenotypes on mice offspring for two consecutive generations | eng |
| dc.type | Tese | por |
| dc.description.abstractOther | Epidemiological and experimental data show that maternal obesity can transmit metabolic, behavioral, and cardiovascular diseases, potentially transmitted by epigenetic mechanisms. Recent literature indicates paternal obesity's role in developing body composition and metabolic diseases by epigenetic modifications on spermatic cells. There is a lack of information about the phenomena in mammals and the dimorphic aspect of this experimental model's metabolic programming. This research aimed to understand if maternal or paternal obesity, separately, modulate the metabolism, behavior, and cardiac function in rodents, for two subsequent generations. Male and female C57BL/6J mice were fed with chow (NC, 6% lipids) or high fat (HF45 and HF60, 45 and 60% lipids, respectively) diet ad libitum for six weeks prior body composition, glycemic metabolism, and behavioral evaluation. Maternal and paternal NC, HF45, and HF60 groups, the F0 generation, were mated with NC animals to obtain F1. To boost the programming effects, the F2 generation was obtained by crossing the F1 generation within their groups. We kept all animals in a chow diet during the experimental protocol, except F0. We observed that F0-HF45 and F0-HF60 male and female had higher body weight and adiposity (female: p<0.01; male: p<0.001) and glycemic metabolism impairment (p<0.05). No significant changes were observed on females regarding pregnancy rate and litter number at birth; however, F0-HF60 females had decreased pups by the end of lactation (p<0.05). Maternal obesity had a more significant impact on MHF45 male offspring, in which F1 had increased body weight (p<0.001), adiposity (p<0.001), and impaired glycemic metabolism (p<0.05). On F2 generation, it was observed not only reduced body weight in this group (p<0.05), but also cardiac defects, showed by decreased ejection fraction (p<0.05) and increased left-ventricle (LF) end-systolic volume (p<0.05). Paternal obesity affected male and female offspring in similar proportions. We observed more significant body weight (p<0.05) and adiposity (p<0.05) in both sexes in the F1-PHF45 group and F1-PHF60 males. On F2 generation, decreased body weight was observed in male and female F2-PHF45 (p<0.05), as well as reduced adiposity in female F2-PHF45 (p<0.01), without changes in glycemic metabolism in both generations. The cardiac function was normal on F1, but a substantial reduction in the ejection fraction and increased left-ventricle (LF) end-systolic volume were detected on F2-PHF45 groups, male (p<0.05) and female (p<0.01). Therefore, we suggest that male offspring was more affected by maternal obesity, while paternal obesity affects both sexes in similar ways, especially regarding the cardiac function. Such dimorphism shows the importance of both sex's studies and the need for additional research on key epigenetic markers regarding phenotype maintenance and transmission to subsequent generations. | eng |
| dc.contributor.advisor1 | Almeida, Norma Aparecida dos Santos | |
| dc.contributor.advisor1ID | 072.340.197-74 | por |
| dc.contributor.referee1 | Almeida, Norma Aparecida dos Santos | |
| dc.contributor.referee2 | Rocha, Fábio Fagundes da| | |
| dc.contributor.referee3 | Malvar, David do Carmo | |
| dc.contributor.referee4 | Silva, Patrícia Cristina Lisboa da | |
| dc.contributor.referee5 | Ayres, Natália Galito Rocha | |
| dc.creator.ID | 116.784.667-27 | por |
| dc.creator.Lattes | http://lattes.cnpq.br/7861398897523675 | por |
| dc.publisher.country | Brasil | por |
| dc.publisher.department | Instituto de Ciências Biológicas e da Saúde | por |
| dc.publisher.initials | UFRRJ | por |
| dc.publisher.program | Programa de Pós-Graduação em Ciências Fisiológicas | por |
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Y.; MING, Z. H.; CHENG, Y.; ZHOU, C. L.; GUO, M. X.; HUANG, Y. T.; YU, D. Q.; SHENG, J. Z.; HUANG, H. F. Diet-Induced Paternal Obesity Impairs Cognitive Function in Offspring by Mediating Epigenetic Modifications in Spermatozoa. Obesity (Silver Spring, Md.), v. 26, n. 11, p. 1749–1757, 2018. | por |
| dc.subject.cnpq | Fisiologia | por |
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