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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

A influ?ncia da perda de peso no perfil inflamat?rio de mulheres com s?ndrome dos ov?rios polic?sticos

Santos, Ana Celly Souza dos 27 March 2015 (has links)
Submitted by Automa??o e Estat?stica (sst@bczm.ufrn.br) on 2016-04-25T22:57:37Z No. of bitstreams: 1 AnaCellySouzaDosSantos_DISSERT.pdf: 1317537 bytes, checksum: b64edb8897e90d29039563de6db801af (MD5) / Approved for entry into archive by Arlan Eloi Leite Silva (eloihistoriador@yahoo.com.br) on 2016-04-27T21:45:33Z (GMT) No. of bitstreams: 1 AnaCellySouzaDosSantos_DISSERT.pdf: 1317537 bytes, checksum: b64edb8897e90d29039563de6db801af (MD5) / Made available in DSpace on 2016-04-27T21:45:33Z (GMT). No. of bitstreams: 1 AnaCellySouzaDosSantos_DISSERT.pdf: 1317537 bytes, checksum: b64edb8897e90d29039563de6db801af (MD5) Previous issue date: 2015-03-27 / A s?ndrome dos ov?rios polic?sticos (SOP) ? considerada a endocrinopatia mais comum na fase reprodutiva da mulher, com preval?ncia que varia entre 15 a 20%. Al?m das altera??es hormonais e reprodutivas, ? comum na SOP a presen?a de fatores de risco para desenvolvimento de doen?as cardiovasculares (DCV) como diabetes mellitus, resist?ncia ? insulina (RI), obesidade visceral, inflama??o cr?nica de baixo grau e dislipidemia. Devido ? elevada frequ?ncia da obesidade associada ? SOP, a perda de peso ? considerada como o tratamento de primeira linha para a s?ndrome por melhorar as altera??es metab?licas e normalizar os andr?genos s?ricos, restaurando a fun??o reprodutiva destas pacientes. Objetivos: avaliar os marcadores inflamat?rios e a RI em mulheres com SOP e ovulat?rias saud?veis com diferentes estados nutricionais e como os par?metros inflamat?rios e hormonais se apresentam ap?s a perda de peso, atrav?s da restri??o cal?rica nas portadoras da s?ndrome. M?todos: O fator de necrose tumoralalfa (TNF-?), a interleucina-6 (IL-6) e a prote?na c-reativa (PCR) foram avaliados em amostras de soro de 40 mulheres em idade reprodutiva. Na primeira fase do estudo, as volunt?rias foram divididas em quatro grupos: Grupo I (n?o eutr?ficas com SOP, n=12); Grupo II (n?o eutr?ficas sem SOP, n=10), Grupo III (eutr?ficas com SOP, n=08) e Grupo IV (eutr?ficas sem SOP, n=10). A categoriza??o dos grupos foi realizada pelo ?ndice de massa corporal (IMC), de acordo com a organiza??o mundial de sa?de (OMS) em n?o eutr?fica, mulheres com IMC ? 25 (kg/m?) e eutr?ficas, IMC entre 18,9-24,9 (kg/m?). A RI foi determinada atrav?s do ?ndice HOMA-IR. Na segunda fase do estudo foi realizada uma interven??o nutricional controlada e os par?metros inflamat?rios foram avaliados em 21 mulheres sobrepeso e obesas com SOP, antes e depois da perda de peso. Todas as pacientes receberam uma dieta hipocal?rica com redu??o de 500 kcal/dia do consumo habitual com concentra??es padr?o de macronutrientes. Resultados: Fase 1: pacientes com SOP apresentaram n?veis aumentados da PCR (p<0,01) e HOMA-IR (p<0,01). Quando divididas por IMC, tanto o grupo n?o eutr?fico com SOP (I) quanto eutr?fico com SOP(III) apresentou n?veis aumentados de PCR (I=2,35?0,55mg/L e III= 2,63?0,65mg/L; p<0,01) e HOMA-IR (I= 2,16?2,54 e III= 1,07?0,55; p<0,01). N?o foram encontradas diferen?as de TNF-? e IL-6 entre os grupos. Fase 2: Ap?s a perda de peso de 5% do peso inicial ocorreu uma redu??o em todos os n?veis s?ricos dos componentes do perfil inflamat?rio avaliados, PCR (154.75 ? 19.33) vs (78.06 ? 9.08), TNF- ? (10.89 ? 5.09) vs (6.39 ? 1.41) e IL6 (154.75 ? 19.33) vs (78.06 ? 9.08) (p < 0.00) em associa??o com a melhora de alguns par?metros hormonais avaliados. Conclus?o: A SOP contribuiu para o surgimento da inflama??o cr?nica e das altera??es no metabolismo da glicose atrav?s do aumento da PCR, da insulina e do HOMA-IR, independente do estado nutricional e a perda de peso melhoraram o estado inflamat?rio e o perfil hormonal das pacientes avaliadas. / The polycystic ovary syndrome (PCOS) is considered the most common endocrine disorder in reproductive age women, with a prevalence ranging from 15 to 20%. In addition to hormonal and reproductive changes, it is common in PCOS the presence of risk factors for developing cardiovascular disease (CVD) and diabetes mellitus, insulin resistance (IR), visceral obesity, chronic low-grade inflammation and dyslipidemia. Due to the high frequency of obesity associated with PCOS, weight loss is considered as the first-line treatment for the syndrome by improving metabolic and normalizes serum androgens, restoring reproductive function of these patients. Objectives: To evaluate the inflammatory markers and IR in women with PCOS and healthy ovulatory with different nutritional status and how these parameters are displayed after weight loss through caloric restriction in with Down syndrome. Methods: Tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6) and C-reactive protein (CRP) were assessed in serum samples from 40 women of childbearing age. The volunteers were divided into four groups: Group I (not eutrophic with PCOS, n = 12); Group II (not eutrophic without PCOS, n = 10), Group III (eutrophic with PCOS, n = 08) and Group IV (eutrophic without PCOS, n = 10). The categorization of groups was performed by body mass index (BMI), according to the World Health Organization (WHO) does not eutrophic, overweight and obesity (BMI> 25 kg / m?) and normal weight (BMI <24.9 kg / m?). IR was determined by HOMA-IR index. In the second phase of the study a controlled dietary intervention was performed and inflammatory parameters were evaluated in 21 overweight and obese women with PCOS, before and after weight loss. All patients received a low-calorie diet with reduction of 500 kcal / day of regular consumption with standard concentrations of macronutrients. Results: Phase 1: PCOS patients showed increased levels of CRP (p <0.01) and HOMAIR (p <0.01). When divided by BMI, both not eutrophic group with PCOS (I) as eutrophic with PCOS (III) showed increased levels of CRP (I = 2.35 ? 0,55mg / L and 2.63 ? III = 0,65mg / L; p <0.01) and HOMA-IR (I = 2.16 ? 2.54 and III = 1.07 ? 0.55; p <0.01). There were no differences in TNF-? and IL-6 between groups. Step 2: After the weight loss of 5% of the initial weight was reduced in all of the components of serum assessed inflammatory profile, PCR (154.75 ? 19:33) vs (78.06 ? 8.9) TNF ? (10.89 ? 5.09) vs (6:39 ? 1:41) and IL6 (154.75 ? 19:33) vs (78.06 ? 08.09) (p <0:00) in association with improvement some hormonal parameters evaluated. Conclusion: PCOS contributed to the development of chronic inflammation and changes in glucose metabolism by increasing CRP, insulin and HOMA-IR, independent of nutritional status. The weight loss, caloric restriction has improved the inflammatory condition and hormonal status of the evaluated patients.
2

O efeito do treinamento intervalado de alta intensidade em componentes celulares e moleculares relacionados ? resist?ncia ? insulina em indiv?duos obesos

Matos, Mariana Aguiar de 20 October 2016 (has links)
Submitted by Jos? Henrique Henrique (jose.neves@ufvjm.edu.br) on 2017-04-27T15:00:50Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) mariana_aguiar_matos.pdf: 2901378 bytes, checksum: 40dbd704043d49a1eee587bb086c4eb4 (MD5) / Approved for entry into archive by Rodrigo Martins Cruz (rodrigo.cruz@ufvjm.edu.br) on 2017-05-16T19:24:00Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) mariana_aguiar_matos.pdf: 2901378 bytes, checksum: 40dbd704043d49a1eee587bb086c4eb4 (MD5) / Made available in DSpace on 2017-05-16T19:24:00Z (GMT). No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) mariana_aguiar_matos.pdf: 2901378 bytes, checksum: 40dbd704043d49a1eee587bb086c4eb4 (MD5) Previous issue date: 2016 / Funda??o de Amparo ? Pesquisa do Estado de Minas Gerais (FAPEMIG) / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico (CNPq) / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior (CAPES) / O excesso de gordura corporal caracter?stico da obesidade est? relacionado a diversas altera??es metab?licas, que incluem a resist?ncia ? insulina. Dentre as medidas n?o farmacol?gicas empregadas para a melhora da sensibilidade ? insulina est? o treinamento f?sico aer?bio, como o treinamento intervalado de alta intensidade (HIIT, do ingl?s high intensity interval training). Sendo assim, esse estudo avaliou os efeitos do HIIT em componentes bioqu?micos, celulares e moleculares relacionados ? resist?ncia ? insulina em obesos. Indiv?duos obesos sens?veis (n=9) e resistentes ? insulina (n=8) foram submetidos a 8 semanas de HIIT, em cicloerg?metro, realizado 3 vezes por semana, com intensidade e volume progressivos (8 a 12 est?mulos; 80 a 110% da pot?ncia m?xima). Amostras de sangue venoso e do m?sculo vasto lateral foram obtidas antes e ap?s o programa de HIIT. Ap?s o programa de treinamento houve aumento da sensibilidade ? insulina nos obesos resistentes ? insulina, mas n?o houve redu??o da massa de gordura. A concentra??o de citocinas no soro, o estresse oxidativo sist?mico e frequ?ncia das c?lulas imunes n?o foram modificadas ap?s o treinamento. No m?sculo esquel?tico, o HIIT promoveu aumento da fosforila??o do substrato do receptor de insulina (IRS) (Tyr612), da Akt (Ser473) e da prote?na quinase dependente de c?lcio/calmodulina (CAMKII) (Thr286), e aumento do conte?do da ?-hidroxiacil-CoA desidrogenase (?-HAD) e citocromo C oxidase (COX-IV). Houve ainda, redu??o da fosforila??o da quinase regulada por sinal extracelular (ERK1/2) nos obesos resistentes ? insulina. Conclu?mos que 8 semanas de HIIT promoveram melhora da sensibilidade ? insulina, modificou componentes da via de sinaliza??o da insulina e do metabolismo oxidativo no m?sculo esquel?tico. Essas altera??es ocorreram independentes de mudan?as na gordura corporal total e de par?metros inflamat?rios sist?micos. / Tese (Doutorado) ? Programa Multic?ntrico de P?s-Gradua??o em Ci?ncias Fisiol?gicas, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2016. / Obesity is characterized by excess of body fat, and its development can lead to a variety of metabolic disorders, including insulin resistance. Exercise is recognized as a non-pharmacological approach to increasing skeletal muscle insulin sensitivity, although the mechanisms are not elucidated. Additionally, the understanding of high intensity interval training (HIIT, high intensity interval training) treat insulin resistance is less understood. Therefore, this study evaluated the effects of HIIT on biochemical, molecular, and cellular markers related to insulin resistance in sedentary obese individuals. Sensitive (n=9) and insulin resistant (n=8) obese individuals (body mass index ? 30 kg/m-2) were engaged in 8 weeks of HIIT using a cycle ergometer. The HIIT was performed 3 times a week, and its intensity and volume progressively increased throughout the training period (from 8 to 12 stimuli; from 80 to 110% of the maximum power). Venous blood and the vastus lateralis muscle samples were obtained before and after the HIIT. HIIT enhanced insulin sensitivity in insulin-resistant obese individuals without changing body fat mass. Cytokine concentration in serum, blood oxidative stress, and frequency of some immune cells were not altered by HIIT. In skeletal muscle, HIIT increased the phosphorylation of insulin receptor substrate (IRS) (Tyr612), Akt (Ser473), and protein kinase dependent calcium/calmodulin (CaMKII) (Thr286). HIIT also increased the expression of ?-hydroxyacyl-CoA dehydrogenase (?-HAD) and cytochrome C oxidase (COX-IV). A reduction of the kinase phosphorylation of extracellular signal-regulated (ERK1/2) was only seen in obese insulin resistant individuals. The results show that 8 weeks of HIIT enhanced insulin sensitivity, modified components of the insulin-signaling pathway, and improved skeletal muscle oxidative metabolism. These changes were independent of alterations in body fat and inflammatory parameters.

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