Дисертації з теми "Cardiac metabolic syndrome"
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Zibadi, Sherma. "Metabolic Syndrome-Induced Cardiac Fibrosis." Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195321.
Повний текст джерелаZullo, Melissa D. "Cardiovascular Disease Management and Functional Capacity in Patients With Metabolic Syndrome." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1232721609.
Повний текст джерелаNAGATA, KOHZO, TOYOAKI MUROHARA, SHOGO WATANABE, YUURI TAKESHITA, SAE OHURA, TAMAYO MURASE, TAKUYA HATTORI, MIWA TAKATSU, and KEIJI TAKAHASHI. "Premature Cardiac Senescence in DahlS.Z-Lepr fa/Lepr fa Rats as a New Animal Model of Metabolic Syndrome." Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/19482.
Повний текст джерелаDonner, Daniel Giordano. "Therapeutic Effects of Selective Androgen Receptor Modulation in the Treatment of Cardiac, Metabolic and Bone Pathologies Associated with Androgen Decline and Obesity." Thesis, Griffith University, 2015. http://hdl.handle.net/10072/367789.
Повний текст джерелаThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Wachowiak, Paul Stephen. "Relationships among Cynical Hostility, Metabolic Syndrome, and Cardiac Structure and Function in Multi-Ethnic Post-Myocardial Infarction Patients: A Structural Modeling Approach." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/291.
Повний текст джерелаVidlund, Mårten. "Glutamate for metabolic intervention in coronary surgery : with special reference to the GLUTAMICS-trial." Doctoral thesis, Örebro universitet, Hälsoakademin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-19757.
Повний текст джерелаMaarman, Gerald Jerome. "The effect of CPT-1 inhibition on myocardial function and resistance to ischemia/reperfusion injury in a rodent model of the metabolic syndrome." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/5354.
Повний текст джерелаENGLISH ABSTRACT: Background: Obesity is associated with dyslipidemia, insulin resistance and glucose intolerance and together these components characterise the metabolic syndrome (Dandona et al. 2005). In the state of obesity, there are high levels of circulating free fatty acids and increased rates of fatty oxidation which inhibit glucose oxidation. This: (i) reduce the heart‘s contractile ability, (ii) exacerbates ischemic/reperfusion injury and (iii) decreases cardiac mechanical function during reperfusion (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Aim: The aim of our study was to investigate the effect of inhibiting fatty acid oxidation, with oxfenicine (4-Hydroxy-L-phenylglycine), on (i) cardiac mechanical function, (ii) mitochondrial respiration, (iii) myocardial tolerance to ischemia/reperfusion injury, (iv) CPT-I expression, MCAD expression, IRS-1 activation, total GLUT- 4 expression and (v) the RISK pathway (ERK42/44 and PKB/Akt). Methods: Male Wistar rats were fed a control rat chow diet or a high calorie diet (HCD) for 16 weeks. The HCD caused diet induced obesity (DIO). The animals were randomly divided into 4 groups [Control, DIO, Control + oxfen and DIO + oxfen]. The drug was administered for the last 8 weeks of feeding (200mg/kg/day). Animals were sacrificed and the hearts were perfused on the Langendorff perfusion system. After being subjected to regional ischemia and two hours of reperfusion, infarct size was determined. A separate series of animals were fed and/or treated and hearts were collected after 25 minutes global ischemia followed by 30 min reperfusion for determination of GLUT- 4, CPT-1, IRS -1, MCAD, ERK (42/44) and PKB/Akt expression/phosphorylation using Western blot analysis. A third series of hearts were excised and used for the isolation of mitochondria. Results: In the DIO rats, chronic oxfenicine treatment improved cardiac mechanical function by improving mitochondrial respiration. Oxfenicine inhibited CPT-1 expression but had no effect on MCAD or GLUT- 4 expression. Oxfenicine decreased IRS-1 iv expression, but not IRS-1 activation. Oxfenicine also improved myocardial tolerance to ischemia/reperfusion without activation of the RISK pathway (ERK & PKB). In the control rats, chronic oxfenicine treatment worsened cardiac mechanical function by adversely affecting mitochondrial respiration. Oxfenicine also worsened myocardial tolerance to ischemia/reperfusion in the control rats without changes in the RISK pathway (ERK & PKB). Oxfenicine had no effect on CPT-1, MCAD or GLUT- 4 expression. Oxfenicine increased IRS-1 expression, but not IRS-1 activity. Conclusion: Chronic oxfenicine treatment improved cardiac mechanical function and myocardial resistance to ischemia/reperfusion injury in obese animals, but worsened it in control animals. The improved cardiac mechanical function and tolerance to ischemia/reperfusion injury may be due to improvement in mitochondrial respiration.
AFRIKAANSE OPSOMMING: Agtergrond: Vetsug word geassosieer met dislipidemie, insulien weerstandigheid en glukose intoleransie, wat saam die metaboliese sindroom karakteriseer (Dandona et al. 2005). Met vetsug is daar ‗n hoë sirkulasie van vetsure, sowel as verhoogde vertsuur oksidasie wat gevolglik glukose oksidasie onderdruk. Dit: (i) verlaag die hart se vermoë om saam te trek, (ii) vererger isgemiese/herperfusie skade en (iv) verlaag kardiale effektiwiteit gedurende herperfusie (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Doel: Die doel van die studie was om die effekte van vetsuur onderdrukking m.b.v. oksfenisien (4-Hidroksie-L-fenielglisien) op (i) meganiese hart funksie, (ii) mitokondriale respirasie, (iii) miokardiale toleransie teen isgemiese/herperfusie skade, (iv) CPT-I uitdrukking, MCAD uitdrukking, IRS-1 aktiwiteit, totale GLUT-4 uitdrukking en (v) die RISK pad (ERK42/44 en PKB/Akt) te ondersoek. Metodes: Manlike Wistar rotte was gevoer met ‗n kontrole rot dieet of ‗n hoë kalorie dieet (HKD) vir 16 weke. Die HKD lei tot dieet-geïnduseerde vetsug (DGV). Die diere was lukraak verdeel in 4 groepe [kontrole, DGV, kontrole + oksfen en DGV + oksfen]. Die behandeling met die middel was toegedien vir die laaste 8 weke van die voeding protokol (200mg/kg/dag). Die diere was geslag en die harte was geperfuseer op die Langendorff perfusie sisteem. Na blootstelling aan streeks- of globale isgemie en 2 ure herperfusie was infark groottes bepaal. ‗n Aparte reeks diere was gevoer en/of behandel en die harte was versamel na 25 minute globale isgemie gevolg deur 30 minute herperfusie vir die bepaling van GLUT-4, CPT 1, IRS -1, MCAD, ERK (42/44) en PKB/Akt uitdrukking/aktivering d.m.v. Western blot analise. ‗n Derde reeks diere was gebruik vir die isolasie van mitokondria. Resultate: In die DGV diere, het kroniese oksfenisien behandeling meganiese hart funksie verbeter d.m.v. die verbetering van mitokondriale respirasie. Oksfenisien het CPT-1 uitdrukking verlaag terwyl GLUT- 4 en MCAD uitdrukking nie geaffekteer was vi nie. Oksfenisien het IRS-1 uitdrukking verlaag, maar nie IRS-1 aktiwiteit nie. Oksfenisien het ook miokardiale weerstand teen isgemiese/herperfusie verbeter met sonder aktivering van die RISK pad (ERK & PKB). In die kontrole diere, het kroniese oksfenisien behandeling die meganiese hart funksie versleg d.m.v. negatiewe effekte op mitokondriale respirasie. Oksfenisien het die miokardiale weerstand teen isgemiese/herperfusie van die kontrole rotte versleg sonder veranderinge in die RISK pad (ERK & PKB). Oksfenisien het geen effek gehad op CPT-1, MCAD en GLUT-4 uitdrukking nie. Oksfenisien het IRS-1 uitdrukking verhoog, maar nie IRS-1 aktiwiteit nie. Samevatting: Kroniese oksfenisien behandeling het die meganiese hart funksie en miokardiale weerstand teen isgemiese/herperfusie skade in die vet diere verbeter, maar versleg in die kontrole diere. Hierdie verbetering van meganiese hart funksie en weerstand teen isgemiese/herperfusie skade kon dalk wees a.g.v. ‗n verbetering in mitokondriale respirasie.
Smith, Wayne. "A pathologic role for angiotensin II and endothelin-1 in cardiac remodelling and ischaemia and reperfusion injury in a rat model of the metabolic syndrome." Thesis, Link to the online version, 2006. http://hdl.handle.net/10019/1217.
Повний текст джерелаMittoux, Aurélia. "Évaluation de la mortalité chez les patients schizophrènes traités par des antipsychotiques dans des conditions normales de prescription en Europe et en Asie." Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10268.
Повний текст джерелаFatica, Erica Marie. "Investigating Cardiac Metabolism in Barth Syndrome Using Induced Pluripotent Stem Cell-Derived Cardiomyocytes." Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu1556630870935279.
Повний текст джерелаNduhirabandi, Frederic. "The role of melatonin in cardioprotection : an investigation into the mechanisms involved in glucose homeostasis, microvascular endothelial function and mitochondrial function in normal and insulin resistant states." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86332.
Повний текст джерелаENGLISH ABSTRACT: Introduction: The cardioprotective actions of the hormone melatonin against myocardial ischaemiareperfusion injury (IRI) are well-established. It has recently been shown to prevent the harmful effects of hyperphagia-induced obesity on the susceptibility of the heart to IRI as well as many of the harmful effects of obesity and insulin resistance. However, the exact mechanism whereby it exerts its beneficial action is still unknown. The aims of this study were to determine the effects of relatively short-term melatonin treatment in a rat model of diet-induced obesity on: (i) biometric and metabolic parameters, lipid peroxidation, myocardial IRI and intracellular signalling (ii) mitochondrial oxidative phosphorylation function (iii) cardiomyocyte glucose uptake and intracellular signalling. In addition, the effects of acute melatonin treatment of cardiac microvascular endothelial cells (CMEC) were determined on cell viability, nitric oxide production (NO), TNF- -induced dysfunction and intracellular signalling. Material and Methods: Male Wistar rats were randomly allocated to two groups for 20 weeks feeding with either standard rat chow or a high calorie diet. Each group was subdivided into 3 groups receiving either water throughout or melatonin (4mg/kg/day, in the drinking water) for the last 6 or 3 weeks of the experimental programme. Hearts, perfused in the working mode, were subjected to ischaemia/reperfusion and infarct size determined. Mitochondria and cardiomyocytes were isolated according to standard techniques and oxidative function and glucose uptake respectively determined. CMEC NO production and cell viability were quantified by FACS analysis of the fluorescent probes, DAF-2/DA and propidium iodide/Annexin V respectively. Intracellular signalling was evaluated using Western blot and appropriate antibodies. Results: The high-calorie diet caused significant increases in body weight gain, visceral adiposity, fasting blood glucose, serum insulin, triglycerides, HOMA-IR index and a concomitant reduction in serum adiponectin levels as well as larger myocardial infarct sizes after exposure to IRI compared to the control, indicating increased susceptibility to damage. Three as well as six weeks of melatonin administration to obese and insulin resistant rats reduced serum insulin levels and the HOMA-IR index. Myocardial infarct size was reduced in both control and diet groups. These effects were associated with increased activation of baseline myocardial STAT- 3 and the RISK pathway during reperfusion. The diet had no effect on the oxidative phosphorylation capacity of mitochondria, isolated from non-perfused hearts (baseline), but melatonin administration for 6 weeks induced a reduction in state 3 respiration rate; mitochondria isolated from diet hearts subjected to global ischaemia, exhibited an attenuated oxidative phosphorylation process which was improved by melatonin treatment. Melatonin in vitro enhanced cardiomycyte insulin stimulated glucose uptake of normal young rats but not of insulin resistant rats. In vivo melatonin treatment for 6 weeks increased basal (in diet group) and insulin stimulated glucose uptake in both control and diet groups. Melatonin (1nM) in vitro caused a significant reduction in necrosis and apoptosis of cultured CMEC, associated with a decrease in nitric oxide availability and eNOS activation and a concomitant increase in PKB/Akt, p38MAPK and AMPK activation. The harmful effects of TNF- treatment on signalling in CMEC could be prevented by co-treatment with melatonin. Conclusions: The results suggest that short-term melatonin treatment was able to significantly attenuate the diet-induced increased myocardial susceptibility to ischaemia/reperfusion damage. It may also improve cardiac glucose homeostasis and mitochondrial oxidative phosphorylation in an insulin resistant state. Melatonin in vitro protects CMEC against apoptosis and necrosis and reduces nitric oxide availability. These beneficial effects of melatonin may ultimately be due to its antioxidant capacity or receptor-mediated actions, but this remains to be established.
AFRIKAANSE OPSOMMING: Inleiding: Die vermoë van die hormoon, melatonien, om die hart teen iskemie/ herperfusiebesering (IHB) te beskerm, is welbekend. Onlangs is ook getoon dat melatonien IHB en verskeie van die nadelige effekte van vetsug en insulienweerstandigheid in hiperfagiegeïnduseerde vetsug kan voorkom. Die meganisme(s) betrokke by hierdie voordelige prosesse is egter grootliks onbekend. Die doel van hierdie studie was om die gevolge van korttermyn melatonienbehandeling in ‘n model van hiperfagiegeïnduseerde vetsug te ondersoek op (i) biometriese en metaboliese parameters, lipiedperoksidasie, miokardiale IHB en intrasellulêre seintransduksie, (ii) mitochondriale oksidatiewe fosforilasie, (iii) glukoseopname en intrasellulêre seintransduksie in kardiomiosiete en aanvullend, (iv) die invloed van akute melatonienbehandeling van kardiale mikrovaskulêre endoteelselle op sellulêre oorlewing, stikstofoksiedproduksie, TNF- - geïnduseerde disfunksie en seintransduksie. Metodiek: Manlike Wistarrotte is ewekansig in twee groep verdeel en vir 20 weke met standaard-rotkos of ‘n hoëkaloriedieet gevoer. Elke groep is in 3 subgroepe verdeel, wat deurgaans water of melatonien (4mg/kg/dag in die drinkwater) vir 3 of 6 weke voor die beëindiging van die eksperiment ontvang het. Harte is geperfuseer volgens die werkharttegniek, blootgestel aan iskemie/herperfusie en die infarktgrootte bepaal. Mitochondria en kardiomiosiete is volgens standaardtegnieke geïsoleer vir bepaling van oksidatiewe funksie en glukoseopname respektiewelik. NO produksie en sellewensvatbaarheid was gekwantifiseer deur vloeisitometriese analises (FACS) van die fluoresserende agense, DAF-2/DA en propidium jodied/Annexin V onderskeidelik. Intrasellulêre seintransduksie is evalueer met behulp van die Western kladtegniek en geskikte antiliggame. Resultate: Die hoëkaloriedieet het ‘n beduidende toename in liggaamsgewig, visserale vet, vastende bloedglukose, seruminsulienvlakke, trigliseriede, HOMA-IR-indeks en ‘n gepaardgaande verlaging in serumadiponektienvlakke tot gevolg gehad, sowel as groter miokardiale infarkte na iskemie/herperfusie. Laasgenoemde dui op ‘n groter vatbaarheid vir iskemiese beskadiging in harte van vetsugtige diere. Drie sowel as ses weke van melatonienbehandeling het die seruminsulienvlakke en HOMAindeks in vetsugtige diere beduidend verlaag, vergeleke met die kontroles. Miokardiale infarktgroottes was verminder in beide kontrole- en vetsuggroepe. Hierdie effekte het met ‘n verhoogde aktivering van basislyn STAT-3 en PKB/Akt en ERKp44/p42 tydens herperfusie gepaard gegaan. Die dieet het geen invloed op die oksidatiewe fosforilasiekapasiteit van mitochondria, geïsoleer uit harte van ongeperfuseerde harte, gehad nie (basislyn), maar melatonienbehandeling vir 6 weke het Staat 3 respirasie verlaag. Mitochondria, geïsoleer uit harte van vetsugtige rotte wat aan globale iskemie onderwerp was, het ‘n onderdrukte oksidatiewe fosforilasieproses gehad, wat egter deur melatonienbehandeling verbeter is. Melatonien in vitro het insuliengestimuleerde glukoseopname deur kardiomiosiete van jong, maar nie vetsugtige rotte nie, verhoog. In vivo melatonientoediening vir 6 weke het egter basale (in die dieetgroep) en insuliengestimuleerde glukoseopname in beide kontrole- en vetsuggroepe verhoog. Toediening van melatonien in vitro aan mikrovaskulêre endoteelselkulture het ‘n beduidende afname in nekrose, apoptose, stikstofoksied- beskikbaarheid en eNOS aktivering teweeggebring, tesame met ‘n verhoogde aktivering van PKB/Akt, p38MAPK en AMPK. Die nadelige effekte van TNF- toediening op seintransduksie in die mikrovaskulêre endoteelselle is deur melatonien voorkom. Gevogtrekkings: Die resultate toon dat melatonien ‘n merkwaardige beskermende effek op die toename in vatbaarheid vir iskemiese beskadiging in vetsugtige rotte gehad het. Dit mag ook miokardiale glukose-homeostase en mitochondriale oksidatiewe funksie in insulienweerstandigheid verbeter. Melatonien in vitro beskerm mikrovaskulêre endoteelselle teen nekrose asook apoptose en verminder die beskikbaarheid van stikstofoksied. Hierdie voordelige effekte van melatonien mag aan sy anti-oksidantvermoëns of stimulasie van die melatonienreseptor toegeskryf word, maar bewyse daarvoor ontbreek nog.
Division of Medical Physiology (Stellenbosch University),
National Research Foundation
Harry Crossley Foundation
Silva, Lucas Raphael Bento e. "Análise da variabilidade e cinética da frequência cardíaca a partir do teste de esforço cardiopulmonar em mulheres com síndrome metabólica: estudo transversal." Universidade Federal de Goiás, 2017. http://repositorio.bc.ufg.br/tede/handle/tede/7139.
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Fundação de Amparo à Pesquisa do Estado de Goiás - FAPEG
Introduction: Metabolic Syndrome (MS) is a metabolic disorder that offers increased risk for cardiovascular diseases. The analysis of heart rate (HR) kinetics during exercise and its variability (HRV) is an important tool in assessing neurocardial integrity. A slow response of the HR at the end of the exercise corresponds to a low performance of the parasympathetic activity. Objective: To compare HR variability at rest and HR kinetics during exerciserecovery (phase-off), post exercise exercise in women with and without MS. Methodology: A cross-sectional study was carried out with 36 women (35-55 years of age), divided into two groups: SM group (GMS, n = 19) and non-SM group (GNMS, n = 17). The volunteers were submitted to the Bruce type limiting cardiopulmonary stress test, and for the evaluation of the HRV at rest, the R-R intervals were captured during 12 minutes in the seated position. The KomolgorovSmirnov test was used to verify the normality of the data and to evaluate the difference between two independent groups the t-Test was used for independent samples or Mann-Whitney test, multivariate analysis (MANOVA), multiple linear regression and Test Of Chi-square. The level of significance was set at 5%. Results: There was a statistically significant difference between the groups in the exponential component (p < 0.005) in the GNSM group and in the "τ" component (p = 0.032), being higher in the GSM group. There was no statistically significant difference in the parameter "FCpico." The GNSM group presented higher HR deltas compared to the SM group in the Δ60, Δ105 and Δ120 groups. GSM presented lower values in the parasympathetic modulation indices when compared to the SP group. GNSM, in contrast to a low correlation between glycemia and the highest values of the exponential component "τ", which showed a negative relation with the CC and BMI variables. Conclusion: The volunteers with MS presented autonomic dysfunction with compromised cardiac-parasympathetic modulation attributed to changes in the glycemic state. The exponential and linear analysis of FCoF can provide us with a sensitive and anticipated indicator of health impairments, proving to be useful to identify changes in cardiac autonomic control in the recovery of physical exercise.
Introdução: A Síndrome Metabólica (SM) é uma desordem metabólica que oferece risco aumentado para as doenças cardiovasculares. A análise da cinética da frequência cardíaca (FC) durante o exercício e de sua variabilidade (VFC) é uma ferramenta importante na avaliação da integridade neurocárdica. Uma resposta lentificada da FC ao término do exercício corresponde a uma baixa atuação da atividade parassimpática. Objetivo: Comparar a variabilidade da FC em repouso e cinética da FC durante a passagem exercício-recuperação (fase-off), pós-exercício em mulheres com e sem SM. Metodologia: Estudo transversal realizado com 36 mulheres (de 35 a 55 anos de idade), subdivididas em dois grupos: grupo Síndrome Metabólica (GSM, n = 19) e grupo não Síndrome Metabólica (GNSM, n = 17). As voluntárias foram submetidas ao teste de esforço cardiopulmonar sintoma limitante do tipo Bruce, e, para a avaliação da VFC em repouso, os intervalos R-R foram captados durante 12 minutos em posição “sentada”. Foram usados o Teste de Komolgorov-Smirnov (para verificar a normalidade dos dados); o Teste-T para amostras independentes ou Teste MannWhitney (para avaliar a diferença entre dois grupos independentes); a análise multivariada – MANOVA (para avaliar a diferença entre os grupos GNSM e GSM em relação aos diferentes tempos dos deltas da frequência cardíaca); a regressão linear múltipla (para avaliar a associação entre os fatores de risco cardiometabólicos, índices da VFC durante o repouso, componentes exponencias e consumo pico de oxigênio – VO2 pico); e o Teste de Qui-Quadrado (para avaliar o relacionamento das variáveis categóricas: presença ou não da SM e o nível de aptidão cardiorrespiratória). O nível de significância foi estabelecido em 5%. Resultados: Houve diferença estatisticamente significante na comparação entre os grupos referente ao componente exponencial “amp” (p < 0.005) no GNSM e ao componente “τ” (p = 0.032), sendo maior no GSM. Não houve diferença estatisticamente significante referente ao parâmetro “FCpico”. O GNSM apresentou maiores valores dos deltas da FC em comparação ao GSM nos Δ60, Δ105 e Δ120. O GSM apresentou menores valores referentes aos índices que representam a modulação parassimpática, quando comparado ao GNSM. O GSM apresentou Resumo xiii relação inversa da glicemia dos baixos níveis do índice SDNN, além de ter sido estabelecida relação direta entre a glicemia e os maiores valores do componente exponencial “τ”. O VO2 pico apresentou relação negativa com as variáveis CC e índice de massa corporal (IMC). Conclusão: As voluntárias com SM apresentaram disfunção autonômica com comprometimento da modulação parassimpática cardiovascular atribuído às alterações no estado glicêmico. A análise exponencial e linear da frequência cardíaca de recuperação (FCoff) pode nos fornecer um indicador sensível e antecipado de comprometimentos à saúde, demonstrando-se útil para identificar as alterações do controle autonômico cardíaco na recuperação do exercício físico.
Rocha, Vinícius Novaes. "Efeitos de diferentes doses de rosuvastatina no metabolismo lipídico e dos carboidratos, morfometria do tecido adiposo e remodelamento cardíaco de camundongos C57BL/6 alimentados com dieta hiperlipídica." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=7925.
Повний текст джерелаThere is a significant association between the prevalence of cardiovascular disease and metabolic syndrome. Evidence shows that obesity is associated with structural and functional changes in the heart. Statins can reduce the endogenous synthesis of cholesterol and are therefore used as an important tool against hypercholesterolemia in obese. The present work aims to study the effects of rosuvastatin in lipid and carbohydrate metabolism, adipose tissue morphometry and cardiac remodeling. In this work we studied the effects of rosuvastatin treatment on the body mass, insulin resistance, lipid profile, blood pressure, cardiac remodeling and structure and ultrastructural changes in the heart of the C57BL/6 male mice fed a high-fat diet. The rosuvastatin treatment reduced levels of blood lipids, improve insulin resistance, reduced blood pressure and body mass of high-fat mice. Furthermore, it attenuated cardiac remodelling, decreasing the interstitial and perivascular fibrosis, and maintained the integrity of mitochondrial morphology, with a lower production of UCP-2. Rosuvastatin had beneficial effects on cardiac changes induced by high-fat diet, as well as in mitochondrial morphology, thus controlled energy production to maintain cardiomyocyte integrity.
Jullian-Desayes, Ingrid. "Biomarqueurs du risque cardio-métabolique dans les pathologies respiratoires chroniques : impact de la prise en charge." Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV020/document.
Повний текст джерелаObstructive sleep apnea (OSA) is associated with related metabolic and cardiovascular comorbidities. Chronic intermittent hypoxia the hallmark of OSA induces deleterious intermediary mechanisms such as oxidative stress, systemic inflammation, insulin resistance and dyslipidemia. Cardiovascular and metabolic comorbidities are also key features of other chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD) and obesity hypoventilation syndrome (OHS). Chronic hypoxia and deleterious intermediary mechanisms also trigger occurrence and progression of non alcoholic fatty liver disease. This link between chronic respiratory diseases and liver injury is observed through modifications of specific liver biomarkers in OSA and COPD. A variety of cardiometabolic biomarkers have been studied for stratification of cardio-metabolic risk and assessing treatment impact in chronic respiratory diseases. The first part of this PhD thesis is a systematic review of cardio-metabolic biomarkers in 3 respiratory diseases: OSA, COPD and OHS.Continuous positive airway pressure (CPAP) the first line therapy for OSA improves symptoms and quality of life. However, CPAP effects on cardio-metabolic consequences remains still debated. In the second part of the PhD thesis, we will address CPAP impact on different cardiometabolic biomarkers and more specifically in markers of liver injury by reporting original results of a randomized controlled trial (RCT).Polypharmacy is usual in patients with OSA, COPD or OHS. Beyond CPAP or non invasive ventilation treatment, it is essential address the contribution of associated medications. Indeed, pharmacological treatments can interfere with the severity of the disease and control of associated comorbidities. The third part of the thesis will present a RCT evaluating Bosentan in hypertensive OSA patients and will present how medications for comorbidities decrease bicarbonate diagnosis value for OHS.We will conclude by underlining the crucial importance of personalized medicine and integrated care in chronic respiratory diseases
Konrad, Signorá Peres. "Alterações metabólicas e hemodinâmicas na obesidade visceral em ratos : repercussões na função autonômica." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2010. http://hdl.handle.net/10183/132802.
Повний текст джерелаCardiovascular disease that has been the leading causes of morbidity and mortality in the global world has the beginning of its pathophysiology in precocious age and, greater predisposition for its development in the validity of the clinical manifestations of the metabolic syndrome as to the glucose intolerance, insulin resistance, dyslipidemia, obesity and hypertension. This study was lead with the objective to evaluate the effect of the cafeteria diet in rats, on morphometric, metabolic and hemodynamic parameters associated with the alterations of autonomic control. Rats (n=32) were distributed in 2 groups, one under cafeteria diet and the other on standard food (24 weeks). At the end of the experimental period data were collected. The treated animals presented bigger abdominal adiposity, increased tryacilglicerides characterizing dyslipidemia and increased of the fasting glycemia. The rate of glucose decay was also reduced showing increased peripheral insulin resistance. It was also observed lower HDL-c levels while values of arterial pressure and heart rate did not change. However significant changes in autonomic control of circulation as reduction of heart rate variability as well as increased sympathovagal balance were also observed. These changes were positively correlated with tryacilglicerides levels indicating that cafeteria diet induced not only alterations of body weight but also of the adipose deposits characterizing visceral (WAT) and muscular fat (BAT). Finally the results suggest that autonomic changes may be the early marker of cardiovascular impairment associated with metabolic illness.
Батаев, Д. А., В. П. Лиходедова, Ю. И. Журавлев та П. К. Алферов. "Качество жизни и эмоциональный фон у пациентов с сердечно-сосудистыми заболеваниями на фоне метаболического синдрома". Thesis, Сумский государственный университет, 2016. http://essuir.sumdu.edu.ua/handle/123456789/47735.
Повний текст джерелаCosta, Fernando Oliveira. "Efeito agudo da galantamina em parâmetros hemodinâmicos e autonômicos em portadores da síndrome metabólica: estudo clínico prospectivo randomizado." Universidade Nove de Julho, 2014. http://bibliotecadigital.uninove.br/handle/tede/1152.
Повний текст джерелаMade available in DSpace on 2015-07-27T14:45:59Z (GMT). No. of bitstreams: 1 Fernando Oliveira Costa.pdf: 1199928 bytes, checksum: f721f323b7b101614061ea44e7dd6cb3 (MD5) Previous issue date: 2014-02-21
The metabolic syndrome (MetS) consists of a combination of conditions that tend to cluster together, and increase the risk of type 2 diabetes and cardiovascular disease. The components of the metabolic syndrome include central (abdominal) obesity, elevated fasting glucose, dyslipidemia (abnormally high triglycerides and low high-density lipoprotein cholesterol), and elevated blood pressure. MetS is also associated with proinflammatory and prothrombotic states, non-alcoholic liver steatosis, obstructive sleep apnea and reproduction disorders. Although a common unifying physiopathological mechanism is not known, central obesity and inflammation play a major role in MetS and upon each of its components. The MetS has reached epidemic proportions and to date there are no proven pharmacological interventions that simultaneously target all of the components of this syndrome. Inflammation plays an important role in the pathogenesis of the MetS. Recently, it was discovered that inflammation can be regulated by neural, cholinergic mechanisms and a cholinergic drug, the acetylcholinesterase inhibitor galantamine suppresses abnormal inflammation and alleviates MetS pathologies in rodents. The fact that galantamine is an approved drug, used to treat patients with Alzheimer´s disease with a known safety profile, will facilitate its clinical application in another situations. We hypothesize that treatment of subjects with the MetS with galantamine will result in alleviation in the MetS clinical conditions and inflammation. The objective of our study was to initiate an investigation on the safety profile of galantamine in MetS patients, with special attention on autonomic, hemodynamic and cognitive parameters. A randomized, double-blind, prospective study evaluated clinical, autonomic, hemodynamic and cognitive variables of patients with MetS in two moments: before treatment (basal state) and after 28 days of treatment with galantamine 8 mg daily. There was a statistical tendency in reducing systolic blood pressure in the HRV with Finometer® in patients under galantamine (124.4 ± 4 vs 119.7 ± 3.7 mmHg, basal and 28 days values, respectively) and also a reduction in diastolic blood pressure (72.5 ± 1.3 vs 67.2 ± 1.7 mmHg, basal and 28 days values, respectively). Paradoxically, an increase in the sympathetic modulation of the heart was observed with the HRV study measuring the LF (nu) value (46.2 ± 3.8 vs 57.1 ± 3.4 basal and 28 days, respectively) and a decrease in the parasympathetic modulation HF (nu) value (53.8 ± 3.8 vs 43.0 ± 3.4, basal and 28 days, respectively). We did not observe any significant change in cognitive domains. Our conclusion is that treatment with galantamine 8 mg exhibits a safe clinical profile and can be used in MetS patients.
A síndrome metabólica consiste na combinação de condições agrupadas e aumentam o risco para diabetes tipo 2 e doença cardiovascular. Seus componentes incluem obesidade central, níveis aumentados de glicose, dislipidemia caracterizada por aumento de triglicérides e baixos níveis de HDL e aumento da pressão arterial. Também está associada a um estado proinflamatório, a um estado protrombótico, a esteatose hepática não-alcoólica, apnéia obstrutiva do sono e a desordens reprodutivas. Apesar da não determinação de um mecanismo fisiopatológico unificador, obesidade central e inflamação parecem ser centrais na síndrome metabólica e nos seus componentes individuais. A síndrome metabólica tem alcançado proporções epidêmicas universais e até o presente não há intervenção farmacológica comprovada que atue simultaneamente em todos os seus componentes. Sabe-se hoje que o processo inflamatório tem um papel importante na patogenia da síndrome. Recentemente foi evidenciado que a inflamação pode ser regulada por mecanismos neurais colinérgicos, e que a galantamina, um inibidor da acetilcolinesterase, suprime a inflamação e atua nos componentes da síndrome diminuindo a patogenia em roedores. O fato de a galantamina ser uma droga já aprovada e de perfil seguro em portadores de demência facilita seu uso em outras situações clínicas. Considerando a hipótese de que a galantamina causará melhora da inflamação e dos outros distúrbios relacionados, o objetivo deste estudo foi iniciar a investigação sobre o perfil de segurança da galantamina em pacientes com síndrome metabólica, em especial, em parâmetros hemodinâmicos, autonômicos e de cognição. Realizamos um estudo prospectivo, duplo-cego e randomizado, que avaliou os dados clínicos e os parâmetros descritos, no momento basal e após 28 dias de uso de galantanima (8mg por dia), em portadores de síndrome metabólica. Houve uma tendência à redução da PAS, avaliada batimento-a-batimento com o Finometer no grupo que usou galantamina (124,4 ± 4 vs 119,7 ± 3,7 mmHg, respectivamente basal e após 28 dias de uso, p=0,04), o mesmo ocorrendo com a PAD (72,5 ± 1,3 vs 67,2 ± 1,7, p=0,005), respectivamente basal e após 28 dias de uso). De forma paradoxal, ocorreu um aumento da atividade simpática na modulação autonômica para o coração, avaliada por meio do estudo da variabilidade da freqüência cardíaca como atestado por um valor LF (nu) (46,2 ± 3,8 vs 57,1 ± 3,4 , p=0,0005)), e redução da modulação parassimpática, representada pelo valor do HF (nu) (53,8 ± 3,8 vs 43,0 ± 3,4, p=0,0005) respectivamente basal e após 28 dias de uso. Não observamos alterações significativas nos testes que avaliam o domínio cognitivo dos indivíduos. Concluímos que a dose utilizada de galantamina tem um perfil de segurança clínica que permite expandir seu uso em pacientes portadores de síndrome metabólica.
Roche, Johanna. "Le sommeil, ses troubles et la santé cardio-métabolique d'adolescents obèses : effets d'une prise en charge associant exercice physique et modification des habitudes alimentaires." Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCE010.
Повний текст джерелаSleep, through its restorative functions, is essential for life. However, lifestyle modifications, sedentary and unhealthy feeding behaviors trigger sleep curtailment and sleep disruption, leading together to weight gain. Obesity is usually associated with obstructive sleep apnea (OSA), and these two diseases both induce metabolic dysfunctions and low-grade systemic inflammation. To the best of our knowledge, no study has assessed the effects of exercise reconditioning and modified food habits on these parameters. The purpose of this work was to assess and compare, from an ancillary study, polysomnographic variables between obese adolescents and normal-weight (NW) controls. In the main study, the effects of a 9-month program (exercise reconditioning, adapted physical activities and modified food habits) on sleep architecture, sleep duration, OSA, biological factors (inflammatory, hormonal, carbohydrates and lipid profiles) and physiological adaptations at exercise were assessed, in order to a better understanding of the roles of cardiorespiratory fitness and sleep disorders on cardio-metabolic health. Thirty-two obese adolescents (age: 14.6 years, BMI z-score: 4.7) were recruited. Every parameters were assessed at admission and post-intervention. Short sleep duration and a high prevalence of OSA (58%) were observed at admission in obese adolescents despite a satisfying sleep architecture, compared with NW controls. Post-intervention, weight loss (11kg) and improved parameters of physiological adaptations at exercise (MAP, VE, VO2peak) were found in every subject and OSA was normalized in 46% of them. Sleep quantity and sleep quality were improved. Decreased C-reactive protein (6.78 vs 10.98 mg/l) and leptin concentrations, and increased adiponectin levels were found, and cardio-metabolic risk (CMR) was decreased. At admission, obesity explains by itself the systemic inflammation whereas the decrease in inflammation, post-intervention, is explained by enhanced cardiorespiratory fitness related to fat-free mass, after controlling for sex, weight loss, change in sleep duration and OSA. Prevention of OSA and metabolic dysfunctions by chronic exercise should be an integral part of the obesity management in youths in order to decrease the risk of cardiovascular morbi-mortality in adulthood
Fonseca, Felipe Xerez Cepêda. "Resposta hemodinâmica, metabólica e ventilatória durante esforço progressivo máximo em pacientes com síndrome metabólica e apneia obstrutiva do sono." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-04022015-145041/.
Повний текст джерелаIntroduction. Metabolic syndrome (MetS) decreases functional capacity (peakVO2). Obstructive sleep apnea (OSA), a comorbidity often found in patients with MetS, leads to an additional increase in the sympathetic nerve activity. We tested the hypotheses that: 1) The overlap of MetS and OSA impairs peakVO2 and hemodynamic, metabolic and ventilatory responses during maximal cardiopulmonary exercise testing (CPET); and 2) Sympathetic hyperactivation is involved in this impairment. Methods. We studied 60 newly diagnosed MetS outpatients (ATP III), sedentary, untreated, divided in 2 groups by the cut off the apnea-hypopnea index of (AHI) >= 15 events/h: MetS+OSA (49±1.7yr, n=30), and MetS-OSA (46±1.4yr, n=30). A healthy age-matched control group was also enrolled (C, 46±1.7yr, n=16). The AHI was evaluated by polysomnography and muscle sympathetic nerve activity (MSNA) by microneurography. The variables evaluated from CEPT were: peakVO2, HR reserve (peakHR-restHR), attenuation of HR recovery (deltaHRR=peakHR-HR at 1st, 2nd, 4th and 6th min), blood pressure response (BP), double product (SBPxHR), ventilation (VE), O2 pulse (VO2/HR), ventilatory equivalent ratio for oxygen (VE/VO2) and ventilatory equivalent ratio for carbon dioxide (VE/VCO2). Results. MetS+OSA and MetS-OSA were similar in physical characteristics and risk factors of MetS. Both groups with MetS had higher MSNA compared with C, and these levels were higher in the MetS+OSA compared to MetS-AOS. No differences among groups were found in the CPET on ventilatory and metabolic variables. However, both groups with MetS showed higher restHR, SBP and DBP (at rest, during exercise and at recovery) and lower peakVO2 and peak O2 pulse compared to C. Both MetS groups had lower HR reserve compared with C, with lower levels on MetS+OSA compared with MetS-OSA. MetS+OSA had lower deltaHRR at 1st (16±2, 18±1 and 24±2 bpm, interaction P=0.008), 2nd (26±2, 32±2 and 40±3 bpm, interaction P < 0.001), 4th (40±2, 50±2 and 61±3 bpm, interaction P < 0.001) and 6th min (48±3, 58±2 e 65±3 bpm, interaction P < 0.02), whereas MetS-OSA had lower deltaHRR at 2nd and 4th compared to C. In addition, MetS+OSA had lower deltaHRR at 4th and 6th min compared to MetS-AOS. Further analysis showed association between MSNA with restHR (R=-0,37; P < 0,001) and between MSNA and deltaHRR at 1st (R=-0.35; P=0.004), 2nd (R=-0.42; P < 0.001) 4th (R=-0,47; P < 0,001) and 6thmin (R=-0,35; P=0,006). Conclusion. The overlap of OSA decreases peakVO2 and potentiates the impairement over hemodynamic responses during exercise in patients with MetS, which may be explained, at least in part, by sympathetic hyperactivation. Therefore, OSA is a comorbidity that could worsen the prognosis in MetS patients
Lin, Yi-Lin, and 林依霖. "Effects of Natural Herbal Extracts on Cardiac disorders of Metabolic Syndrome Animal Models." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/35007224715357736447.
Повний текст джерела中國醫藥大學
基礎醫學研究所碩士班
101
Metabolic syndrome, also known as insulin resistance syndrome, a metabolic disorder involving multifaceted syndrome, their typical complications include obesity, diabetes. Our research was divided into two parts, involving two kind of typical complications diabetes and obesity, and different natural herbal extracts were given to investigate the effectiveness of our measure. Diabetes and cardiovascular diseases among the top ten causes of death ranked in the second and fifth respectively, and among the diabetes are more causes of death about 80% come from the concurrent cardiovascular diseases. Previous studies point out that diabetes easily cause inflammation, cardiac hypertrophy, myocardial apoptosis and cardiac fibrosis, leading to myocardial remodeling affecting cardiac function and finally cause heart failure. Anthocyanin is a strong antioxidants, and shows effectiveness of cardiovascular protection. Many studies indicate that Anthocyanin could balance blood sugar in whole body. Firstly our aim is to identify if Anthocyanin extracted from purple rice exerts protective effect in diabetes hearts. The five-week-old male Wistar rats were administered with streptozotocin to induce β cells damage, insulin secretion impaired as Type 1 diabetes. Animal were randomly divided into normal group, DM group (by intraperitoneal injection STZ 55 mg / kg), DM plus anthocyanin group (250 mg / kg / day, feeding four weeks). After treatment, the H & E stain, Masson''s trichrome stain, TUNEL, IHC stain and Western Blotting array were applied to observe the changes in heart tissues and protein expression. Secondly our aim is to identify whether Andrographi paniculata extracts could protect myocardial damage in high-fat diet induced obesity mice. Previous results pointed out that the main bioactive ingredient of Andrographi paniculata extract, andrographolide has anti-inflammatory and anti-apoptotic effects. Our research animals were divided into three group of normal, obesity (induced by high fat diet), obesity plus Andrographi paniculata extracts gavage (2 g / kg / day, feeding one week). Same experimental techniques were applied to observe whether Andrographi paniculata extracts could protect high-fat diet-induced obesity heart damage. In the first part of the diabetes, those followed increase of myocardial inflammatory signaling pathways, and further accompanied by cardiac hypertrophy, myocardial apoptosis, fibrosis and associated proteins were significantly expressed. Furthermore, significant reduction of heart function index EF (blood ejection fraction), and FS (systolic fraction) were of served, suggesting the results of myocardial tissue damage and loss of heart function. But these pathological, biochemical and functional indicators were improved significantly by given Anthocyanin. However, we also found myocardial inflammation signaling pathway were increased in the second part of the obese mice, and leads to cardiac hypertrophy, apoptosis. But given the short-term feeding Andrographi paniculata extracts also showed significant inhibition effect. Therefore, our study strongly suggest that Anthocyanin and Andrographi paniculata extracts supplement can be used for prevention and treatment of cardiovascular disease in metabolic syndrome patients.
Chinali, Marcello. "Cardiac Markers of Preclinical Disease in Adolescents with the Metabolic Syndrome: the Strong Heart Study." Tesi di dottorato, 2008. http://www.fedoa.unina.it/3246/1/tesi_di_dottorato_Marcello_Chinali.pdf.
Повний текст джерелаBehring, Jessica Belle. "Evaluating changes in reversible cysteine oxidation of cardiac proteins as metabolic syndrome develops into cardiovascular disease." Thesis, 2016. https://hdl.handle.net/2144/19057.
Повний текст джерелаRueda-Clausen, Christian Federico. "Long-term cardiovascular and metabolic effects of hypoxia-induced intrauterine growth restriction." Phd thesis, 2011. http://hdl.handle.net/10048/1768.
Повний текст джерелаKhan, Danish. "Role of SIRT6 in the Regulation of Glucose Metabolism and Fatty Acid Uptake in Heart." Thesis, 2020. https://etd.iisc.ac.in/handle/2005/5077.
Повний текст джерелаMateus, Tiago Duarte Cordeiro. "Study of the metabolome and muscle strength measures for the characterization of patients with myotonic dystrophy type 1." Master's thesis, 2021. http://hdl.handle.net/10773/30819.
Повний текст джерелаA distrofia miotônica tipo 1 (DM1) é uma doença hereditária autossómica dominante causada por uma alteração que leva a uma expansão anormal de repetições instáveis de CTG na região 3' não traduzida do gene da proteína quinase da distrofia miotônica (DMPK). DM1 é caracterizado por miotonia, fraqueza muscular distal progressiva e por envolvimento multissistémica, nomeadamente cataratas, dores musculares, disfunções cardíacas e respiratórias, disfunções endócrinas (resistência à insulina, síndrome metabólica, dislipidemia), cancro e alterações no sistema nervoso central (SNC). Doentes com DM1 apresentam frequência de síndrome metabólica maior do que na população geral. Assim, o estudo do metaboloma é de grande importância, pois pode fornecer novos ideias sobre as vias moleculares afetadas nas doenças DM1, bem como discriminar entre os diferentes graus de gravidade em doentes com DM1 e também pode levar ao desenvolvimento de novas terapêuticas metabólicas. Dadas as alterações metabólicas previamente descritas e observadas em doentes com DM1, consideramos que a avaliação do perfil metabólico destes doentes é de grande importância. Portanto, elaborou-se uma revisão da literatura para resumir as alterações metabólicas previamente descritas em doentes com DM1 e a relação da Lipina com as alterações metabólicas na DM1 (Capítulo I). Essencialmente, os estudos anteriores mostraram uma clara alteração metabólica entre os doentes com DM1 e os grupos controlo, nomeadamente o aumento dos níveis de colesterol total, lipoproteína de baixa densidade, triacilglicerol, insulina e resistência HOMA-insulina, o aumento dos níveis de glicose, assim como a diminuição dos níveis de lipoproteína de alta densidade. Esta revisão também demonstrou uma potencial relação entre a Lipina e a sua associação com as anormalidades metabólicas encontradas em doentes com DM1, nomeadamente os papéis metabólicos no tecido adiposo, músculo esquelético, fígado e a sua associação com a dislipidemia e a resistência à insulina, que é uma das características em doentes com DM1. O perfil metabólico dos doentes com DM1 foi então avaliado pela técnica de espectroscopia ATR FTIR, em conjunto com a análise multivariada, sendo que é adequada para fornecer um perfil (bio) químico dos doentes com DM1 e controlos. Essencialmente, fibroblastos derivados de DM1 e controlos foram utilizados, e os resultados demonstraram uma clara discriminação dentro de fibroblastos derivados de DM1 com diferentes repetições de CTG e idades de início da doença, o que significa que estes podem ter um perfil metabólico distinto. Esta discriminação pode ser atribuída principalmente ao metabolismo lipídico alterado na região 1800-1500 cm-1 . Também foi possível discriminar entre os grupos controlo e fibroblastos derivados de DM1 do Instituto Coriell e Centro Hospitalar do Tâmega e Sousa na região de 3000-2800 cm-1 (Capítulo II). Além disso, foi feita uma revisão sistemática para reunir informações de todos os resultados e medidas utilizadas para avaliar a força muscular em doentes adultos com DM1 (Capítulo IV). Foi avaliada a força muscular cardíaca, esquelética e respiratória. Resumidamente, a revisão sistemática demonstrou uma utilização consistente da ecocardiografia, teste muscular quantitativo, teste muscular manual e manometria para avaliar a força muscular cardíaca, esquelética e respiratória. As medidas escolhidas para avaliar a força muscular foram: (1) fração de ejeção para a força do musculo cardíaco; (2) torque isométrico muscular, força de preensão e conselho de pesquisa médica (0-5 pontos e 0-60 pontos) para a força do músculo esquelético; (3) pressão inspiratória máxima e pressão expiratória máxima para a força dos músculos respiratórios. Em conclusão, os resultados sugerem que há uma necessidade de estudos adicionais relativamente ao metabolismo lipídico em doentes com DM1, não apenas para caracterizar melhor estes doentes, como também para compreender o mecanismo subjacente das anormalidades lipídicas e ter novas noções sobre a Lipina na DM1. A espectroscopia FTIR é uma ferramenta valiosa para caracterizar doentes com diferentes severidades da DM1, o que é crucial para um diagnóstico adequado e para estudos futuros. Reunimos com sucesso as medidas mais consensuais e importantes para avaliar a força muscular. Os resultados obtidos foram importantes e úteis, pois serão valiosos para avaliação da força muscular em futuros ensaios clínicos e estudos observacionais, principalm
Mestrado em Biologia Molecular e Celular
ROCHE, Johanna. "Le sommeil, ses troubles et la santé cardio-métabolique d'adolescents obèses : effets d'une prise en charge associant exercice physique et modification des habitudes alimentaires." Thesis, 2018. http://www.theses.fr/2018UBFCE010.
Повний текст джерелаSleep, through its restorative functions, is essential for life. However, lifestyle modifications, sedentary and unhealthy feeding behaviors trigger sleep curtailment and sleep disruption, leading together to weight gain. Obesity is usually associated with obstructive sleep apnea (OSA), and these two diseases both induce metabolic dysfunctions and low-grade systemic inflammation. To the best of our knowledge, no study has assessed the effects of exercise reconditioning and modified food habits on these parameters. The purpose of this work was to assess and compare, from an ancillary study, polysomnographic variables between obese adolescents and normal-weight (NW) controls. In the main study, the effects of a 9-month program (exercise reconditioning, adapted physical activities and modified food habits) on sleep architecture, sleep duration, OSA, biological factors (inflammatory, hormonal, carbohydrates and lipid profiles) and physiological adaptations at exercise were assessed, in order to a better understanding of the roles of cardiorespiratory fitness and sleep disorders on cardio-metabolic health. Thirty-two obese adolescents (age: 14.6 years, BMI z-score: 4.7) were recruited. Every parameters were assessed at admission and post-intervention. Short sleep duration and a high prevalence of OSA (58%) were observed at admission in obese adolescents despite a satisfying sleep architecture, compared with NW controls. Post-intervention, weight loss (11kg) and improved parameters of physiological adaptations at exercise (MAP, VE, VO2peak) were found in every subject and OSA was normalized in 46% of them. Sleep quantity and sleep quality were improved. Decreased C-reactive protein (6.78 vs 10.98 mg/l) and leptin concentrations, and increased adiponectin levels were found, and cardio-metabolic risk (CMR) was decreased. At admission, obesity explains by itself the systemic inflammation whereas the decrease in inflammation, post-intervention, is explained by enhanced cardiorespiratory fitness related to fat-free mass, after controlling for sex, weight loss, change in sleep duration and OSA. Prevention of OSA and metabolic dysfunctions by chronic exercise should be an integral part of the obesity management in youths in order to decrease the risk of cardiovascular morbi-mortality in adulthood