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Die Rolle von Apelin bei Adipositas und gestörter GlukosetoleranzKrist, Joanna 12 November 2014 (has links) (PDF)
Apelin ist ein Adipokin, das Einfluß auf die Glukosehomöostase hat und vermutlich eine wichtige Rolle in der Regulation von Adipositas und den damit assoziierten Erkrankungen einnimmt. Die Effekte von Apelin scheinen metabolisch günstig zu sein.
In dieser Arbeit wurden zunächst Apelin-Serumkonzentrationen und metabolische Parameter bei 740 Studienteilnehmern bestimmt und in einer Querschnittsstudie (n=629) sowie in drei Interventionsstudien (n=111) dargestellt. In einer Subgruppe (n=161) wurde die mRNA-Expression von Apelin und dessen Rezeptor APJ im viszeralen und subkutanen Fettgewebe bei Patienten mit Typ-2-Diabetes genauer untersucht. Im Rahmen der Interventionsstuden wurde der Einfluß von 12 Wochen körperlichem Training (n=60), 6 Monaten hypokalorischer Mischkost (n=19) und bariatrischer Chirurgie (n=32) auf den Serum-Apelinspiegel sowie Zusammenhänge mit Gewichtsreduktion, verbesserter Insulinsensitivität und subklinischer Inflammation analysiert.
Die höchsten Apelin-Serumkonzentrationen fanden sich beim adipösen Typ-2-Diabetiker. Die Apelin-Serumkonzentration korrelierte aber auch unabhängig vom Bodymassindex signifikant mit Parametern für Insulinresistenz und subklinischer Inflammation. Die Apelin-Expression war in den unterschiedlichen Fettgewebsdepots bei normal glukosetoleranten Patienten gleich, beim Typ-2-Diabetiker mit insgesamt höherer Expression überwog sie im viszeralen Fettgewebe. Nach allen Interventionsstudien kam es zur Abnahme der Apelin-Serumkonzentration und korrelierte auch dann signifikant mit einer verbesserten Insulinsensitivität, wenn es zu keiner Gewichtsreduktion kam.
Die Apelinkonzentration im Serum sowie die Expression im Fettgewebe ist nicht nur vom Bodymassindex abhängig, sondern steht im direkten Zusammenhang mit Insulinsensitivität und inflammatorischen Prozessen. Die unterschiedliche fettdepotspezifische Regulation unterstreicht die pathogenetische Bedeutung eines „kranken“ viszeralen Fettgewebes in der Entwicklung von Typ-2-Diabetes, wobei Apelin als metabolisch günstiges Adipokin vermutlich eine kompensatorische Rolle einnimmt.
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Auswirkungen eines zwölfmonatigen kontrollierten Trainingsprogramms auf die Leptin-, Adiponectin- und Progranulin-Serumkonzentrationen sowie Parameter des Lipidstoffwechsels bei Patienten mit Typ 2 DiabetesSchaarschmidt, Wiebke 21 November 2011 (has links) (PDF)
Die Prävalenz des Typ 2 Diabetes ist in den letzten Jahren deutlich angestiegen. Neben einer gesunden Ernährungsweise ist die Erhöhung der körperlichen Aktivität ein wichtiger Bestandteil in der Basistherapie des Typ 2 Diabetes. Körperliches Training führt zu einer Reihe metabolischer Veränderungen wie zur Reduktion der Fettmasse, zur Verbesserung der Glukosehomöostase, des Lipidprofils und zur Normalisierung zirkulierender Adipokine aus dem Fettgewebe.
Ziel dieser Arbeit war es, die Auswirkungen eines zwölfmonatigen, kontrollierten, praxisnahen, kombinierten Kraft-Ausdauer-Trainingsprogramms auf das Körpergewicht, Parameter des Lipidstoffwechsels (Gesamt-, LDL-, HDL-Cholesterin- und Triglyzerid-Serumkonzentrationen) sowie die Serumkonzentrationen der Adipokine Leptin, Adiponectin und Progranulin bei Patienten mit Typ 2 Diabetes zu untersuchen.
Für die prospektive offene Interventionsstudie wurden initial 710 Patienten mit Typ 2 Diabetes untersucht, von denen 156 die Ein- und Ausschlusskriterien für die Studie erfüllten. Es wurden die Daten von 120 Patienten (77 Frauen, 43 Männer) analysiert, von denen nach Abschluss des zwölfmonatigen Trainingsprogramms vollständige Datensätze vorlagen. Die Patienten trainierten zweimal pro Woche für jeweils 60 + 15 Minuten bei 50-70% ihrer individuellen maximalen Leistungsfähigkeit, die zu Beginn der Studie mittels Spiroergometrie ermittelt wurde. Das Training umfasste jeweils 20 Minuten Aufwärm- und Abkühlphase, 20 Minuten Fahrradergometer-Training, 20 Minuten Training am Rudergerät und 20 Minuten Krafttraining an Krafttrainingsgeräten. Die Messung der Zielparameter erfolgte vor Beginn der Intervention sowie nach drei, sechs und zwölf Monaten körperlichen Trainings.
Das zwölfmonatige Trainingsprogramm führte zu einer signifikanten Reduktion der Gesamt- und LDL-Cholesterin-, Triglyzerid- sowie der Progranulin-Serumkonzentrationen, während sich die zirkulierenden Leptinspiegel nicht veränderten. Die HDL-Cholesterin und Adiponectin-Serumkonzentrationen waren in Folge des Trainingsprogramms signifikant erhöht. Diese Veränderungen waren weitgehend unabhängig von der Entwicklung des Körpergewichts, das sich im Verlauf der Studie nicht signifikant veränderte.
Zusammengefasst zeigt die Untersuchung, dass ein zwölfmonatiges, moderates und praxistaugliches Trainingsprogramm signifikant und unabhängig von Verbesserungen des Körpergewichts die Serumkonzentrationen der Adipokine Adiponectin und Progranulin sowie von Parametern des Lipidstoffwechsels verbessert.
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Ενδομήτρια καθυστέρηση ανάπτυξης (IURG) : παθογενετικοί μηχανισμοίΓερονάτσιου, Αικατερίνη 19 January 2011 (has links)
Η ενδομήτρια καθυστέρηση ανάπτυξης ορίζεται ως παθολογική μείωση του ρυθμού εμβρυικής ανάπτυξης που καταλήγει σε ένα έμβρυο το οποίο δεν έχει την αναμενόμενη ανάπτυξη σύμφωνα με την ηλικία κύησης και το οποίο διατρέχει κίνδυνο αυξημένης περιγεννητικής νοσηρότητας και θνησιμότητας.
Ενδομήτρια καθυστέρηση ανάπτυξης είναι η ανικανότητα του εμβρύου να διατηρήσει τον αναμενόμενο ρυθμό ανάπτυξης ανεξάρτητα αν το βάρος του είναι κάτω από τη 10η εκατοστιαία θέση. Όταν η ανάπτυξη του εμβρύου είναι κάτω από την 5η εκατοστιαία θέση τότε ίσως να μπορεί να θεωρηθεί πραγματική ενδομήτρια καθυστέρηση ανάπτυξης.
Σύμφωνα με το αμερικανικό κολέγιο γυναικολόγων και μαιευτήρων American College of Obstetricians and Gynecologists (ACOG) η ενδομήτρια καθυστέρηση ανάπτυξης ορίζεται ως το έμβρυο που αποτυγχάνει να έχει τον αναμενόμενο ρυθμό ανάπτυξης.
Πολλές φορές οι όροι ενδομήτρια καθυστέρηση ανάπτυξης (IUGR) και μικρό για την ηλικία κύησης (SGA) συγχέονται και για αυτό το λόγο διευκρινίζεται ότι ο όρος μικρό για την ηλικία κύησης (SGA) αναφέρεται σε έμβρυο του οποίου το εκτιμώμενο βάρος είναι κάτω από τη 10η εκατοστιαία θέση. Από το σύνολο των μικρών για την ηλικία κύησης (SGA) εμβρύων το 40% είναι υγιή, 20% είναι μικρά εξαιτίας χρωμοσωμικών και περιβαλλοντικών παραγόντων και 40% διατρέχουν ιδιαίτερα αυξημένο κίνδυνο ενδομήτριου θανάτου και σχετίζονται με ενδομήτρια καθυστέρηση ανάπτυξης.
Η ενδομήτρια καθυστέρηση ανάπτυξης είναι μια πολυσυστηματική διαταραχή και διακρίνεται σε:
Α) Συμμετρική. Όταν η ανάπτυξη της κεφαλής και της κοιλιάς επιβραδύνονται συμμετρικά. Είναι λιγότερο συχνή, 20%-30%.
Β) Ασύμμετρη. Δυσανάλογη ελάττωση του μεγέθους της κοιλιάς σε σχέση με αυτό της κεφαλής. Είναι περισσότερο συχνή, 70%-80%, και οφείλεται συνήθως σε μητροπλακουντιακή ανεπάρκεια και συμβαίνει μετά την 28η εβδομάδα. Στη φάση αυτή γίνεται η μεγαλύτερη εναπόθεση λίπους.
Η ενδομήτρια καθυστέρηση ανάπτυξης αποτελεί κύριο πρόβλημα στην περιγεννητική ιατρική, είναι η ΔΕΥΤΕΡΗ αιτία θανάτου μετά την προωρότητα. 52% των ανεξήγητων ξαφνικών θανάτων των εμβρύων συσχετίζονται με ανάπτυξη IUGR. 10% των περιπτώσεων περιγεννητικής θνησιμότητας στην Ευρώπη είναι αποτέλεσμα μη διαγνωσμένης IUGR. Η επίπτωση της ενδομήτριας καθυστέρησης ανάπτυξης είναι 8% στον γενικό πληθυσμό. / Intrauterine growth restriction (IUGR) is the failure of the fetus to achieve his/her intrinsic growth potential and is associated with significantly increased perinatal morbidity and mortality.
IUGR affects 10% of pregnancies and perinatal mortality rates are 4-8 times higher for infants with this disorder.
Intrauterine growth restriction is not a specific disease entity with a unique pathophysiology, but the result of suboptimal intrauterine growth conditions in conjunction with a variety of disorders from genetic to metabolic, vascular, coagulative, autoimmune, as well as infectious.
Newborns with intrauterine growth restriction (IUGR) present reduced fat mass and undergo adaptational changes of endocrine/metabolic mechanisms as a result of intrauterine malnutrition. Recently, it was shown that fat-secreted adipokines such as visfatin, a novel adipokine improving glucose tolerance through insulin-mimetic effects, and vaspin , profoundly influence insulin sensitivity and energy metabolism.
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Role of Adipose-to-Muscle Communication in PCB126-induced Metabolic DefectsCaron, Audrey 20 June 2018 (has links)
Despite the importance of muscle in the development of type 2 diabetes, few studies have investigated the effect of polychlorinated biphenyls (PCBs) on muscle energy metabolism. Previous results from our lab suggested that PCB126 exposure induced an indirect negative effect on muscle mitochondrial function. Since PCBs are stored in adipose tissue, we hypothesized that PCB126 alters adipokine secretion which in turn affects muscle metabolism. Objectives. Study the adipose-to-muscle communication in PCB126-induced metabolic defects. Methods. Communication between adipocytes and myotubes was reproduced by exposing C2C12 or mouse primary myotubes to the conditioned medium (CM) of 3T3L1 adipocytes exposed to environmentally relevant PCB126 levels. Results. PCB126 significantly increased adipokine secretion and decreased mitochondrial function, glucose uptake and glycolysis in insulin resistant (IR) but not in insulin sensitive 3T3L1. However, exposure of myotubes to CM of IR 3T3L1 only decreased glucose uptake and insulin sensitivity, without altering myotubes glycolysis or mitochondrial function. Conclusion. Our results suggest that the increased adipokine secretion by adipocytes could explain the decreased muscle glucose uptake and insulin sensitivity when exposed to PCB126.
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Níveis séricos de adipocinas e ácidos graxos em pacientes comperiodontite crônica generalizada / Serum levels of adipokines and fatty acids in patients with chronic periodontitisManuela Rubim Camara Sete 03 December 2013 (has links)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / O tecido adiposo é um grande reservatório de mediadores biologicamente ativos, tais como as adipocinas.As principaissãoa leptina, a resistina e a adiponectina,que estão presentes em processos inflamatórios e podem estar diretamente ligadas à doença periodontal. Os ácidos graxos teriam um papel regulador sobre essas adipocinas. O objetivo do trabalho foicomparar as concentrações de leptina, resistina e adiponectina e de ácido docosahexaenoico (DHA), ácido docosapentaenoico(DPA), ácido eicosapentaenoico(EPA) e ácido araquidônico (AA),no sangue dos pacientes com periodontite crônica generalizada e com gengivite. Como objetivo secundário, avaliar a razão entreessas substâncias no soro desses pacientes.Participaram do estudo 15 pacientes sistemicamente saudáveis com periodontite crônica generalizada (grupo teste, idade média: 45.7 9.4 anos) e 15 com gengivite (grupo controle, idade média 32.1 7.8 anos). Foram registrados os parâmetros médicos e periodontais e amostras sanguíneas foram coletadas. As concentraçõesno soro de ácidos graxos foram analisadas por cromatografia gasosa e as adipocinas foram analisadas pelo método multiensaio multiplex. Ascomparações entre as variáveis foram analisadas pelo teste Mann-Whitneye as correlações pelo teste de Spearman. Não houve diferença significante entre os níveis de adipocinas entre os grupos. Quanto aos níveis de DHA, DPA, EPA e AA, houve diferença significativamente maior para o grupo de pacientes com periodontite comparado ao grupo com gengivite.As razões entre res/DHA, res/AA, adipon/DHA, adipon/AA e adipon/DPA foram significantemente menores para o grupo periodontite. Não houve correlação entre as adipocinas e os parâmetros clínicos analisados e entre os níveis de adipocinas e ácidos graxos. Concluímos que aperiodontite crônica generalizada apresenta diferenças significativamente maiores nos níveis dos ácidos graxos quando comparada à gengivite.As adipocinas, resistina e adiponectina,apresentaram uma tendência a valores menores no grupo periodontite. Os resultados das razões sugerem uma menor proporção de resistina e adiponectina em relação aos ácidos graxos na periodontite. / Adipose tissue is a large reservoir of biologically active mediators, such as adipokines. The main ones are leptin, resistin and adiponectin, which are present in inflammatory processes and can be directly linked to periodontal disease. Fatty acids might have a regulatory role on these adipokines. The aim of this study was to compare the concentrations of leptin, resistin and adiponectin and docosahexaenoic acid(DHA), docosapentaenoic acid (DPA), eicosapentaenoic acid(EPA) and arachidonic acid (AA), in the blood of patients with generalized chronic periodontitis and gingivitis. Secondary objective was to evaluate the ratio of these substances in the serum of these patients. Participants were 15 systemically healthy patients with chronic periodontitis (test group, mean age: 45.7 9.4 years) and 15 with gingivitis (control group, mean age 32.1 7.8 years). We recorded medical and periodontal parameters and collected blood samples. Serum concentrations of fatty acids were analyzed by gas chromatography and adipokines were analyzed by multiplex bead immunoassay. Comparisons between variables were analyzed by Mann - Whitney test and correlations using the Spearman test. There was no significant difference between the levels of adipokines between groups. Considering the levels of DHA, DPA, EPA and AA, there was difference significantly higher for the group of patients with periodontitis compared to the group with gingivitis. The ratios res/DHA, res/AA, adipon/DHA, adipon/AA and adipon/DPA were significantly lower for the group periodontitis. There was no correlation between adipokines and clinical parameters analyzed and between levels of adipokines and fatty acids. We conclude that generalized chronic periodontitis differs significantly higher levels of fatty acids when compared to gingivitis. Adipokines, resistin and adiponectin, showed a tendency to lower values in periodontitis. Reasonss results suggest a smaller proportion of adiponectin and resistin in relation to the fatty acids in periodontitis.
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Perda de peso, indicadores do metabolismo de carboidratos e produção de citocinas em cãesBrunetto, Márcio Antonio [UNESP] 26 February 2010 (has links) (PDF)
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brunetto_ma_dr_jabo.pdf: 3892215 bytes, checksum: 28d3da2d4850b5fc4716adca9b80b1a3 (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / O aumento dos depósitos corporais de gordura está relacionado com profundas alterações de algumas funções fisiológicas que podem resultar em redução da tolerância à glicose e resistência insulínica. O presente estudo objetivou avaliar os efeitos da perda de peso sobre parâmetros bioquímicos, metabólicos, hormonais e de composição corporal em cães naturalmente obesos, em fase estática a pelo menos 12 meses e após a perda de 20% de peso corporal em comparação com um grupo de cães em condição corporal ideal. O grupo 1 (G1) foi composto por 10 cães obesos com escore de condição corporal igual ou superior a 9 e com porcentagem de gordura corporal média igual a 45,72 ± 1,51%. O grupo 2 (G2) foi composto pelos cães do G1 após a perda de 20% do peso inicial, que passou a apresentar 33,53 ± 1,92% de massa gorda (p<0,001). No grupo 3 (G3), foram incluídos 10 cães da raça beagle, com escore de condição corporal entre 4 e 5, com porcentagem de gordura corporal média igual a 18,36 ± 1,38% (p<0,01). A tolerância à glicose e a sensibilidade insulínica foram avaliados através do teste intravenoso de tolerância à glicose (TIVTG) e pelo teste pós-prandial de glicose e insulina (TPPGI) nos três grupos experimentais. A interação entre tempo e tratamento (grupo experimental) foi significativa para a glicemia (p<0,05), sendo diferentes os grupos G1 x G3 e G2 apresentou valores de glicemia intermediários nos dois testes. No TIVTG, o pico da glicemia nos três grupos experimentais foi observado logo no primeiro minuto após a infusão da glicose. Nos tempos 1,0; 2,5 e 5,0 minutos os valores de glicemia foram estatisticamente menores para G3 em relação à G1. No TPPGI os G1 e G2 apresentaram secreção tardia de insulina, evidenciado por maior área abaixo da curva da insulina no intervalo de 60-360 minutos. Os animais obesos (G1) apresentaram maiores concentrações... / The increase of fat corporal deposits is related with deep alterations of some physiologic functions, which can result in reduction of glucose tolerance and insulin resistance. The present study intended to evaluate the effects of weight loss over different biochemical, metabolic, hormonal and corporal composition parameters in dogs naturally obese, in static phase for at least 12 months, and to compare them after loss of 20% of corporal weight with a group of dogs in ideal corporal condition. The group 1 (G1) was composed by 10 obese dogs with body condition score equal or superior to 9 and with mean corporal fat percentage equal to 45.72 ± 1.51%. Group 2 (G2) was composed by the dogs of G1 after loss of 20% of initial weight, presenting at this moment 33.53 ± 1.92% of corporal fat (p<0.001). In group 3 (G3), 10 beagle dogs were included, with body condition score between 4 and 5, mean percentage of corporal fat equal to 18.36 ± 1.38% (p<0.01). Glucose tolerance and insulin sensibility were measured in the three groups through intravenous glucose tolerance test (TIVTG) and glucose and insulin postprandial test (TPPGI). The interaction between time and treatment (experimental group) was significant for the glycemia (p <0.05), being different the groups G1 x G3 and G2 presented intermediate glycemia values in both tests. In TIVTG, the glycemic peak in the three experimental groups was observed in the first minute after the infusion of glucose. In moments 1.0; 2.5 and 5.0 minutes glycemia values were statistically lower to G3 in comparison to G1. In TPPGI the G1 and G2 groups presented later secretion of insulin, demonstrated for bigger insulin under the curve area from times 60-360 minutes. Obese animals (G1) presented higher serum concentrations of circulating adipokines, leptin, TNF- α and IL-6 than G3 and these values were significantly reduced after weight loss
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Rekrutierung von Immunzellen in das perivaskuläre Fettgewebe bei Adipositas – Bedeutung von Leptin / Recruitment of immune cells into perivascular adipose tissue in obesity - Effect of leptinHerzberg, Sebastian 14 June 2018 (has links)
No description available.
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Investigação da expressão de genes do metabolismo lipídico em pacientes com Diabetes Mellitus tipo 2, Dislipidemia e Doença Periodontal Crônica /Silva, Romerito Lins da. January 2016 (has links)
Orientador: Raquel Mantuaneli Scarel Caminaga / Banca: Bruno César de Vasconcelos Gurgel / Banca: Joni Aususto Cirelli / Resumo: O Diabetes Mellitus tipo 2 (DM2) e a Dislipidemia são doenças metabólicas que podem induzir a progressão de doenças coexistentes com patogênese inflamatória semelhante, como a doença periodontal (DP). Adipocinas são proteínas produzidas pelo tecido adiposo que possuem atividade metabólica, podendo influenciar o estado hiperinflamatório do hospedeiro. O objetivo deste estudo foi investigar a influência do DM2 (metabolicamente compensado ou descompensado), Dislipidemia e DP crônica, na expressão de genes relacionados à adipocinas em células mononucleares do sangue periférico (PBMC) e buscar correlacionar a expressão desses genes com o perfil clínico periodontal, glicêmico e lipídico. Investigaram-se cinco grupos de pacientes (30 indivíduos cada): G1 (diabetes descompensado, dislipidemia e doença periodontal), G2 (diabetes compensado, dislipidemia e doença periodontal), G3 (dislipidemia e doença periodontal), G4 (apenas doença periodontal) e G5(sistemicamente e periodontalmente saudável). Os pacientes foram submetidos a exame periodontal completo e avaliação bioquímica dos perfis glicêmico e lipídico. Foi extraído RNA do sangue de cada paciente para investigação da expressão dos genes Adiponectina (ADIPOQ), Receptor 1 da Adiponectina (ADIPOR1), Leptina (LEP) e Resistina (RETN) por meio da Transcriptase Reversa seguida de Reação em Cadeia da Polimerase quantitativa em tempo real (RT-qPCR). Para a expressão gênica realizou-se o teste de Kruskal-Wallis, seguido pelo pós-teste de Du... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Type 2 Diabetes Mellitus (T2D) and dyslipidemia are metabolic diseases that can induce the progression of coexisting inflammatory injury and they have similar pathogenesis to chronic periodontitis (CP). Adipokines are proteins produced by fat tissue that have metabolic activity and can influence the host hyper-inflammatory state. The aim of this study was to investigate in poorly or well-controlled T2D and normoglycemic individuals, both conditions associated with dyslipidemia and CP, the systemic expression of adipokines genes and its correlation with glycemic, lipid and periodontal profiles. One hundred fifty patients were separated into groups (G) of 30 subjects each: (G1) poorly controlled T2D with dyslipidemia and CP; (G2) wellcontrolled T2D with dyslipidemia and CP; (G3) normoglycemic individuals with dyslipidemia and CP; (G4) individuals with CP; (G5) systemic and periodontal healthy individuals (control). All patients underwent physical and periodontal examination and biochemical evaluation of glycemic and lipid profiles. Total RNA was extracted from peripheral blood mononuclear cells (PBMC) of patients for gene expression investigation of: Adiponectin (ADIPOQ), Adiponectin Receptor 1 (ADIPOR1), Leptin (LEP) and Resistin (RETN) by Reverse Transcriptase followed by real-time quantitative Polymerase Chain Reaction (RT-qPCR). Gene expression was evaluated by Kruskal- Wallis test followed by Dunn's post-test. Correlations among clinical, biochemical and gene expressions w... (Complete abstract click electronic access below) / Mestre
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Níveis séricos de adipocinas e ácidos graxos em pacientes comperiodontite crônica generalizada / Serum levels of adipokines and fatty acids in patients with chronic periodontitisManuela Rubim Camara Sete 03 December 2013 (has links)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / O tecido adiposo é um grande reservatório de mediadores biologicamente ativos, tais como as adipocinas.As principaissãoa leptina, a resistina e a adiponectina,que estão presentes em processos inflamatórios e podem estar diretamente ligadas à doença periodontal. Os ácidos graxos teriam um papel regulador sobre essas adipocinas. O objetivo do trabalho foicomparar as concentrações de leptina, resistina e adiponectina e de ácido docosahexaenoico (DHA), ácido docosapentaenoico(DPA), ácido eicosapentaenoico(EPA) e ácido araquidônico (AA),no sangue dos pacientes com periodontite crônica generalizada e com gengivite. Como objetivo secundário, avaliar a razão entreessas substâncias no soro desses pacientes.Participaram do estudo 15 pacientes sistemicamente saudáveis com periodontite crônica generalizada (grupo teste, idade média: 45.7 9.4 anos) e 15 com gengivite (grupo controle, idade média 32.1 7.8 anos). Foram registrados os parâmetros médicos e periodontais e amostras sanguíneas foram coletadas. As concentraçõesno soro de ácidos graxos foram analisadas por cromatografia gasosa e as adipocinas foram analisadas pelo método multiensaio multiplex. Ascomparações entre as variáveis foram analisadas pelo teste Mann-Whitneye as correlações pelo teste de Spearman. Não houve diferença significante entre os níveis de adipocinas entre os grupos. Quanto aos níveis de DHA, DPA, EPA e AA, houve diferença significativamente maior para o grupo de pacientes com periodontite comparado ao grupo com gengivite.As razões entre res/DHA, res/AA, adipon/DHA, adipon/AA e adipon/DPA foram significantemente menores para o grupo periodontite. Não houve correlação entre as adipocinas e os parâmetros clínicos analisados e entre os níveis de adipocinas e ácidos graxos. Concluímos que aperiodontite crônica generalizada apresenta diferenças significativamente maiores nos níveis dos ácidos graxos quando comparada à gengivite.As adipocinas, resistina e adiponectina,apresentaram uma tendência a valores menores no grupo periodontite. Os resultados das razões sugerem uma menor proporção de resistina e adiponectina em relação aos ácidos graxos na periodontite. / Adipose tissue is a large reservoir of biologically active mediators, such as adipokines. The main ones are leptin, resistin and adiponectin, which are present in inflammatory processes and can be directly linked to periodontal disease. Fatty acids might have a regulatory role on these adipokines. The aim of this study was to compare the concentrations of leptin, resistin and adiponectin and docosahexaenoic acid(DHA), docosapentaenoic acid (DPA), eicosapentaenoic acid(EPA) and arachidonic acid (AA), in the blood of patients with generalized chronic periodontitis and gingivitis. Secondary objective was to evaluate the ratio of these substances in the serum of these patients. Participants were 15 systemically healthy patients with chronic periodontitis (test group, mean age: 45.7 9.4 years) and 15 with gingivitis (control group, mean age 32.1 7.8 years). We recorded medical and periodontal parameters and collected blood samples. Serum concentrations of fatty acids were analyzed by gas chromatography and adipokines were analyzed by multiplex bead immunoassay. Comparisons between variables were analyzed by Mann - Whitney test and correlations using the Spearman test. There was no significant difference between the levels of adipokines between groups. Considering the levels of DHA, DPA, EPA and AA, there was difference significantly higher for the group of patients with periodontitis compared to the group with gingivitis. The ratios res/DHA, res/AA, adipon/DHA, adipon/AA and adipon/DPA were significantly lower for the group periodontitis. There was no correlation between adipokines and clinical parameters analyzed and between levels of adipokines and fatty acids. We conclude that generalized chronic periodontitis differs significantly higher levels of fatty acids when compared to gingivitis. Adipokines, resistin and adiponectin, showed a tendency to lower values in periodontitis. Reasonss results suggest a smaller proportion of adiponectin and resistin in relation to the fatty acids in periodontitis.
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Vliv adipocytárních hormonů (leptin a adiponectin) na predikci váhového úbytku a následného přírůstku (weight regain) / Adipokines (leptin and adiponectin) as predictors of weight loss and weight regain during one year period following the 10-week low caloric diet (NUGENOB study)Drahoš, Jan January 2010 (has links)
In the Czech republic, about 20% of women and 16% of men are obese. The key role in the etiology of obesity plays the imbalance between energy intake and expenditure, which is influenced by many factors, including leptin and adiponectin. Leptin is secreted mainly from adipocytes and it's levels increase with cell fat content and body fat percentage. Leptin itself is supposed to lead to weight loss, both by decreasing appetite and increasing energy expenditure. But high levels of leptin can be a signal of so called leptin resistance, a state in which leptin is losing it's effects. Adiponectin is secreted exclusively from adipose tissue. In obese people, lower levels of adiponectin were proven (i.e. adiponectin levels are in a negative correlation with body fat percentage). That's consistent with the fact that adiponectin is affecting a range of metabolic prosesses and thus improves insulin sensitivity and metabolic profile. For evaluation, we used a database of almost 750 subjects, that was build under the Nugenob study, conducted in 8 cities in 7 european countries. Al the participants were measured their anthropometric and biochemical parameters at the baseline and after 10 weeks of a standardized weight reduction program. The czech center retested the patient once again 1 year after the initial...
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