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Orientador: Daisy Maria Fávero Salvadori / Coorientador: João Paulo de Castro Marcondes / Resumo: A obesidade é uma doença de etiologia multifatorial, resultante de interações complexas entre fatores genéticos e ambientais. No entanto, o aumento acentuado de sua incidência, precocidade e severidade não foram ainda totalmente elucidados. Dentre os inúmeros fatores de risco, diversos achados sugerem, também, que estímulos estressores (p.ex. diabete, alterações nutricionais) na vida intrauterina podem promover alterações genéticas e epigenéticas, predispondo ao desenvolvimento tardio de doenças e disfunções metabólicas, como a obesidade. Assim, o presente estudo foi delineado com o objetivo de avaliar a possível relação entre o Diabetes melittus gestacional (DMG) e a predisposição do recém-nascido para o desenvolvimento de obesidade na vida adulta. Para tanto, foram incluídos no estudo gestantes saudáveis e gestantes diagnosticadas com DMG e seus respectivos recém-nascidos. Adicionalmente, adultos obesos e eutróficos foram incluídos como população de referência (controle). Considerando a relação entre o diabete e a obesidade com a disfunção mitocondrial, foi avaliado o perfil de expressão de gênica e proteica de SOD2 (superóxido desmutase 2), PPARα (receptor ativador da proliferação de peroxissomos alfa) e PPARGC-1β (receptor ativador da proliferação de peroxissomos gamma coativador 1 beta), relacionados ao metabolismo mitocondrial, em sangue do cordão umbilical e sangue periférico (população de referência), e o perfil de expressão gênica em células de placenta (faces materna e fetal). Primeiramente, nossos resultados demonstraram que indivíduos obesos apresentavam aumento da expressão gênica e proteica de SOD2, PPARα e PPARGC-1β no tecido sanguíneo quando comparados aos eutróficos (p < 0,05). No entanto, o mesmo não foi observado no tecido placentário (expressão gênica) e no sangue do cordão umbilical (expressão gênica e protéica) dos recém-nascidos das gestantes com DMG e... / Abstract: Obesity is a multifactorial disease involving complexes interactions between genetic and environmental agents. However, the increased incidence, early onset and severity of this disease, are still not well understood. Several findings have demonstrated that in utero stressors (diabetes, cigarettes, and/or alcohol consumption, etc) can promote genetic and epigenetic changes predisposing to late development of diseases and metabolic disorders, such as obesity. The present study was designed to evaluate the possible relationship between gestational Diabetes mellitus (GDM) and newborn predisposition to obesity his later life. Healthy and GDM pregnant women and their respective newborns were included. Additionally, obese and eutrophic adults were recruted as reference population. Considering the relationship between diabetes and obesity with mitochondrial dysfunction, gene and protein related to mitochondrial metabolism (SOD2 (superoxide dismutase 2), PPARα (peroxisome proliferator-activated receptor alpha) and PPARGC-1β(peroxisome proliferatoractivated receptor gamma coactivador beta) were evaluated in cells from cord and peripheral blood (reference population), and in placenta cells (gene expression profile in maternal and fetal sides). Our results showed an increased gene and protein expression (SOD2, PPARα and PPARGC-1β) in peripheral blood from obese compared to euthrophic subjects (p <0.05). However, the same result was not observed in the placental tissue (gene expression) and in umbilical cord blood cells (gene and protein expression) from GDM women and their respective newborn compared to the non diabetic group, i.e., GDM was not an effective agent to promote transcriptional changes in SOD2, PPARα PPARGC-1β in maternal and fetal sides of placenta, and transcriptional and translational changes in umbilical cord blood cells. In conclusion, SOD2, PPARα and PPARGC-1β gene and protein expression were confirmed as potential ... / Mestre

Made available in DSpace on 2015-12-10T14:22:49Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-01-19. Added 1 bitstream(s) on 2015-12-10T14:29:01Z : No. of bitstreams: 1 000851402.pdf: 1086924 bytes, checksum: d01cb9f4eba10b500b059e2fe7102a41 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / A obesidade é uma doença de etiologia multifatorial, resultante de interações complexas entre fatores genéticos e ambientais. No entanto, o aumento acentuado de sua incidência, precocidade e severidade não foram ainda totalmente elucidados. Dentre os inúmeros fatores de risco, diversos achados sugerem, também, que estímulos estressores (p.ex. diabete, alterações nutricionais) na vida intrauterina podem promover alterações genéticas e epigenéticas, predispondo ao desenvolvimento tardio de doenças e disfunções metabólicas, como a obesidade. Assim, o presente estudo foi delineado com o objetivo de avaliar a possível relação entre o Diabetes melittus gestacional (DMG) e a predisposição do recém-nascido para o desenvolvimento de obesidade na vida adulta. Para tanto, foram incluídos no estudo gestantes saudáveis e gestantes diagnosticadas com DMG e seus respectivos recém-nascidos. Adicionalmente, adultos obesos e eutróficos foram incluídos como população de referência (controle). Considerando a relação entre o diabete e a obesidade com a disfunção mitocondrial, foi avaliado o perfil de expressão de gênica e proteica de SOD2 (superóxido desmutase 2), PPARα (receptor ativador da proliferação de peroxissomos alfa) e PPARGC-1β (receptor ativador da proliferação de peroxissomos gamma coativador 1 beta), relacionados ao metabolismo mitocondrial, em sangue do cordão umbilical e sangue periférico (população de referência), e o perfil de expressão gênica em células de placenta (faces materna e fetal). Primeiramente, nossos resultados demonstraram que indivíduos obesos apresentavam aumento da expressão gênica e proteica de SOD2, PPARα e PPARGC-1β no tecido sanguíneo quando comparados aos eutróficos (p < 0,05). No entanto, o mesmo não foi observado no tecido placentário (expressão gênica) e no sangue do cordão umbilical (expressão gênica e protéica) dos recém-nascidos das gestantes com DMG e... / Obesity is a multifactorial disease involving complexes interactions between genetic and environmental agents. However, the increased incidence, early onset and severity of this disease, are still not well understood. Several findings have demonstrated that in utero stressors (diabetes, cigarettes, and/or alcohol consumption, etc) can promote genetic and epigenetic changes predisposing to late development of diseases and metabolic disorders, such as obesity. The present study was designed to evaluate the possible relationship between gestational Diabetes mellitus (GDM) and newborn predisposition to obesity his later life. Healthy and GDM pregnant women and their respective newborns were included. Additionally, obese and eutrophic adults were recruted as reference population. Considering the relationship between diabetes and obesity with mitochondrial dysfunction, gene and protein related to mitochondrial metabolism (SOD2 (superoxide dismutase 2), PPARα (peroxisome proliferator-activated receptor alpha) and PPARGC-1β(peroxisome proliferatoractivated receptor gamma coactivador beta) were evaluated in cells from cord and peripheral blood (reference population), and in placenta cells (gene expression profile in maternal and fetal sides). Our results showed an increased gene and protein expression (SOD2, PPARα and PPARGC-1β) in peripheral blood from obese compared to euthrophic subjects (p <0.05). However, the same result was not observed in the placental tissue (gene expression) and in umbilical cord blood cells (gene and protein expression) from GDM women and their respective newborn compared to the non diabetic group, i.e., GDM was not an effective agent to promote transcriptional changes in SOD2, PPARα PPARGC-1β in maternal and fetal sides of placenta, and transcriptional and translational changes in umbilical cord blood cells. In conclusion, SOD2, PPARα and PPARGC-1β gene and protein expression were confirmed as potential ...

Indiana University-Purdue University Indianapolis (IUPUI) / Objectives: To determine (1) whether prescribed and delivered energy and protein intakes during the first two weeks of life met Ziegler’s estimated requirements for Very Low Birth Weight (VLBW) infants, (2) if actual energy during the first week of life correlated with time to regain birth weight and reach full enteral nutrition (EN) defined as 100 kcal/kg/day, (3) if growth velocity from time to reach full EN to 36 weeks’ postmenstrual age (PMA) met Ziegler’s estimated fetal growth velocity (16 g/kg/day), and (4) growth outcomes at 36 weeks’ PMA. Study design: Observational study of feeding, early nutrition and early growth of 40 VLBW infants ≤ 30 weeks GA at birth in three newborn intensive care units NICUs. Results: During the first week of life, the percentages of prescribed and delivered energy (69% [65 kcal/kg/day]) and protein (89% [3.1 g/kg/day]) were significantly less than theoretical estimated requirements. Delivered intakes were 15% less than prescribed because of numerous interruptions in delivery and medical complications. During the second week, the delivered intakes of energy (90% [86 kcal/kg/day]) and protein (102% [3.5 g/kg/day]) improved although the differences between prescribed and delivered were consistently 15%. Energy but not protein intake during the first week was significantly related to time to reach full EN. Neither energy nor protein intake significantly correlated with days to return to birth weight. The average growth velocity from the age that full EN was attained to 36 weeks’ PMA (15 g/kg/day) was significantly less than the theoretical estimated fetal growth velocity (16 g/kg/day) (p<0.03). A difference of 1 g/kg/day represents a total deficit of 42 - 54 grams over the course of a month. At 36 weeks’ PMA, 53% of the VLBW infants had extrauterine growth restriction, or EUGR (<10th percentile) on the Fenton growth grid and 34% had EUGR on the Lubchenco growth grid. Conclusions: The delivered nutrient intakes were consistently less than 15% of the prescribed intakes. Growth velocity between the age when full EN was achieved and 36 weeks’ PMA was 6.7% lower than Ziegler’s estimate. One-third to one-half of the infants have EUGR at 36 weeks’ PMA.