Adipocinas e o diabetes mellitus gestacional
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Data
2013-10-30
Autores
Lobo, Thalita Frutuoso [UNIFESP]
Orientadores
Daher, Silvia [UNIFESP]
Tipo
Dissertação de mestrado
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Introdução: A obesidade é uma condição inflamatória que predispõe ao desenvolvimento do Diabetes Mellitus Gestacional (DMG). Algumas mulheres obesas desenvolvem uma forma mais precoce de DMG, antes do aumento fisiológico da secreção de hormônios placentários hiperglicemiantes que ocorre por volta da 24ª semana da gestação. Ainda não está claro qual seria o perfil de adipocinas séricas dessas gestantes que desenvolvem esta forma precoce de DMG. Objetivo: Avaliar mediadores da resposta inflamatória na 1ª metade da gestação em mulheres pré-obesas e obesas, procurando associar os achados com o diagnóstico de DMG precoce (até 20 semanas). Métodos: Este estudo do tipo coorte prospectivo recrutou gestantes com sobrepeso (IMC pré-gestacional >25 Kg/m 2) na 1ª metade da gestação, sem outras co-morbidades. Foi colhido sangue para avaliar os níveis séricos de adipocinas, e para análise de polimorfismos genéticos. Todas as participantes realizaram teste de tolerância oral a glicose com 75g (TTOG) até a 20ª semana de gestação; aquelas com 1 ou mais valores anormais (jejum 92-125 mg/dL, 1h 180-199 mg/dL, 2 h 153-199 mg/dL) receberam o diagnóstico de DMG, segundo os critérios do IADPSG. Todas as gestantes foram acompanhadas até o final da gestação e aquelas que desenvolveram DMG posteriormente ou qualquer outra complicação clínica ou obstétrica foram excluídas das análises. Foram comparados os achados dos exames laboratoriais entre as gestantes com e sem DMG precoce. As concentrações séricas de adiponectina, leptina, resistina, grelina e visfatina foram mensuradas por ELISA, e os polimorfismos genéticos pela técnica de PCR-RFLP. Resultados: Um total de 93 gestantes com sobrepeso foi incluído nas análises: 33 desenvolveram DMG precoce e 60 tiveram uma gestação saudável sem nenhuma complicação. Os níveis séricos de adiponectina foram significantemente mais baixos e os de leptina mais altos no grupo que desenvolveu DMG precoce (p=0,02, p=0,01; respectivamente). A razão adiponectina/leptina foi menor no grupo DMG (p=0,003). Não encontramos alterações das concentrações séricas de resistina, grelina e visfatina relacionadas ao DMG. O polimorfismo -2548 G/A do gene de Leptina mostrou associação com DMG precoce (p=0,02). Conclusão: Gestantes com sobrepeso com DMG precoce têm níveis de adiponectina significantemente menores e de leptina significantemente maiores na 1ª metade da gravidez do que gestantes saudáveis. Além disso, o polimorfismo -2548 G/A do gene de Leptina parece estar associado à doença.
Introduction: Obesity is an inflammatory condition that predisposes to the development of Gestational Diabetes Mellitus (GDM). Some obese women develop early-onset GDM, before the physiological increase in secretion of placental hyperglycemic hormones that occurs around the 24th week of pregnancy. The adipokine profile of these women who develop early-onset GDM remains unclear. Objective: To assess inflammatory response mediators in the 1st half of pregnancy in pre-obese and obese women, trying to relate the findings to the diagnosis of early onset GDM (before the 20th week). Methods: This prospective cohort study recruited overweight pregnant women (pre-pregnancy BMI> 25 kg / m2 ) in the 1st half of pregnancy without other co-morbidities. Blood was collected to evaluate serum adipokines, and for the analysis of genetic polymorphisms. All participants underwent a 75g oral glucose tolerance test (OGTT) up to the 20th week of pregnancy; those with 1 or more abnormal values (fasting 92-125 mg/dL, 1h 180-199 mg/dL, 2 h 153 - 199 mg/dL) were diagnosed with GDM according to the criteria of the IADPSG. All women were followed until the end of pregnancy and those who subsequently developed GDM or any other clinical or obstetric complications were excluded from the analysis. We compared the results of laboratory tests among pregnant women with and without early-onset GDM. Serum concentrations of adiponectin, leptin, resistin, ghrelin and visfatin were determined by ELISA, and genetic polymorphisms by PCR-RFLP. Results: A total of 93 overweight pregnant women were included in the analysis: 33 developed early onset GDM and 60 had a healthy pregnancy with no complications. Serum adiponectin levels were significantly lower and leptin levels were significantly higher in the early-onset GDM group (p = 0.02, p = 0.01, respectively). The adiponectin/leptin ratio was lower in the early-onset GDM group (p = 0.003). We did not identify significant differences in the levels of resistin, ghrelin and visfatin related to GDM. The leptin gene -2548 G/A polymorphism was associated with early-osnet GDM (p = 0.02). Conclusion: Overweight pregnant women with early-onset GDM have significantly lower levels of adiponectin and significantly higher levels of leptin in the first half of pregnancy, than healthy pregnant women. Inaddition, the leptin gene -2548 G/A polymorphism seems to be associated with the disease.
Introduction: Obesity is an inflammatory condition that predisposes to the development of Gestational Diabetes Mellitus (GDM). Some obese women develop early-onset GDM, before the physiological increase in secretion of placental hyperglycemic hormones that occurs around the 24th week of pregnancy. The adipokine profile of these women who develop early-onset GDM remains unclear. Objective: To assess inflammatory response mediators in the 1st half of pregnancy in pre-obese and obese women, trying to relate the findings to the diagnosis of early onset GDM (before the 20th week). Methods: This prospective cohort study recruited overweight pregnant women (pre-pregnancy BMI> 25 kg / m2 ) in the 1st half of pregnancy without other co-morbidities. Blood was collected to evaluate serum adipokines, and for the analysis of genetic polymorphisms. All participants underwent a 75g oral glucose tolerance test (OGTT) up to the 20th week of pregnancy; those with 1 or more abnormal values (fasting 92-125 mg/dL, 1h 180-199 mg/dL, 2 h 153 - 199 mg/dL) were diagnosed with GDM according to the criteria of the IADPSG. All women were followed until the end of pregnancy and those who subsequently developed GDM or any other clinical or obstetric complications were excluded from the analysis. We compared the results of laboratory tests among pregnant women with and without early-onset GDM. Serum concentrations of adiponectin, leptin, resistin, ghrelin and visfatin were determined by ELISA, and genetic polymorphisms by PCR-RFLP. Results: A total of 93 overweight pregnant women were included in the analysis: 33 developed early onset GDM and 60 had a healthy pregnancy with no complications. Serum adiponectin levels were significantly lower and leptin levels were significantly higher in the early-onset GDM group (p = 0.02, p = 0.01, respectively). The adiponectin/leptin ratio was lower in the early-onset GDM group (p = 0.003). We did not identify significant differences in the levels of resistin, ghrelin and visfatin related to GDM. The leptin gene -2548 G/A polymorphism was associated with early-osnet GDM (p = 0.02). Conclusion: Overweight pregnant women with early-onset GDM have significantly lower levels of adiponectin and significantly higher levels of leptin in the first half of pregnancy, than healthy pregnant women. Inaddition, the leptin gene -2548 G/A polymorphism seems to be associated with the disease.
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Citação
LOBO, Thalita Frutuoso. Adipocinas e o diabetes mellitus gestacional. 2013. 150 f. Dissertação (Mestrado) - Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), São Paulo, 2013.