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Diabetes gestacional
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A Diabetes Gestacional pode ser explicada pela Hipótese de Pederson, Freinkel, Metzger e Barker, como um conflito entre dois sistemas, materno e fetal, no qual hiperglicémia materna conduz a hiperinsulinémia e adipogénese fetais, sobretudo no terceiro trimestre da gestação.
Os potenciais alvos mecanísticos da resistência à insulina serão o IRS-1, a PI3K, o GLUT-4, os PPARs e a PC-1. E como marcadores surgirão a progesterona, os recetores de prolactina, os micro-RNAs como o 326, e citocinas como TNF-alfa, leptina, adiponectina e IL-6.
Os principais fatores de risco serão o peso antes e durante a gestação, a dieta, a idade materna, uma DG prévia, a PCOS e a etnicidade.
As complicações podem advir de três parâmetros: hiperglicémia materna, hiperglicémia e hiperinsulinémia fetais. Esses levam à produção de AGEs que potenciarão pré-eclâmpsia, a formação de ROS que despoletará alterações congénitas, e a promoção do anabolismo que culminará na macrossomia e adiposidade, podendo ainda findar em lesões microcirculatórias e hipóxia. E, mais grave ainda, na angústia respiratória do recém-nascido.
O tratamento pode ser comportamental baseado-se numa dieta de baixo índice glicémico, recomendando-se um regime mediterrânico pois promove um bom consumo de polifenóis e PUFAs. Completando com exercício físico o sucesso rondará entre os 75 a 80% dos casos.
Farmacologicamente a primeira linha poderá ser a insulina ou a metformina. A insulina permite o melhor controlo glicémico, não atravessa a placenta e logo não promove imprinting metabólico. Já a metformina, evita a hipoglicémia e macrossomia neonatais, além de possibilitar melhor controlo de peso. Como segunda linha, existe a glibenclamida que é inferior em eficácia e segurança.
Durante a gestação, além da glicémia deve-se vigiar a proteinúria e o ganho de peso, e a partir de testes antenatais decidir-se se se deve induzir o parto antes das 39 semanas. Recomendar-se-á cesariana se o peso fetal for superior a 4,5kg.
Após a gravidez, deve-se seguir a utente, observando a HbA1c e promovendo o bom estilo de vida que reduz a incidência de diabetes em 35%.
A DG é um marcador de doença cardiovascular e, como tal, essa família deve ser acompanhada pelo sistema nacional de saúde.
Gestational Diabetes can be explained by the Pederson-Freinkel-Metzger-Barker Hypothesis, as a conflict between two systems, maternal and fetal, where maternal hyperglycemia leads to fetal hyperinsulinemia and adipogenesis, mainly in the third trimester of pregnancy. The mechanistic targets for insulin resistance will be IRS-1, PI3K, GLUT-4, PPARs and PC-1. Progesterone, prolactin receptors, micro-RNAs such as 326, and cytokines such as TNF-alpha, leptin, adiponectin and IL-6 appear as markers for GD. The main risk factors will be weight, diet, maternal age, previous GD, PCOS and ethnicity. Complications can arise from three parameters: maternal hyperglycemia, fetal hyperglycemia and hyperinsulinemia. These will lead to the production of AGEs – a key for pre-eclampsia, the formation of ROS – a trigger for congenital changes, and to anabolism promotion, which will result in macrosomia and adiposity. On other hand, disturbances in endothelium could be responsible for hypoxia appearance. And even worse, respiratory distress of the newborn. In a first place, treatment will be non-pharmacological and will be based on a low glycemic index diet, especially a Mediterranean diet as it promotes a good consumption of polyphenols and PUFAs. Combining this approach with physical activity appealing, success rate will be around 75 to 80%. In a pharmacological strategy, the first line may be insulin or metformin. Insulin is known to achieve a good glycemic control and does not cross the placenta – so doesn’t appear to be a cause of metabolic imprinting. Metformin, on the other hand, prevents neonatal hypoglycemia and macrosomia, in addition to enabling better weight control. As a second line, there is glibenclamide which is inferior in efficacy and safety. During childbirth, in addition to blood glucose, proteinuria and weight gain should be monitored, and antenatal tests are needed to be done to understand if stress conditions suggest labor induction or not before 39 weeks. Cesarean section will be recommended if fetal weight exceeds 4.5 kg. After pregnancy, the mother should be followed, observing HbA1c and promoting a good lifestyle that will reduces the incidence of diabetes about 35%. GD is a marker of cardiovascular disease and, as such, this family must be surveilled by a national health system program.
Gestational Diabetes can be explained by the Pederson-Freinkel-Metzger-Barker Hypothesis, as a conflict between two systems, maternal and fetal, where maternal hyperglycemia leads to fetal hyperinsulinemia and adipogenesis, mainly in the third trimester of pregnancy. The mechanistic targets for insulin resistance will be IRS-1, PI3K, GLUT-4, PPARs and PC-1. Progesterone, prolactin receptors, micro-RNAs such as 326, and cytokines such as TNF-alpha, leptin, adiponectin and IL-6 appear as markers for GD. The main risk factors will be weight, diet, maternal age, previous GD, PCOS and ethnicity. Complications can arise from three parameters: maternal hyperglycemia, fetal hyperglycemia and hyperinsulinemia. These will lead to the production of AGEs – a key for pre-eclampsia, the formation of ROS – a trigger for congenital changes, and to anabolism promotion, which will result in macrosomia and adiposity. On other hand, disturbances in endothelium could be responsible for hypoxia appearance. And even worse, respiratory distress of the newborn. In a first place, treatment will be non-pharmacological and will be based on a low glycemic index diet, especially a Mediterranean diet as it promotes a good consumption of polyphenols and PUFAs. Combining this approach with physical activity appealing, success rate will be around 75 to 80%. In a pharmacological strategy, the first line may be insulin or metformin. Insulin is known to achieve a good glycemic control and does not cross the placenta – so doesn’t appear to be a cause of metabolic imprinting. Metformin, on the other hand, prevents neonatal hypoglycemia and macrosomia, in addition to enabling better weight control. As a second line, there is glibenclamide which is inferior in efficacy and safety. During childbirth, in addition to blood glucose, proteinuria and weight gain should be monitored, and antenatal tests are needed to be done to understand if stress conditions suggest labor induction or not before 39 weeks. Cesarean section will be recommended if fetal weight exceeds 4.5 kg. After pregnancy, the mother should be followed, observing HbA1c and promoting a good lifestyle that will reduces the incidence of diabetes about 35%. GD is a marker of cardiovascular disease and, as such, this family must be surveilled by a national health system program.
Descrição
Trabalho Final de Mestrado Integrado, Ciências Farmacêuticas, 2022, Universidade de Lisboa, Faculdade de Farmácia.
Palavras-chave
Adipogénese Controlo de peso vs insulina vs metformina Imprinting metabólico Inflamação sistémica Unidades materna e feto-placentária Mestrado integrado - 2022