| Literature DB >> 31152867 |
Marilza Vieira Cunha Rudge1, Angélica Mercia Pascon Barbosa2, Luis Sobrevia3, Rafael Bottaro Gelaleti4, Raghavendra Lakshmana Shetty Hallur4, João Paulo Castro Marcondes4, Daisy Maria Fávero Salvadori5, Caroline Baldini Prudêncio4, Claudia Garcia Magalhães6, Roberto Costa6, Joelcio Francisco Abbade6, José Eduardo Corrente7, Iracema de Mattos Paranhos Calderon8.
Abstract
Mild gestational hyperglycemia (MGH), as assessed using the normal oral glucose tolerance test (OGTT) and detection of an altered glycemic profile, is associated with adverse perinatal outcome. This study described the results of 40 years of research conducted at the Perinatal Diabetes Research Centre at São Paulo State University (UNESP), Brazil, on the maternal MGH environment and placental markers. This study also described the unidirectional relationship between MGH and excessive fetal growth, also supplying moderator analysis. In addition to hyperglycemia, MGH is associated with an increased incidence of hypertension, metabolic syndrome, persistent insulin resistance after pregnancy, and high risk of developing type 2 diabetes mellitus (T2DM) after pregnancy. Structural changes and functional abnormalities resulting from MGH were observed in placenta. The fully adjusted model concluded that the predictor variable (MGH), which creates a complex environment for the fetus, has a direct effect on excessive birth weight and produces a z-score for ratios of birth weight to gestational age of ≥2. Maternal age, pre-pregnancy BMI, number of previous pregnancies, numbers of prenatal visits, and 1 h OGTT are moderator variables that impact MGH and excessive fetal growth. These results show that maternal MGH has some characteristics associated with similar long-term T2DM development and similar adverse perinatal results to those of gestational diabetes mellitus (GDM) mothers, making it an intermediate maternal and placental marker between normoglycemic and GDM mothers.Entities:
Keywords: Apoptosis; Cytokines; Gene expression; Gestational diabetes mellitus; IRS-1 gene; Inflammatory mediators; Insulin resistance; Large for gestational age; Mild gestational hyperglycemia; Moderator analysis; Natural killer cells; Placenta
Year: 2019 PMID: 31152867 DOI: 10.1016/j.bbadis.2019.05.014
Source DB: PubMed Journal: Biochim Biophys Acta Mol Basis Dis ISSN: 0925-4439 Impact factor: 5.187