Metformin in overweight and obese women with gestational diabetes: a propensity score-matched study

Bettencourt‐Silva, Rita; Neves, João Sérgio; Ferreira, Maria João; Souteiro, Pedro; Belo, Sandra; Oliveira, Ana I.; Carvalho, Davide; Namora, Gabriela; Montenegro, Nuno; Queirós, Joana

doi:10.1007/s12020-019-02043-3

Cited by 8 publications

(3 citation statements)

References 35 publications

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“…Therefore, metformin could be useful in the antenatal management of women with PCOS or other disorders with altered glucose metabolism, as shown before [ 6 – 8 , 10 , 19 , 48 , 49 ]. On the other hand, studies of women with gestational diabetes, diabetes mellitus or obesity show that the risk of preeclampsia, caesarean section or preterm birth is lower [ 14 , 15 ] or similar when the effect of metformin is compared to the placebo or to insulin [ 15 – 17 , 20 ]. In fact, in our analysis the risk of preeclampsia was lower in women without PCOS with metformin (at least before 24 weeks).…”

Section: Discussionmentioning

confidence: 99%

Pregnancy, perinatal and childhood outcomes in women with and without polycystic ovary syndrome and metformin during pregnancy: a nationwide population-based study

Fornes

Simin

Nguyen

et al. 2022

Reprod Biol Endocrinol

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Background Polycystic Ovary Syndrome (PCOS) is an endocrine disorder that affects women in reproductive age and represents an unfavourable risk factor for several pregnancy and perinatal outcomes. Despite, no guidelines or pharmaceutical strategies for treating PCOS during pregnancy are available. The aim of this study is to determine the association between polycystic ovary syndrome with or without metformin and the pregnancy, perinatal outcomes as well as the risk of obesity in children born to these mothers. Methods In this nationwide population-based cohort study based in Swedish population, all singleton births (n = 1,016,805) from 686,847 women since 2006 up to 2016 were included. Multivariable logistic and Cox regression modelling with odds ratios (OR) and hazard ratios (HR) and 95% confidence intervals were used to study the association between the exposure of maternal PCOS, metformin during pregnancy (or the combination of both) and: 1) Pregnancy outcomes: preeclampsia, gestational diabetes, caesarean section, and acute caesarean section, 2) Perinatal outcomes: preterm birth, stillbirth, low birth weight, macrosomia, Apgar < 7 at 5 min, small for gestational age and large for gestational age, and 3) Childhood Obesity. Results PCOS in women without metformin use during pregnancy was associated with higher risks of preeclampsia (OR = 1.09, 1.02–1.17), gestational diabetes (OR = 1.71, 1.53–1.91) and caesarean section (OR = 1.08, 1.04–1.12), preterm birth (OR = 1.30, 1.23–1.38), low birth weight (OR = 1.29, 1.20–1.38), low Apgar scores (OR = 1.17, 1.05–1.31) and large for gestational age (OR = 1.11, 1.03–1.20). Metformin use during pregnancy (in women without PCOS) was associated with a 29% lower risks of preeclampsia (OR = 0.71, 0.51–0.97), macrosomia and large for gestational age. Obesity was more common among children born to mothers with PCOS without metformin (HR = 1.61, 1.44–1.81); and those with metformin without PCOS (HR = 1.67, 1.05–2.65). PCOS with metformin was not associated with any adverse outcome. Conclusion PCOS was associated with increased risks of adverse pregnancy and perinatal outcomes and childhood obesity. Metformin appears to reduce these risks in mothers with polycystic ovary syndrome and their children; but may increase the risk of childhood-obesity in children form women without PCOS.

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Section: Discussionmentioning

confidence: 99%

Pregnancy, perinatal and childhood outcomes in women with and without polycystic ovary syndrome and metformin during pregnancy: a nationwide population-based study

Fornes

Simin

Nguyen

et al. 2022

Reprod Biol Endocrinol

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“…MET, an oral hypoglycemic agent, has been widely applied as a standard first-line therapy for T2DM due to its low cost, safety profile, and potential cardiovascular benefits ( Zhou et al., 2001 ; DeFronzo et al., 2016 ), which has been shown to exert hypoglycemic effect by suppressing hepatic gluconeogenesis caused by elevated secretion of GLP-1 and related peptides via an intestinal AMP-activated protein kinase-dependent pathway ( Inzucchi et al., 2014 ). MET has also been identified to have the function of preventing excessive gestational weight gain and therefore could be used to prevent excessive weight gain during pregnancy ( Balsells et al., 2015 ; Bettencourt-Silva et al., 2019 ). Thus, MET is now the preferred option for GDM treatment considering its advantage of reducing maternal weight gain compared with insulin.…”

Section: Introductionmentioning

confidence: 99%

Metformin Ameliorates Gestational Diabetes Mellitus-Induced Endothelial Dysfunction via Downregulation of p65 and Upregulation of Nrf2

et al. 2020

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Gestational diabetes mellitus (GDM) causes oxidative stress in mothers and infants and causes vascular endothelial dysfunction, which is a key factor for maternal and fetal cardiovascular diseases in the later stage of GDM, seriously threatening the life and health of mothers and infants. Nowadays, metformin (MET) has been discovered to improve endothelial function, but studies regarding the mechanism of MET improving endothelial cell function and alleviating endothelial function under hyperglycemia are still extremely limited. We aimed to investigate whether MET exerts its protective role against hyperglycemia-induced endothelial dysfunction through p65 and Nrf2. In our studies, applying cell migration assay and tube formation assay, we observed an obvious improvement of endothelial function under MET-treated, as characterized by that MET accelerated GDM-attenuated migration and angiogenesis of HUVECs. And ELISA assay results uncovered that Nrf2 expression level was decreased in GDM placenta, HVUECs and maternal serum comparing with normal group, however activation Nrf2 largely ameliorated tube formation under hyperglycemic condition. Furthermore, MET elevated the Nrf2 expression level and the level of nuclear Nrf2 accumulation in hyperglycemic HUVECs. Besides, preliminary evidence predicted that Nrf2 expression was modulated by transcription factor p65, which was increased in GDM peripheral blood, placenta and HUVECs, and suppression of p65 could recover GDM-induced suppression of angiogenesis. In addition, we also confirmed MET restores the GDM-induced angiogenesis impairment may via downregulation of p65 and upregulation of Nrf2. Taken together, the endothelial protective effect of MET under GDM (HG) conditions could be partly attributed to its role in downregulating p65 and upregulating Nrf2.

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“…The incidence of GDM uctuates widely due to differences in geographical area, ethnicity and diagnostic criteria [2,3]. Long-term uncontrolled blood glucose in patients with GDM may have serious adverse effects on the mothers and fetus, such as preeclampsia, cesarean section, macrosomia, premature rupture of membrane, neonatal hypoglycemia and so on [4,5]. At present, the exact pathogenesis of GDM is still not throughly clear, but the IR and the chronic subclinical in ammatory process caused by immune system dysfunction are considered as the main factors for the development of GDM [6].…”

Section: Introductionmentioning

confidence: 99%

High Level of Complement Factor Ba Within 11 to 17 Weeks of Gestation Increases the Risk of Subsequent Gestational Diabetes: A Propensity Score-Matched Study

Shen

Jun-xian

Tian³

et al. 2021

Preprint

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Background: Several studies have shown that the over activation of complement factor B(CFB) was related to obesity, insulin resistance(IR) and type 2 diabetes mellitus. This study was to assess whether circulating complement factor Ba (CFBa) within 11 to 17 weeks of gestation is associated with subsequent gestational diabetes mellitus (GDM) or not.Methods: Biochemical parameters and blood samples were collected from 399 pregnant women within 11 to 17 weeks of gestation. At 24 to 28 weeks of pregnancy, all participants underwent 75-g oral glucose tolerance test (fasting for more than 8 hours before blood sampling) and were assigned to GDM group(n=80) and normal control group(n=319). Perinatal data were collected after delivery. A propensity score-matched (PSM) analysis was performed to reduce the impact of confounding factors on glucose metabolism during pregnancy between the two groups.Results: Two groups of 74 well-matched patients who maintained balance in terms of baseline characteristics. The levels of CFBa in pregnant women who later developed GDM were significantly higher than those in healthy pregnant women [0.4(0.1-0.8) vs. 0.2(0.2-0.3), P=0.031]. Logistic regression results confirmed that the level of CFBa was an independent influencing factor for the occurrence of GDM (OR=1.52, 95% CI: 1.25-1.85, P=0.000). Further grouping according to the quartile of CFBa level, it was found that the incidence of GDM in category 3 was markedly higher than that in the first and the second categories. Conclusions: High level of the CFBa within 11 to 17 weeks of gestation increased the risk of subsequent GDM, and maybe a biomarker for predicting GDM.

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Metformin in overweight and obese women with gestational diabetes: a propensity score-matched study

Cited by 8 publications

References 35 publications

Pregnancy, perinatal and childhood outcomes in women with and without polycystic ovary syndrome and metformin during pregnancy: a nationwide population-based study

Pregnancy, perinatal and childhood outcomes in women with and without polycystic ovary syndrome and metformin during pregnancy: a nationwide population-based study

Metformin Ameliorates Gestational Diabetes Mellitus-Induced Endothelial Dysfunction via Downregulation of p65 and Upregulation of Nrf2

High Level of Complement Factor Ba Within 11 to 17 Weeks of Gestation Increases the Risk of Subsequent Gestational Diabetes: A Propensity Score-Matched Study

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