Weight gain in pregnancy: can metformin steady the scales?

Adams, Jacquelyn H.; Poehlmann, John; Racine, Jenna L.; Iruretagoyena, J. Igor; Eddy, Allison A.; Hoppe, Kara K.; Stewart, Katharina; Rhoades, J.; Antony, Kathleen M.

doi:10.1080/14767058.2022.2044775

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…There are very few studies that report the association of metformin with weight loss in pregnant women. The results of a single-center retrospective cohort study that enrolled pregnant women with type 2 diabetes or prediabetes showed that metformin exposure during pregnancy was associated with less excess weight gain and a higher proportion of weight reduction [27]. This study suggests that the use of metformin in pregnant women may help in avoiding excess weight gain and its associated comorbidities.…”

Section: Discussionmentioning

confidence: 76%

Maternal Metformin Treatment Reprograms Maternal High-Fat Diet-Induced Hepatic Steatosis in Offspring Associated with Placental Glucose Transporter Modifications

Huang

Tiao

Lin

et al. 2022

IJMS

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Maternal high-fat (HF) diet exposure in utero may affect fetal development and cause metabolic problems throughout life due to lipid dysmetabolism and oxidative damage. Metformin has been suggested as a potential treatment for body weight reduction and nonalcoholic fatty liver disease, but its reprogramming effect on offspring is undetermined. This study assesses the effects of maternal metformin treatment on hepatic steatosis in offspring caused by maternal HF diet. Female rats were fed either a control or an HF diet before conception, with or without metformin treatment during gestation, and placenta and fetal liver tissues were collected. In another experiment, the offspring were fed a control diet until 120 d (adult stage). Metformin treatment during pregnancy ameliorates placental oxidative stress and enhances placental glucose transporter 1 (GLUT1), GLUT3, and GLUT4 expression levels through 5’ adenosine monophosphate-activated protein kinase (AMPK) activation. Maternal metformin treatment was shown to reprogram maternal HF diet-induced changes in offspring fatty liver with the effects observed in adulthood as well. Further validation is required to develop maternal metformin therapy for clinical applications.

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Section: Discussionmentioning

confidence: 76%

Maternal Metformin Treatment Reprograms Maternal High-Fat Diet-Induced Hepatic Steatosis in Offspring Associated with Placental Glucose Transporter Modifications

Huang

Tiao

Lin

et al. 2022

IJMS

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“…follow-up has demonstrated increased weight, body mass index, and adiposity at mid-childhood following in utero metformin exposure (Tarry-Adkins et al, 2019). Despite these concerns, there continues to be interest in the use of metformin in pregnancy for potential preeclampsia prevention, reduced maternal weight gain in obese pregnancies, and lower miscarriage rate among pregnancies complicated by polycystic ovarian syndrome (Syngelaki et al, 2016;Løvvik et al, 2019;Adams et al, 2022). However, the mechanisms underlying these potential beneficial outcomes remain unknown.…”

Section: Open Access Edited Bymentioning

confidence: 99%

Metformin impairs trophoblast metabolism and differentiation in a dose-dependent manner

Nashif

Mahr

Jena

et al. 2023

Front. Cell Dev. Biol.

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Metformin is a widely prescribed medication whose mechanism of action is not completely defined and whose role in gestational diabetes management remains controversial. In addition to increasing the risk of fetal growth abnormalities and preeclampsia, gestational diabetes is associated with abnormalities in placental development including impairments in trophoblast differentiation. Given that metformin impacts cellular differentiation events in other systems, we assessed metformin’s impact on trophoblast metabolism and differentiation. Using established cell culture models of trophoblast differentiation, oxygen consumption rates and relative metabolite abundance were determined following 200 µM (therapeutic range) and 2000 µM (supra-therapeutic range) metformin treatment using Seahorse and mass-spectrometry approaches. While no differences in oxygen consumption rates or relative metabolite abundance were detected between vehicle and 200 µM metformin-treated cells, 2000 µM metformin impaired oxidative metabolism and increased the abundance of lactate and TCA cycle intermediates, α-ketoglutarate, succinate, and malate. Examining differentiation, treatment with 2000 μM, but not 200 µM metformin, impaired HCG production and expression of multiple trophoblast differentiation markers. Overall, this work suggests that supra-therapeutic concentrations of metformin impair trophoblast metabolism and differentiation whereas metformin concentrations in the therapeutic range do not strongly impact these processes.

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“…However, metformin is no longer considered a first line medication for GDM since long term follow up has demonstrated increased weight, body mass index, and adiposity at mid-childhood following in utero metformin exposure (Tarry-Adkins et al, 2019). Despite these concerns, there continues to be interest in use of metformin in pregnancy for potential preeclampsia prevention, reduced maternal weight gain in obese pregnancies, and lower miscarriage rate among pregnancies complicated by polycystic ovarian syndrome (Syngelaki et al, 2016;Løvvik et al, 2019;Adams et al, 2022). However, the mechanisms underlying these potential beneficial outcomes remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Metformin impairs trophoblast metabolism and differentiation in dose dependent manner

Nashif

Mahr

Jena

et al. 2023

Preprint

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Metformin is a widely prescribed medication whose mechanism of action in not completely defined and whose role in gestational diabetes management remains controversial. In addition to increasing risks of fetal growth abnormalities and preeclampsia, gestational diabetes is associated with abnormalities in placental development including impairments in trophoblast differentiation. Given that metformin impacts cellular differentiation events in other systems, we assessed metformin's impact on trophoblast metabolism and differentiation. Using established cell culture models of trophoblast differentiation, oxygen consumption rates and relative metabolite abundance were determined following 200 μM (near-physiologic) and 2000 μM (supra-physiologic) metformin treatment using Seahorse and mass-spectrometry approaches. While no differences in oxygen consumption rates or relative metabolite abundance was detected between vehicle and 200 μM metformin treated cells, 2000 μM metformin impaired oxidative metabolism and increased abundance of lactate and TCA cycle intermediates, α-ketoglutarate, succinate, and malate. Examining differentiation, treatment with 2000 μM, but not 200 μM metformin, impaired HCG production and expression of multiple trophoblast differentiation markers. Overall, this work suggests that supra-physiologic concentrations of metformin impairs trophoblast metabolism and differentiation whereas physiologic concentrations of metformin do not strongly impact these processes.

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Weight gain in pregnancy: can metformin steady the scales?

Cited by 3 publications

References 24 publications

Maternal Metformin Treatment Reprograms Maternal High-Fat Diet-Induced Hepatic Steatosis in Offspring Associated with Placental Glucose Transporter Modifications

Maternal Metformin Treatment Reprograms Maternal High-Fat Diet-Induced Hepatic Steatosis in Offspring Associated with Placental Glucose Transporter Modifications

Metformin impairs trophoblast metabolism and differentiation in a dose-dependent manner

Metformin impairs trophoblast metabolism and differentiation in dose dependent manner

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