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Ginecología y obstetricia de México

versão impressa ISSN 0300-9041

Resumo

AYALA-YANEZ, Rodrigo et al. Metformin: Cellular and molecular interactions and its’ impact in obstetrics. Literature review. Ginecol. obstet. Méx. [online]. 2020, vol.88, n.3, pp.161-175.  Epub 30-Ago-2021. ISSN 0300-9041.  https://doi.org/10.24245/gom.v88i3.3598.

OBJECTIVE:

Identify the most recognized cellular mechanisms and their relations to obstetric pathology, determining molecular pathways for potential therapeutic use.

METHODOLOGY:

After a bibliographical search done in Pubmed and Cochrane database of MeSH terms: “metformin”, “cellular mechanisms”, “AMPK”, “LKB1”, “gestational diabetes”, “abortion”, “preeclampsia”, in the periods comprehending 2000 through 2019, a total of 49 references were selected, on the basis of the criteria established by the objective of this review.

RESULTS:

With 49 selected references, we found that metformin regulates adenosine monophosphate protein kinase (AMPK) and LKB1, both who which participate in metabolic mechanisms, activating second messengers who stimulate or inhibit processes like gluconeogenesis, steroid and protein synthesis and cellular growth. This drug actually acts by inhibiting complex I of the mitochondrial respiration process, impacting various cell functions. Gestational diabetes, abortion and preeclampsia are three obstetric pathologies selected due to their incidence and relevance, as well as the fact that metformin is being used for their treatment. We also identified the mechanisms for gastrointestinal symptoms where OCT-1, PMAT and 5-HT are involved and may be therapeutic targets. The association of cell mechanisms influenced by metformin are part of various metabolic pathways, being the ones in gestational diabetes the most, well known due to experience with diabetes mellitus.

CONCLUSIONS:

Although metformin has a clear role in gestational diabetes, results are insufficient to identify its’ role in abortion. As for preeclampsia, the mechanisms identified have a greater preventive and therapeutic potential.

Palavras-chave : Metformin; Cellular mechanisms; AMPK; LKB1; Gestational Diabetes; Preeclampsia; Abortion.

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