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RESEARCH PRODUCT
Metformin induces lipid changes on sphingolipid species and oxidized lipids in polycystic ovary syndrome women.
Mariona JovéMilagros RochaAntonio Hernández-mijaresReinald PamplonaVictor M. VictorIrene PradasAlba NaudíCelia BañulsSusana Rovira-llopissubject
Endocrine reproductive disordersmedicine.medical_specialtyendocrine system diseasesmedicine.drug_classlcsh:Medicinemedicine.disease_causeArticleInternal medicinemedicineHumansAndrostenedionelcsh:ScienceSphingolipidsMultidisciplinarybusiness.industrylcsh:Rdigestive oral and skin physiologynutritional and metabolic diseasesLipid metabolismMetabolismAndrogenSphingolipidPolycystic ovaryMetforminMetforminOxidative StressEndocrinologyLipidomicslcsh:QFemalebusinessOxidation-ReductionOxidative stressmedicine.drugPolycystic Ovary Syndromedescription
Metformin is one of the treatments used for pcoS pathology decreasing body weight, plasma androgen, FSH and glucose levels. Unfortunately, there is little known about metformin’s effects on lipid metabolism, a crucial process in pcoS pathology. We have employed a lipidomic approach to explore alterations in the plasma lipid profile of patients with PCOS following metformin treatment. The aim is to offer new insights about the effect of metformin in PCOS patients. Plasma samples were obtained from 27 subjects prior to and following 12 weeks of metformin treatment. A detailed biochemical characterization and lipidomic profile was performed. Metformin reduces BMI, HOMA-IR, fSH and androstenedione and increases DHeA-S but no changes were found in glucose levels after treatment. Multivariate statistics revealed a specific lipidomic signature due to the effect of 12 weeks of metformin treatment in pcoS patients. this signature includes changes in sphingolipid metabolism suggesting a crosstalk between these lipid species and the androgenic metabolism and a decrease in oxidized lipids reinforcing that metformin treatment improves oxidative stress status. our study confirms the specific effect of metformin in lipid metabolism on women with PCOS after 12 weeks of treatment. We thank Maria Rosa Gomez and David Argiles for technical support. This research was funded by grants from Carlos III Health Institute (ISCIII) (PI16/1083, PI16/0301) to V.M.V and M.R, respectively and CIBERehd (CB06/04/0071)−initiatives of the ISCIII to M.R and V.M.V, the European Regional Development Fund (ERDF “A way to build Europe”). Unrestricted grant from Menarini S.A to M.R. V.M.V. and M.R. are recipients of contracts from the Ministry of Health of the Valencian Regional Government and Carlos III Health Institute (CES10/030 and CP10/0360, respectively). R. P. is recipient of contracts from the Spanish Ministry of Economy and Competitiveness, Institute of Health Carlos III (grant number PI14/00328); Spanish Ministry of Science, Innovation and Universities (grant number RTI2018-099200-B-I00), and the Generalitat of Catalonia, Department of Health (grant number SLT002/16/00250) and Department of Business and Knowledge (grant number 2017SGR696). This study has been co-financed by FEDER funds from the European Union (‘A way to build Europe’). I.P. received a predoctoral fellowship from the Lleida University. S.R-LL. is recipient of a Juan de la Cierva contract from Spanish Ministry of Economy and Competitiveness (FJCI-2015-25040). C.B. is recipient of a Sara Borrell contract from Institute of Health Carlos III (CD14/00043). M.J is a Serra Húnter Fellow.
year | journal | country | edition | language |
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2019-01-18 | Scientific reports |