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Maternal selenium status is profoundly involved in metabolic fetal programming by modulating insulin resistance, oxidative balance and energy homeostasis

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Abstract

Purpose

High and low levels of selenium (Se) have been related to metabolic disorders in dams and in their offspring. Their relationship to oxidative balance and to AMP-activated protein kinase (AMPK) is some of the mechanisms proposed. The aim of this study is to acquire information about how Se is involved in metabolic programming.

Methods

Three experimental groups of dam rats were used: control (Se: 0.1 ppm), Se supplemented (Se: 0.5 ppm) and Se deficient (Se: 0.01 ppm). At the end of lactation, the pups’ metabolic profile, oxidative balance, Se levels, selenoproteins and IRS-1 hepatic expression, as well as hepatic AMPK activation were measured.

Results

The experimental groups present deep changes in Se homeostasis, selenoproteins and IRS-1 hepatic expression, oxidative balance, AMPK activation ratio and insulin levels. They do, however, have different metabolic profiles.

Conclusions

High- and low-Se diets are linked to insulin resistance, yet the mechanisms involved are completely opposite.

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Acknowledgements

Grants from Andalusian Regional Government for its support to CTS-193 research group.

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Authors and Affiliations

Authors

Contributions

MLO and FN were responsible for the study concept and design. AM and FN were responsible for acquisition of animal data. MLO was responsible for data analysis and interpretation of findings. MLO drafted the manuscript. FN and OC provided critical revision of the manuscript. All authors critically reviewed content and approved final version for publication. OC was responsible to find financing for the study.

Corresponding author

Correspondence to Fátima Nogales.

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Conflict of interest

On behalf of all authors, the corresponding author states that there is no conflict of interest.

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Ojeda, M.L., Nogales, F., Membrilla, A. et al. Maternal selenium status is profoundly involved in metabolic fetal programming by modulating insulin resistance, oxidative balance and energy homeostasis. Eur J Nutr 58, 3171–3181 (2019). https://doi.org/10.1007/s00394-018-1861-4

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  • DOI: https://doi.org/10.1007/s00394-018-1861-4

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