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other·preclinical research, biomedical research, endocrinology, nutrition, obstetrics and gynecology·PMC10647445

Effects of Gestational Diabetes Mellitus and Selenium Deficiency on the Offspring Growth and Blood Glucose Mechanisms of C57BL/6J Mice

Nutrients · 10 authors, 2 centres

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TL;DR

This preclinical mouse study used S961-induced gestational diabetes mellitus (GDM) and selenium (Se) deficiency to examine effects on offspring growth, glucose metabolism, oxidative stress, and PI3K/Akt signaling in four experimental groups (control, GDM, Se deficiency, GDM+Se deficiency). The central result is that GDM and maternal Se deficiency affect offspring through oxidative stress and PI3K/Akt signaling, with pronounced sex differences: effects persist into adulthood in females but dissipate in males.

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Offspring were assessed at weaning (4 weeks) and adulthood (8 weeks) for body weight, fasting blood glucose, oral glucose tolerance, renal Se content, hepatic oxidative stress markers (GSH-Px, SOD, MDA), organ coefficients, and PI3K/Akt pathway protein expression. GDM increased lactating offspring obesity susceptibility with gender-specific differences persisting into adulthood. Se deficiency reduced SOD activity in female adult offspring but only in male weaning offspring. Combined GDM and Se deficiency increased abnormal glucose metabolism risk in female offspring from weaning to adulthood, with the influence diminishing in males. Effects on PI3K/Akt signaling mirrored this sex-dependent trend. Se deficiency model was confirmed by significantly lower renal Se content. Limitations include the indirect translational relevance of mouse models to human GDM and the use of a pharmacological rather than metabolic GDM induction method.

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other

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preclinical research

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ORIGINAL PAPER

PMC10647445

Effects of Gestational Diabetes Mellitus and Selenium Deficiency on the Offspring Growth and Blood Glucose Mechanisms of C57BL/6J Mice

Nutrients

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ABSTRACT

This study aimed to explore the effects and mechanisms of maternal gestational diabetes mellitus (GDM) and selenium (Se) deficiency on the growth and glucose metabolism of offspring. Female C57BL/6J mice were divided into four groups as follows: a control group, a GDM group, a Se deficiency group, and a GDM with Se deficiency group. GDM animal models were established via S961. Pregnant mice fed their offspring until weaning. Then, offspring continued to be fed with a basic diet until adulthood. Body weight and fasting blood glucose were measured weekly. Se content, oxidative stress indicators, and the protein expression of the PI3K/Akt signaling pathway were detected. GDM increased susceptibility to obesity in lactating offspring, with gender differences observed in adult offspring. The effect of Se deficiency on SOD activity only appeared in female offspring during adulthood but was shown in male offspring during weaning though it disappeared during adulthood. GDM and Se deficiency increased the risk of abnormal glucose metabolism in female offspring from weaning to adulthood but gradually decreased in male offspring. The influence on the expression of PI3K/Akt signaling pathway-related proteins showed the same trend. GDM and Se deficiency affected the growth and glucose metabolism of offspring through oxidative stress and PI3K/Akt signaling pathway-related proteins, and gender differences existed.

CITATION EXPORT

Wenhui Xu, Jiayu Gong, Yifei Chen et al.. Effects of Gestational Diabetes Mellitus and Selenium Deficiency on the Offspring Growth and Blood Glucose Mechanisms of C57BL/6J Mice. Nutrients. (2023). https://doi.org/10.3390/nu15214519

AUTHORS

10 · 2 CENTRES

Wenhui Xu, Jiayu Gong, Yifei Chen, Yiru Chen, Shutong Chen, Yanyan Wu, Yuan He, Chenxu Li, Haitao Yu, Lin Xie

1School of Public Health, Jilin University, Changchun 130012, China; [email protected] (W.X.); [email protected] (J.G.); [email protected] (Y.C.); [email protected] (S.C.); [email protected] (Y.W.); [email protected] (Y.H.); [email protected] (C.L.)
2Clinical Nutrition Department, Third Hospital of Jilin University, Changchun 130032, China; [email protected]

EDITOR / REVIEWER

Didier Vieau, Takao Kimura