Mitochondrial dysfunction in the fetoplacental unit in gestational diabetes mellitus

Sobrevía, Luis; Valero, Paola; Grismaldo, Adriana; Villalobos-Labra, Roberto; Pardo, Fabián; Subiabre, Mario; Armstrong, Gael; Toledo, Fernando; Vega, Sofía; Cornejo, Marcelo; Fuentes, Gonzalo; Marı́n, Reinaldo

doi:10.1016/j.bbadis.2020.165948

Cited by 28 publications

(41 citation statements)

References 139 publications

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“…Some studies have shown that pregnant women and fetuses have relatively independent adiponectin regulatory systems. Adiponectin cannot directly pass through the placental barrier, and offspring are not affected by maternal adiponectin levels [43]. This conclusion confirms that there is no correlation between the APN level of offspring mice in adulthood and that of maternal mice in early pregnancy.…”

Section: Discussionsupporting

confidence: 60%

Effects of exogenous adiponectin supplementation in early pregnant PCOS mice on the metabolic syndrome of adult female offspring

et al. 2021

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Objective PCOS is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities. At present, PCOS has been confirmed to have a certain genetic background. Compared with healthy women, the vast majority of PCOS patients have hyperandrogenemia, and this excessive androgen exposure during pregnancy may affect the development of female fetuses. The aim of the current study was to investigate the effect of adiponectin intervention during early pregnancy of obese mice with PCOS on the metabolic phenotype of adult female offspring. Methods After the PCOS model was established, C57BL/6J mice were divided into maternal-control, maternal-PCOS, and maternal-PCOS + APN groups. DHEA-induced PCOS mice were supplemented with adiponectin (10 mg/kg/day) in the early pregnancy in order to eliminate adverse hormone exposure and then traced for endocrine indicators in their adult female offspring, which were observed for metabolism syndrome or endocrine disturbance and exhibited the main effects of APN. To further explore the underlying mechanism, the relative expressions of phosphorylated AMPK, PI3K, and Akt were detected in the ovaries of offspring mice. Results The serum testosterone level of the maternal-PCOS + APN group in early pregnancy was significantly lower than that of the maternal-PCOS group (p < 0.01). The serum testosterone level in the offspring-PCOS + APN group was significantly lower than in the offspring-PCOS group (p <0.05), the diestrus time characterized by massive granulocyte aggregation in the estrus cycle was significantly shorter than in the offspring-PCOS group (p<0.05), and the phenotypes of PCOS-like reproductive disorders and metabolic disorders, such as obesity, insulin resistance, impaired glucose tolerance, and hyperlipidemia, were also significantly improved in the offspring-PCOS + APN group (p < 0.05). Compared with the control group, the expression levels of phosphorylated AMPK, PI3K, and Akt in the offspring-PCOS group were significantly decreased (p < 0.05), while those in the offspring-PCOS + APN group were significantly increased (p < 0.05). Conclusions APN intervention in early pregnancy significantly reduced the adverse effects of maternal obesity and high androgen levels during pregnancy on female offspring and corrected the PCOS-like endocrine phenotype and metabolic disorders of adult female offspring. This effect may be caused by the activation of the AMPK/PI3K-Akt signaling pathway in PCOS offspring mice.

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Section: Discussionsupporting

confidence: 60%

Effects of exogenous adiponectin supplementation in early pregnant PCOS mice on the metabolic syndrome of adult female offspring

et al. 2021

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“…Some studies have shown that pregnant women and fetuses have relatively independent adiponectin regulatory systems. Adiponectin cannot directly pass through the placental barrier, and offspring are not affected by maternal adiponectin levels [43]. This conclusion con rms that there is no correlation between the APN level of offspring mice in adulthood and that of maternal mice in early pregnancy.…”

Section: Discussionmentioning

confidence: 69%

Effects of Exogenous Adiponectin Supplementation in Early Pregnant PCOS Mice on the Metabolic Syndrome of Adult Female Offspring

Zuo

Liao

Zhang

et al. 2020

Preprint

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Objective: PCOS is a heterogeneous endocrine disorder with both reproductive and metabolic abnormalities. At present, PCOS has been confirmed to have a certain genetic background. Compared with healthy women, the vast majority of PCOS patients have hyperandrogenemia, and this excessive androgen exposure during pregnancy may affect the development of female fetuses. The aim of the current study was to investigate the effect of adiponectin intervention during early pregnancy of obese mice with PCOS on the metabolic phenotype of adult female offspring.Methods: After the PCOS model was established, C57BL/6J mice were divided into maternal-control, maternal-PCOS, and maternal-PCOS+APN groups. DHEA-induced PCOS mice were supplemented with adiponectin (10 mg/kg/day) in the early pregnancy in order to eliminate adverse hormone exposure and then traced for endocrine indicators in their adult female offspring, which were observed for metabolism syndrome or endocrine disturbance and exhibited the main effects of APN. To further explore the underlying mechanism, the relative expressions of phosphorylated AMPK, PI3K, and Akt were detected in the ovaries of offspring mice.Results: The serum testosterone level of the maternal-PCOS+APN group in early pregnancy was significantly lower than that of the maternal-PCOS group (p < 0.01). The serum testosterone level in the offspring-PCOS+APN group was significantly lower than in the offspring-PCOS group (p＜0.05), the diestrus time characterized by massive granulocyte aggregation in the estrus cycle was significantly shorter than in the offspring-PCOS group (p＜0.05), and the phenotypes of PCOS-like reproductive disorders and metabolic disorders, such as obesity, insulin resistance, impaired glucose tolerance, and hyperlipidemia, were also significantly improved in the offspring-PCOS+APN group (p＜0.05). Compared with the control group, the expression levels of phosphorylated AMPK, PI3K, and Akt in the offspring-PCOS group were significantly decreased (p＜0.05), while those in the offspring-PCOS+APN group were significantly increased (p＜0.05).Conclusions: APN intervention in early pregnancy significantly reduced the adverse effects of maternal obesity and high androgen levels during pregnancy on female offspring and corrected the PCOS-like endocrine phenotype and metabolic disorders of adult female offspring. This effect may be caused by the activation of the AMPK/PI3K-Akt signaling pathway in PCOS offspring mice.

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“…Alterations in the natural physiological adaptations ensuring the normal growth and development of the foetus lead to the development of adult metabolic disorders, including overweight and obesity, diabetes mellitus, hypertension and cancer. [1][2][3][4][5][6][7][8] An increasing prevalence of type 2 diabetes mellitus (T2DM) has been reported worldwide. [9][10][11] Moreover, T2DM together with obesity 11,12 lead to a metabolic condition called diabesity.…”

Section: Introductionmentioning

confidence: 99%

Gestational diabesity and foetoplacental vascular dysfunction

et al. 2021

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Gestational diabetes mellitus (GDM) shows a deficiency in the metabolism of Dglucose and other nutrients, thereby negatively affecting the foetoplacental vascular endothelium. Maternal hyperglycaemia and hyperinsulinemia play an important role in the aetiology of GDM. A combination of these and other factors predisposes women to developing GDM with pre-pregnancy normal weight, viz. classic GDM. However, women with GDM and prepregnancy obesity (gestational diabesity, GDty) or overweight (GDMow) show a different metabolic status than women with classic GDM. GDty and GDMow are associated with altered l-arginine/nitric oxide and insulin/adenosine axis signalling in the human foetoplacental microvascular and macrovascular endothelium. These alterations differ from those observed in classic GDM. Here, we have reviewed the consequences of GDty and GDMow in the modulation of foetoplacental endothelial cell function, highlighting studies describing the modulation of intracellular pH homeostasis and the potential implications of NO generation and adenosine signalling in GDty-associated foetal vascular insulin resistance. Moreover, with an increase in the rate of obesity in women of childbearing 2 of 15 | CORNEJO Et al.

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Mitochondrial dysfunction in the fetoplacental unit in gestational diabetes mellitus

Cited by 28 publications

References 139 publications

Effects of exogenous adiponectin supplementation in early pregnant PCOS mice on the metabolic syndrome of adult female offspring

Effects of exogenous adiponectin supplementation in early pregnant PCOS mice on the metabolic syndrome of adult female offspring

Effects of Exogenous Adiponectin Supplementation in Early Pregnant PCOS Mice on the Metabolic Syndrome of Adult Female Offspring

Gestational diabesity and foetoplacental vascular dysfunction

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