Influence of prenatal stress on metabolic abnormalities induced by postnatal intake of a high-fat diet in BALB/c mice

Juárez, Yamila Raquel; Quiroga, Sofía; Prochnik, Andrés; Wald, Miriam; Tellechea, Mariana Lorena; Genaro, Ana Marı́a; Burgueño, Adriana Laura

doi:10.1017/s2040174420000987

Cited by 4 publications

(2 citation statements)

References 83 publications

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“…[ 58 ] Consistent with previous reports, [ 59,60 ] we observed an increased expression of the leptin mRNA in adipose tissue of young adult offspring exposure to maternal and/or post‐weaning HFD, although serum leptin level only increased in MHC group at 9 weeks old. We also observed a dramatically increase in resistin gene expression, which was consistent with an earlier report, [ 61 ] but an increase in resistin serum level was not observed. Whether the inconsistency between mRNA and secreted protein level is related to pre‐translational modification needs further confirmation.…”

Section: Discussionsupporting

confidence: 93%

Sex‐Specific Effects of Maternal and Post‐Weaning High‐Fat Diet on Adipose Tissue Remodeling and Asprosin Expression in Mice Offspring

Zhao

Jiang

Chen

et al. 2022

Molecular Nutrition Food Res

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Scope Perinatal high‐fat diet (HFD) increases risk of metabolic disorders in offspring. Adipose tissue remodeling is associated with metabolic syndrome. The current study characterizes the profile of maternal HFD‐induced changes in adipose tissue remodeling and adipokines expression in mice offspring. Methods and Results Female C57BL/6 mice are fed with CHOW or HFD for 2 weeks before mating, throughout gestation and lactation. At weaning, pups are randomly fed with CHOW or HFD, resulting in eight groups according to sex and maternal diet: Male CHOW‐CHOW (MCC), Male CHOW‐HFD (MCH), Male HFD‐CHOW (MHC), Male HFD‐HFD (MHH), Female CHOW‐CHOW (FCC), Female CHOW‐HFD (FCH), Female HFD‐CHOW (FHC), and Female HFD‐HFD (FHH). Increased body weight, impaired glucose tolerance, increased adipose tissue mass and hypertrophy, and decreased circulating asprosin level are only observed in male offspring exposure to maternal HFD. Serum asprosin level negatively correlates with fasting blood glucose, serum cholesterol (CHO), and high‐density lipoprotein (HDL) levels, while positively correlates with serum low‐density lipoprotein (LDL) and glutamate‐oxaloacetate transaminase (GOT) levels in male offspring. A combination of genetic and biochemical analyses of adipokines shows the depot‐ and sex‐specific changes in response to maternal and/or post‐weaning HFD. Conclusion This study's results reveal the differential metabolic changes in response to maternal and/or post‐weaning HFD in male and female offspring. The effect of maternal HFD on metabolic phonotype is more obvious in male offspring, supporting the notion that males are more susceptible to HFD‐induced metabolic disorders.

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Section: Discussionsupporting

confidence: 93%

Sex‐Specific Effects of Maternal and Post‐Weaning High‐Fat Diet on Adipose Tissue Remodeling and Asprosin Expression in Mice Offspring

Zhao

Jiang

Chen

et al. 2022

Molecular Nutrition Food Res

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“…Prenatal stress also exerts sex-specific effects on metabolism, although findings are mixed. This includes evidence of a female specific elevation in cholesterol levels, and a male specific fall in body weight in prenatally stressed mice (531), whereas others report a male specific increase in cholesterol and triglycerides (532).…”

Section: Sex Effectsmentioning

confidence: 99%

The sex-dependent response to psychosocial stress and ischaemic heart disease

Helman

Headrick

Stapelberg

et al. 2023

Front. Cardiovasc. Med.

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Stress is an important risk factor for modern chronic diseases, with distinct influences in males and females. The sex specificity of the mammalian stress response contributes to the sex-dependent development and impacts of coronary artery disease (CAD). Compared to men, women appear to have greater susceptibility to chronic forms of psychosocial stress, extending beyond an increased incidence of mood disorders to include a 2- to 4-fold higher risk of stress-dependent myocardial infarction in women, and up to 10-fold higher risk of Takotsubo syndrome—a stress-dependent coronary-myocardial disorder most prevalent in post-menopausal women. Sex differences arise at all levels of the stress response: from initial perception of stress to behavioural, cognitive, and affective responses and longer-term disease outcomes. These fundamental differences involve interactions between chromosomal and gonadal determinants, (mal)adaptive epigenetic modulation across the lifespan (particularly in early life), and the extrinsic influences of socio-cultural, economic, and environmental factors. Pre-clinical investigations of biological mechanisms support distinct early life programming and a heightened corticolimbic-noradrenaline-neuroinflammatory reactivity in females vs. males, among implicated determinants of the chronic stress response. Unravelling the intrinsic molecular, cellular and systems biological basis of these differences, and their interactions with external lifestyle/socio-cultural determinants, can guide preventative and therapeutic strategies to better target coronary heart disease in a tailored sex-specific manner.

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Maternal preconception stress produces sex-specific effects at the maternal:fetal interface to impact offspring development and phenotypic outcomes

Cissé,

Montgomery,

Zierden

et al. 2023

Biology of Reproduction

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Entering pregnancy with a history of adversity, including adverse childhood experiences (ACEs) and racial discrimination stress, is a predictor of negative maternal and fetal health outcomes. Little is known about the biological mechanisms by which preconception adverse experiences are stored and impact future offspring health outcomes. In our maternal preconception stress (MPS) model, female mice underwent chronic stress from postnatal days 28–70 and were mated two weeks post-stress. MPS dams blunted the pregnancy-induced shift in the circulating extracellular vesicle proteome and reduced glucose tolerance at mid-gestation, suggesting a shift in pregnancy adaptation. To investigate MPS effects at the maternal:fetal interface, we probed the mid-gestation placental, uterine, and fetal brain tissue transcriptome. Male and female placentas differentially regulated expression of genes involved in growth and metabolic signaling in response to gestation in an MPS dam. We also report novel offspring sex- and MPS- specific responses in the uterine tissue apposing these placentas. In the fetal compartment, MPS female offspring reduced expression of neurodevelopmental genes. Using a ribosome-tagging transgenic approach we detected a dramatic increase in genes involved in chromatin regulation in a PVN enriched neuronal population in females at PN21. While MPS had an additive effect on high fat diet induced weight gain in male offspring, both MPS and high fat diet were necessary to induce significant weight gain in female offspring. These data highlight the preconception period as a determinant of maternal health in pregnancy and provides novel insights into mechanisms by which maternal stress history impacts offspring developmental programming.

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Influence of prenatal stress on metabolic abnormalities induced by postnatal intake of a high-fat diet in BALB/c mice

Cited by 4 publications

References 83 publications

Sex‐Specific Effects of Maternal and Post‐Weaning High‐Fat Diet on Adipose Tissue Remodeling and Asprosin Expression in Mice Offspring

Sex‐Specific Effects of Maternal and Post‐Weaning High‐Fat Diet on Adipose Tissue Remodeling and Asprosin Expression in Mice Offspring

The sex-dependent response to psychosocial stress and ischaemic heart disease

Maternal preconception stress produces sex-specific effects at the maternal:fetal interface to impact offspring development and phenotypic outcomes

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