Maternal high fat diet programs hypothalamic-pituitary-adrenal function in adult rat offspring

Niu, Xiaoting; Wu, Xingwang; Ying, Anna; Shao, Baiqi; Li, Xiaofeng; Zhang, Wanli; Lin, Chengcheng; Lin, Yuanshao

doi:10.1016/j.psyneuen.2018.12.003

Cited by 20 publications

(11 citation statements)

References 42 publications

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“…In mice and rats, maternal HFD has been reported to lead to increased maternal levels of corticosterone, which under this diet more readily passed through the placenta to the fetus [120]. The offspring had long-term elevated corticosterone levels, a dysregulated HPA-axis and were more sensitive to stressors with amygdala playing a role [121]. In humans, higher maternal early pregnancy BMI was reported to be associated with lower morning salivary cortisol in the offspring at adult age [122].…”

Section: Glucocorticoids and The Hypothalamicpituitary-adrenal (Hpa) mentioning

confidence: 99%

Relationship of prenatal maternal obesity and diabetes to offspring neurodevelopmental and psychiatric disorders: a narrative review

et al. 2020

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Obesity and diabetes is a worldwide public health problem among women of reproductive age. This narrative review highlights recent epidemiological studies regarding associations of maternal obesity and diabetes with neurodevelopmental and psychiatric disorders in offspring, and provides an overview of plausible underlying mechanisms and challenges for future human studies. A comprehensive search strategy selected terms that corresponded to the domains of interest (maternal obesity, different types of diabetes, offspring cognitive functions and neuropsychiatric disorders). The databases searched for articles published between January 2010 and April 2019 were PubMed, Web of Science and CINAHL. Evidence from epidemiological studies strongly suggests that maternal pre-pregnancy obesity is associated with increased risks for autism spectrum disorder, attention-deficit hyperactivity disorder and cognitive dysfunction with modest effect sizes, and that maternal diabetes is associated with the risk of the former two disorders. The influence of maternal obesity on other psychiatric disorders is less well studied, but there are reports of associations with increased risks for offspring depression, anxiety, schizophrenia and eating disorders, at modest effect sizes. It remains unclear whether these associations are due to intrauterine mechanisms or explained by confounding family-based sociodemographic, lifestyle and genetic factors. The plausible underlying mechanisms have been explored primarily in animal models, and are yet to be further investigated in human studies.

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Section: Glucocorticoids and The Hypothalamicpituitary-adrenal (Hpa) mentioning

confidence: 99%

Relationship of prenatal maternal obesity and diabetes to offspring neurodevelopmental and psychiatric disorders: a narrative review

et al. 2020

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“…For example, Sasaki et al's finding of decreased basal corticosterone in adult offspring was conducted in the middle of the light cycle, whereas Walker and colleagues found increased basal corticosterone during the dark but not light cycle (Sasaki et al, 2013;Walker et al, 2008). Niu et al sampled basal plasma corticosterone over a 24-h period and found an overall increase secondary to increases in both pulse frequency and amplitude of corticosterone secretion (Niu et al, 2019). Consistent with Sasaki's group, however, Niu and colleagues went on to demonstrate that offspring have heighted stress responsivity, exhibiting increased corticosterone levels and slower negative feedback following acute restraint stress, and additionally that they exhibit attenuated habituation to repeated restraint stress (Niu et al, 2019).…”

Section: Hpa Axis and Neuroendocrine Hormonesmentioning

confidence: 99%

“…Niu et al sampled basal plasma corticosterone over a 24-h period and found an overall increase secondary to increases in both pulse frequency and amplitude of corticosterone secretion (Niu et al, 2019). Consistent with Sasaki's group, however, Niu and colleagues went on to demonstrate that offspring have heighted stress responsivity, exhibiting increased corticosterone levels and slower negative feedback following acute restraint stress, and additionally that they exhibit attenuated habituation to repeated restraint stress (Niu et al, 2019). Niu also showed that maternal HFD-induced stress sensitization was dependent on the amygdala (Niu et al, 2019).…”

Section: Hpa Axis and Neuroendocrine Hormonesmentioning

confidence: 99%

Maternal stressors and the developmental origins of neuropsychiatric risk

Khambadkone

Cordner

Tamashiro

2020

Frontiers in Neuroendocrinology

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The maternal environment during pregnancy is critical for fetal development and perinatal perturbations can prime offspring disease risk. Here, we briefly review evidence linking two wellcharacterized maternal stressors -psychosocial stress and infection -to increased neuropsychiatric risk in offspring. In the current climate of increasing obesity and globalization of the Western-style diet, maternal overnutrition emerges as a pressing public health concern. We focus our attention on recent epidemiological and animal model evidence showing that, like psychosocial stress and infection, maternal overnutrition can also increase offspring neuropsychiatric risk. Using lessons learned from the psychosocial stress and infection literature, we discuss how altered maternal and placental physiology in the setting of overnutrition may contribute to abnormal fetal development and resulting neuropsychiatric outcomes. A better understanding of converging pathophysiological pathways shared between stressors may enable development of interventions against neuropsychiatric illnesses that may be beneficial across stressors.

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“…In the mother, elevated CORT and inflammatory molecules can be transmitted to developing offspring both prenatally and during lactation [63][64][65]. It is possible that exposures to elevated levels of CORT and inflammation during these critical points in development program HPA axis activity and glucocorticoid signalling in offspring, enabling adaptation to chronic inflammation experienced in perinatal life [27][28][29][30][31][32][33]. Inasmuch as these alterations rendered by perinatal cues of inflammation do not match the postnatal environment, they may constitute a developmental mechanism leading to phenotypic changes in behavior later in life.…”

Section: Sex-specific Alterations To Cort+lps Challenge In Hfd Offspringmentioning

confidence: 99%

“…In humans, maternal high-fat diet (HFD) is linked to metabolic disorders and anxiety in children [20][21][22][23][24][25][26]. In rodents, offspring born to obese dams, exhibit altered levels of GR and inflammatory genes in brain regions that regulate the HPA axis [27][28][29][30][31][32][33]. For example, our lab found increases in NFκB and IL6 transcript levels in the amygdala of females in basal conditions, along with decreased levels of CORT in serum of both sexes [27].…”

Section: Introductionmentioning

confidence: 98%

Maternal high-fat diet induces sex-specific changes to glucocorticoid and inflammatory signaling in response to corticosterone and lipopolysaccharide challenge in adult rat offspring

Wijenayake

Rahman

Lum

et al. 2020

J Neuroinflammation

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Background: Maternal obesity as a result of high levels of saturated fat (HFD) consumption leads to significant negative health outcomes in both mother and exposed offspring. Offspring exposed to maternal HFD show sexspecific alterations in metabolic, behavioral, and endocrine function, as well as increased levels of basal neuroinflammation that persists into adulthood. There is evidence that psychosocial stress or exogenous administration of corticosterone (CORT) potentiate inflammatory gene expression; however, the response to acute CORT or immune challenge in adult offspring exposed to maternal HFD during perinatal life is unknown. We hypothesize that adult rat offspring exposed to maternal HFD would show enhanced pro-inflammatory gene expression in response to acute administration of CORT and lipopolysaccharide (LPS) compared to control animals, as a result of elevated basal pro-inflammatory gene expression. To test this, we examined the effects of acute CORT and/or LPS exposure on pro and anti-inflammatory neural gene expression in adult offspring (male and female) with perinatal exposure to a HFD or a control house-chow diet (CHD).Methods: Rat dams consumed HFD or CHD for four weeks prior to mating, during gestation, and throughout lactation. All male and female offspring were weaned on to CHD. In adulthood, offspring were 'challenged' with administration of exogenous CORT and/or LPS, and quantitative PCR was used to measure transcript abundance of glucocorticoid receptors and downstream inflammatory markers in the amygdala, hippocampus, and prefrontal cortex.(Continued on next page) Results: In response to CORT alone, male HFD offspring showed increased levels of anti-inflammatory transcripts, whereas in response to LPS alone, female HFD offspring showed increased levels of pro-inflammatory transcripts. In addition, male HFD offspring showed greater pro-inflammatory gene expression and female HFD offspring exhibited increased anti-inflammatory gene expression in response to simultaneous CORT and LPS administration.Conclusions: These findings suggest that exposure to maternal HFD leads to sex-specific changes that may alter inflammatory responses in the brain, possibly as an adaptive response to basal neuroinflammation.

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Maternal high fat diet programs hypothalamic-pituitary-adrenal function in adult rat offspring

Cited by 20 publications

References 42 publications

Relationship of prenatal maternal obesity and diabetes to offspring neurodevelopmental and psychiatric disorders: a narrative review

Relationship of prenatal maternal obesity and diabetes to offspring neurodevelopmental and psychiatric disorders: a narrative review

Maternal stressors and the developmental origins of neuropsychiatric risk

Maternal high-fat diet induces sex-specific changes to glucocorticoid and inflammatory signaling in response to corticosterone and lipopolysaccharide challenge in adult rat offspring

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