Fetal Endocrinology

Katugampola, Harshini; Gevers, Evelien; Dattani, Mehul

doi:10.1002/9781119152712.ch3

Cited by 4 publications

(4 citation statements)

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“…Studies show that these are observed from the very early neonatal, prepubertal and post-pubertal periods and appear to persist through to adulthood [121][122][123][124]. Research indicates that excessive cortisol exposure during early gestation triggers an early shift from tissue accretion to differentiation, thereby reducing fetal growth in various vital organs such as the brain, heart, liver, kidney and adrenal glands [125][126][127]. This process often leads to the clinical manifestation of intrauterine growth restriction (IUGR), characterized by the development of growth-retarded fetuses [128,129].…”

Section: Discussionmentioning

confidence: 99%

Pregestational Prediabetes Induces Maternal Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation and Results in Adverse Fetal Outcomes: Influences on HPA Axis and Development

Ngema,

Xulu,

Khathi

et al. 2024

Preprint

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Maternal type 2 diabetes mellitus (T2DM) has been shown to result in fetal programming of the hypothalamus-pituitary-adrenal (HPA) axis, leading to adverse fetal outcomes. T2DM is preceded by prediabetes and shares similar pathophysiological complications. However, no studies have investigated the effects of maternal prediabetes on fetal HPA axis function and postnatal offspring development, hence this study. Pre-diabetic (PD) and non-pre-diabetic (NPD) female Sprague Dawley rats were mated with non-prediabetic males. After gestation, male pups born from the PD and NPD groups were collected. Markers of HPA axis function, adrenocorticotropin hormone (ACTH) and corticosterone were measured in all dams and pups. Glucose tolerance and expression of mineralocorticoid (MR) and glucocorticoid (GR) receptors were further measured in all pups at birth and their developmental milestones. The results demonstrated increased basal concentrations of ACTH and corticosterone in the dams from the PD group by comparison to NPD. Furthermore, the results show an increase in pups ACTH and corticosterone concentrations, impaired glucose tolerance and dysregulated MR and GR expression in the PD group at all developmental milestones. These observations reveal that pregestational prediabetes is associated with maternal dysregulation of the HPA axis, impacting offspring HPA axis development along with impaired glucose handling.

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Section: Discussionmentioning

confidence: 99%

Pregestational Prediabetes Induces Maternal Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation and Results in Adverse Fetal Outcomes: Influences on HPA Axis and Development

Ngema,

Xulu,

Khathi

et al. 2024

Preprint

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show abstract

“…Studies show that there is increased adrenocortical function in children in the juvenile period who were exposed to GC in utero with increased fasting cortisol concentrations in adults [150,151]. The upregulation of postnatal HPA function in other species may reflect changes in the HPA axis at the level of the hypothalamus, pituitary or adrenal gland itself [152,153].…”

Section: Discussionmentioning

confidence: 99%

Pregestational Prediabetes Induces Maternal Hypothalamic–Pituitary–Adrenal (HPA) Axis Dysregulation and Results in Adverse Foetal Outcomes

Ngema,

Xulu,

Ngubane

et al. 2024

IJMS

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Maternal type 2 diabetes mellitus (T2DM) has been shown to result in foetal programming of the hypothalamic–pituitary–adrenal (HPA) axis, leading to adverse foetal outcomes. T2DM is preceded by prediabetes and shares similar pathophysiological complications. However, no studies have investigated the effects of maternal prediabetes on foetal HPA axis function and postnatal offspring development. Hence, this study investigated the effects of pregestational prediabetes on maternal HPA axis function and postnatal offspring development. Pre-diabetic (PD) and non-pre-diabetic (NPD) female Sprague Dawley rats were mated with non-prediabetic males. After gestation, male pups born from the PD and NPD groups were collected. Markers of HPA axis function, adrenocorticotropin hormone (ACTH) and corticosterone, were measured in all dams and pups. Glucose tolerance, insulin and gene expressions of mineralocorticoid (MR) and glucocorticoid (GR) receptors were further measured in all pups at birth and their developmental milestones. The results demonstrated increased basal concentrations of ACTH and corticosterone in the dams from the PD group by comparison to NPD. Furthermore, the results show an increase basal ACTH and corticosterone concentrations, disturbed MR and GR gene expression, glucose intolerance and insulin resistance assessed via the Homeostasis Model Assessment (HOMA) indices in the pups born from the PD group compared to NPD group at all developmental milestones. These observations reveal that pregestational prediabetes is associated with maternal dysregulation of the HPA axis, impacting offspring HPA axis development along with impaired glucose handling.

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“…The complications include IUGR, altered gene expression, HPA axis programming, glucose intolerance, increased risk of developing T2DM, and cardiovascular diseases, among others [ 67 , 137 , 184 , 185 , 186 ].…”

Section: Figurementioning

confidence: 99%

A Review of Fetal Development in Pregnancies with Maternal Type 2 Diabetes Mellitus (T2DM)-Associated Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation: Possible Links to Pregestational Prediabetes

Ngema,

Xulu,

Ngubane

et al. 2024

Biomedicines

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Research has identified fetal risk factors for adult diseases, forming the basis for the Developmental Origins of Health and Disease (DOHaD) hypothesis. DOHaD suggests that maternal insults during pregnancy cause structural and functional changes in fetal organs, increasing the risk of chronic diseases like type 2 diabetes mellitus (T2DM) in adulthood. It is proposed that altered maternal physiology, such as increased glucocorticoid (GC) levels associated with a dysregulated hypothalamic-pituitary-adrenal (HPA) axis in maternal stress and T2DM during pregnancy, exposes the fetus to excess GC. Prenatal glucocorticoid exposure reduces fetal growth and programs the fetal HPA axis, permanently altering its activity into adulthood. This programmed HPA axis is linked to increased risks of hypertension, cardiovascular diseases, and mental disorders in adulthood. With the global rise in T2DM, particularly among young adults of reproductive age, it is crucial to prevent its onset. T2DM is often preceded by a prediabetic state, a condition that does not show any symptoms, causing many to unknowingly progress to T2DM. Studying prediabetes is essential, as it is a reversible stage that may help prevent T2DM-related pregnancy complications. The existing literature focuses on HPA axis dysregulation in T2DM pregnancies and its link to fetal programming. However, the effects of prediabetes on HPA axis function, specifically glucocorticoid in pregnancy and fetal outcomes, are not well understood. This review consolidates research on T2DM during pregnancy, its impact on fetal programming via the HPA axis, and possible links with pregestational prediabetes.

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Fetal Endocrinology

Cited by 4 publications

References 351 publications

Pregestational Prediabetes Induces Maternal Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation and Results in Adverse Fetal Outcomes: Influences on HPA Axis and Development

Pregestational Prediabetes Induces Maternal Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation and Results in Adverse Fetal Outcomes: Influences on HPA Axis and Development

Pregestational Prediabetes Induces Maternal Hypothalamic–Pituitary–Adrenal (HPA) Axis Dysregulation and Results in Adverse Foetal Outcomes

A Review of Fetal Development in Pregnancies with Maternal Type 2 Diabetes Mellitus (T2DM)-Associated Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation: Possible Links to Pregestational Prediabetes

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