Obesity and regulation of human placental lactogen production in pregnancy

Cattini, Peter A.; Jin, Yan; Jarmasz, Jessica S.; Noorjahan, Noshin; Bock, Margaret E.

doi:10.1111/jne.12859

Cited by 21 publications

(25 citation statements)

References 95 publications

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“…On the other hand, placental lactogens are exclusively synthesized during pregnancy by fetal syncytiotrophoblasts and include human placental lactogen (hPL), human chorionic somatomammotropin A and B (hCS-A and hCS-B), and the placental growth hormone (PGH). Evolutionary studies indicate that placental lactogens are closely related in their chemical structure to the human Growth Hormone (GH) as a result of three duplications and one deletion in the GH gene [ 88 ]. Derived from this structural homology, lactogens share with GH their binding capacity to both somatogenic and lactogenic receptors [ 89 ].…”

Section: Role Of Placenta In the Endocrine Milieu Of Gdmmentioning

confidence: 99%

Immunoendocrine Dysregulation during Gestational Diabetes Mellitus: The Central Role of the Placenta

Olmos-Ortíz

Flores-Espinosa

Díaz

et al. 2021

IJMS

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Gestational Diabetes Mellitus (GDM) is a transitory metabolic condition caused by dysregulation triggered by intolerance to carbohydrates, dysfunction of beta-pancreatic and endothelial cells, and insulin resistance during pregnancy. However, this disease includes not only changes related to metabolic distress but also placental immunoendocrine adaptations, resulting in harmful effects to the mother and fetus. In this review, we focus on the placenta as an immuno-endocrine organ that can recognize and respond to the hyperglycemic environment. It synthesizes diverse chemicals that play a role in inflammation, innate defense, endocrine response, oxidative stress, and angiogenesis, all associated with different perinatal outcomes.

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Section: Role Of Placenta In the Endocrine Milieu Of Gdmmentioning

confidence: 99%

Immunoendocrine Dysregulation during Gestational Diabetes Mellitus: The Central Role of the Placenta

Olmos-Ortíz

Flores-Espinosa

Díaz

et al. 2021

IJMS

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“…The transgene may be inserted randomly or may be inserted into a selected genetic locus. Random insertion is simpler, but tissue expression may be influenced by proximity to strong enhancer elements; this potential problem can be avoided by adding locus control regions to the transgene, but at the cost of a larger and more complex transgene ( 15 ). Further, the genetic background of the mouse strain must be considered, as outcomes may vary with genetic background.…”

Section: Micementioning

confidence: 99%

Lessons From APOL1 Animal Models

et al. 2021

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African-Americans have a three-fold higher rate of chronic kidney disease compared to European-Americans. Much of this excess risk is attributed to genetic variants in APOL1, encoding apolipoprotein L1, that are present only in individuals with sub-Saharan ancestry. Although 10 years have passed since the discovery of APOL1 renal risk variants, the mechanisms by which APOL1 risk allele gene products damage glomerular cells remain incompletely understood. Many mechanisms have been reported in cell culture models, but few have been demonstrated to be active in transgenic models. In this narrative review, we will review existing APOL1 transgenic models, from flies to fish to mice; discuss findings and limitations from studies; and consider future research directions.

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“…Given the importance of placental hormones for fetal growth, maternal nurturing and the offspring’s behavioural outcomes, placental endocrine insufficiency may mediate the well-established relationship between prenatal adversities experienced by the mother and these undesirable outcomes for both her and her offspring. Evidence that these observations in experimental models are relevant to human pregnancy may come from studies of maternal obesity ( 70 , 71 ) and depression ( 72 , 73 ) where lower level of placental lactogen has been reported. However, further work is required to link specific placental hormone deficiencies to neurological disorders in human populations.…”

Section: Discussionmentioning

confidence: 96%

Placental endocrine insufficiency programs anxiety, deficits in cognition and atypical social behaviour in offspring

Harrison

Creeth

Tyson

et al. 2021

Human Molecular Genetics

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Abnormally elevated expression of the imprinted PHLDA2 gene has been reported in the placenta of human babies that are growth restricted in utero in several studies. We previously modelled this gene alteration in mice and found that just two-fold increased expression of Phlda2 resulted in placental endocrine insufficiency. In addition, elevated Phlda2 was found to drive fetal growth restriction (FGR) of transgenic offspring and impaired maternal care by their wild type mothers. Being born small and being exposed to suboptimal maternal care have both been associated with the increased risk of mental health disorders in human populations. In the current study we probed behavioural consequences of elevated Phlda2 for the offspring. We discovered increased anxiety-like behaviours, deficits in cognition and atypical social behaviours, with the greatest impact on male offspring. Subsequent analysis revealed alterations in the transcriptome of the adult offspring hippocampus, hypothalamus, and amygdala, regions consistent with these behavioural observations. The inclusion of a group of fully wild type controls raised in a normal maternal environment allowed us to attribute behavioural and molecular alterations to the adverse maternal environment induced by placental endocrine insufficiency rather than the specific gene change of elevated Phlda2. Our work demonstrates that a highly common alteration reported in human fetal growth restriction is associated with negative behavioural outcomes later in life. Importantly, we also establish the experimental paradigm that placental endocrine insufficiency can program atypical behaviour in offspring highlighting the under-appreciated role of placental endocrine insufficiency in driving disorders of later life behaviour.

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Obesity and regulation of human placental lactogen production in pregnancy

Cited by 21 publications

References 95 publications

Immunoendocrine Dysregulation during Gestational Diabetes Mellitus: The Central Role of the Placenta

Immunoendocrine Dysregulation during Gestational Diabetes Mellitus: The Central Role of the Placenta

Lessons From APOL1 Animal Models

Placental endocrine insufficiency programs anxiety, deficits in cognition and atypical social behaviour in offspring

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