30th anniversary for the developmental origins of endocrinology

Limesand, Sean W.; Thornburg, Kent L.; Harding, Jane E

doi:10.1530/joe-19-0227

Cited by 12 publications

(8 citation statements)

References 16 publications

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“…A recent meta-analysis with over four million individuals showed a 50% increase in T2DM onset in those with abnormal birth weight,15 defined as either too low (<3000 g) or too high (>4500 g). The U-shaped risk curve adds evidence to the hypothesis of the fetal origin of the metabolic syndrome 16. This hypothesis postulates that intrauterine adversity triggers various adaptations in anticipation of similar conditions in postnatal life,17 sparing vital organs such as the brain at the expense of other organs such as the pancreas.…”

Section: Introductionmentioning

confidence: 79%

“…The mechanism by which extreme birth weight increases the risk of diabetes onset is still unclear,16 and our work here was not aimed to address this. The leading hypothesis in metabolic science, first developed by Hales and Barker,17 posits that in-utero adversity leads to epigenetic changes that allow the fetus to cope with a predicted adverse environment by prioritizing energy storage.…”

Section: Discussionmentioning

confidence: 98%

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Birth weight, family history of diabetes and diabetes onset in schizophrenia

Fernández-Egea

Walker

Ziauddeen

et al. 2020

BMJ Open Diab Res Care

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IntroductionThe prevalence of diabetes in schizophrenia is twice that in the general population, but there are few reliable predictors of which individuals will develop glucose dysregulation.ObjectiveTo test if abnormal birth weight (either too low or too high) and parental diabetes, both variables that can be ascertained in the clinic, can predict diabetes onset in patients with schizophrenia.Research design and methodsElectronic records of a cohort of 190 clozapine-treated patients (37% treated for more than 20 years) and Cox regression survival analysis (with any type of glucose dysregulation as the event) to account for differences in length of treatment before the event and age at clozapine treatment initiation.ResultsAge at clozapine initiation (Exp(B)=1.098; p<0.001), family history of diabetes (Exp(B)=2.299; p=0.049) and birth weight2 (Exp(B)=0.999; p=0.013) were significant predictors of glucose dysregulation onset, while gender was not (Exp(B)=0.1.350; p=0.517). Among individuals with 10 years of follow-up, 80% of those with both abnormal birth weight and a family history of diabetes developed diabetes compared with 56% with only abnormal birth weight, 40% with only a family history of diabetes and 20% in those with neither.ConclusionsSince 48% of cases had at least one risk factor and 6% had both risk factors, there is a substantial proportion of patients for whom preventive strategies could be implemented.

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Section: Introductionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 98%

Birth weight, family history of diabetes and diabetes onset in schizophrenia

Fernández-Egea

Walker

Ziauddeen

et al. 2020

BMJ Open Diab Res Care

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“…The research in DOHaD, which has increased substantially from the 1990s, has shown that the maternal environment during pregnancy can affect programming during development and increase the risk of offspring developing long-term diseases [ 3 , 4 ]. Professor David Barker was one of the pioneer researchers to demonstrate the DOHaD phenomenon in his epidemiological studies in 1989, linking perinatal weight and the subsequent growth trajectory with health and disease risk in later life [ 5 , 6 ]. Since the development of the DOHaD hypothesis, many authors have linked birth weight with the development of NCDs.…”

Section: Introductionmentioning

confidence: 99%

Epigenetics in the Uterine Environment: How Maternal Diet and ART May Influence the Epigenome in the Offspring with Long-Term Health Consequences

Peral-Sanchez

Hojeij

Ojeda

et al. 2021

Genes

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The societal burden of non-communicable disease is closely linked with environmental exposures and lifestyle behaviours, including the adherence to a poor maternal diet from the earliest preimplantation period of the life course onwards. Epigenetic variations caused by a compromised maternal nutritional status can affect embryonic development. This review summarises the main epigenetic modifications in mammals, especially DNA methylation, histone modifications, and ncRNA. These epigenetic changes can compromise the health of the offspring later in life. We discuss different types of nutritional stressors in human and animal models, such as maternal undernutrition, seasonal diets, low-protein diet, high-fat diet, and synthetic folic acid supplement use, and how these nutritional exposures epigenetically affect target genes and their outcomes. In addition, we review the concept of thrifty genes during the preimplantation period, and some examples that relate to epigenetic change and diet. Finally, we discuss different examples of maternal diets, their effect on outcomes, and their relationship with assisted reproductive technology (ART), including their implications on epigenetic modifications.

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“…It is well established that a suboptimal intrauterine environment results in fetal adaptations with adverse consequences persisting after birth, throughout the lifespan and in future generations (1)(2)(3)(4)(5). An adverse intrauterine environment has been associated with the development of a wide range of non-communicable diseases, including obesity, diabetes and cardiovascular disease (2,(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of mechanistic target of rapamycin signaling decreases levels of O-GlcNAc transferase and increases serotonin release in the human placenta

et al. 2020

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Changes in placental function, in particular down-regulation of placental O-GlcNAc transferase (OGT) in response to maternal stress and increased placental secretion of serotonin into the fetal circulation following maternal infection, have been mechanistically linked to adverse neurodevelopment in mice. We hypothesized that mTOR signaling is a key regulator of trophoblast serotonin synthesis and OGT protein expression and that serotonin is secreted by the human placenta into the fetal circulation. Placental homogenates (n=46) from elective terminations at 8-22 weeks of gestation and from healthy term women were sexed and the protein levels of OGT and enzymes involved in serotonin synthesis was determined. Primary human trophoblast (PHT) cells were isolated from normal term placenta (n=27), cultured and transfected (n=8) with siRNA targeting a scramble sequence (control), raptor (inhibits mTOR Complex 1), or rictor (inhibits mTOR Complex 2). Subsequently, conditioned media and PHT cell lysates were collected. Free serotonin concentration was measured using ELISA in cell culture media and in platelet-depleted normal term umbilical vein and artery plasma (n=38). Both mTORC1 and mTORC2 inhibition down-regulated OGT levels in PHT cells. The level of serotonin synthesis enzyme TPH-1 was higher in early gestation female placentas and at term serotonin concentration was 3-fold higher in the umbilical vein than in the umbilical artery. Inhibition of mTORC2, but not mTORC1, increased cultured PHT cell serotonin secretion. Our data is consistent with the model that mTOR signaling is a key regulator of trophoblast serotonin synthesis and OGT protein expression.

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30th anniversary for the developmental origins of endocrinology

Cited by 12 publications

References 16 publications

Birth weight, family history of diabetes and diabetes onset in schizophrenia

Birth weight, family history of diabetes and diabetes onset in schizophrenia

Epigenetics in the Uterine Environment: How Maternal Diet and ART May Influence the Epigenome in the Offspring with Long-Term Health Consequences

Inhibition of mechanistic target of rapamycin signaling decreases levels of O-GlcNAc transferase and increases serotonin release in the human placenta

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