Prenatal programming of adult thyroid function by alcohol and thyroid hormones

Wilcoxon, Jennifer Slone; Redei, Eva E.

doi:10.1152/ajpendo.00022.2004

Cited by 56 publications

(78 citation statements)

References 69 publications

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“…Dams in the ethanol groups consumed 95.272.3 ml/day, and dams in the PF groups consumed 104.272.7 ml/day of their respective isocaloric diets, as previously reported. 31 This amount of ethanol-diet consumption is not different from the alcohol intake of dams of the same strain and age, which produced blood ethanol levels of 80 mg/100 ml at 0900 h and 127 mg/100 ml at 2000 h, as reported previously. 41 The body weight of alcohol-consuming dams was significantly lower than both of those on PF or control diets as described previously.…”

Section: Methodssupporting

confidence: 80%

“…The experimental procedures and morphometric analysis of the animals employed in these studies have been previously described in detail. 31 Briefly, adult male and female Sprague-Dawley rats (viral free, 56-58 days of age; Harlan, Indianapolis, IN, USA) were housed individually in a temperature-and humiditycontrolled vivarium with regular light-dark cycles (lights on at 0700 h and off at 1900 h). After 7 days of acclimatization, rats were mated by placing a female in the male cage overnight.…”

Section: Animalsmentioning

confidence: 99%

“…30 Our laboratory has recently demonstrated that alcohol-consuming rat dams have suppressed levels of plasma TSH, 3,3 0 ,5-triiodothyronine (T3), and T4, and their adult offspring show the classic hypothyroid hormonal profile. 31 We hypothesized that some of the behavioral abnormalities of FAE offspring are due to the suppressive effects of alcohol on the maternal and fetal hypothalamic-pituitary-thyroid (HPT) axes. Therefore, we elevated maternal thyroid hormone levels in utero to test this hypothesis.…”

mentioning

confidence: 99%

“…The thyroid hormone milieu and HPT function of the alcoholconsuming and control dams, with and without T4 administration, and their offspring are described in detail previously. 31 The goals of the present study were to determine the effects of FAE and prenatal T4 administration on the adult offspring's spatial learning and memory and depressive behavior, and on the expression of genes known to be associated with these behaviors in specific brain regions. The selected genes, GAP-43 [32][33][34] and glucocorticoid receptor (GR), 35 have been extensively studied and implicated in learning, and GR has also been suggested to influence behavior in the FST.…”

mentioning

confidence: 99%

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Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

et al. 2005

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Children prenatally exposed to alcohol typically exhibit behavioral abnormalities, including hyperactivity, learning deficits, and an increased prevalence of depression. Similar impairments are found in children of hypothyroid mothers, and we have shown that alcohol-consuming rat dams have suppressed hypothalamic-pituitary-thyroid (HPT) function. Therefore, we hypothesized that suppressed maternal thyroid hormonal milieu may contribute to the deleterious consequences of prenatal alcohol exposure. We aimed first to confirm and then to reverse the behavioral deficits in the fetal alcohol exposed (FAE) rat offspring by administration of thyroxine (T4) to the alcohol-consuming dams. Adult offspring prenatally exposed to ethanol (FAE; 35% ethanol-derived calories), pair-fed (PF) or control (C) diets were tested in the Morris water maze (MWM), the forced swim test (FST), and the open field test (OFT) to assess spatial learning, depressive behavior, and exploratory behavior/anxiety, respectively. Adult FAE offspring took longer to locate a hidden platform in the MWM and showed increased depressive behavior in the FST both of which were reversed by administration of T4 to the alcohol-consuming mother. We found sex and brain regionspecific alterations in expression of genes involved in these behaviors in FAE adult offspring. Specifically, decreased hippocampal GAP-43 mRNA levels in adult FAE females and decreased glucocorticoid receptor (GR) expression in the amygdala of male and female FAE offspring were observed. The decreased mRNA levels of GAP-43 and GR were normalized by T4 treatment to the alcohol-consuming mother. Our results suggest that the suppressed HPT function of the alcohol-consuming mother contributes to the behavioral and cognitive dysfunctions observed in the offspring. Prenatal alcohol exposure has long-term developmental consequences, 1-3 and in humans alcohol is recognized as a teratogen leading to long-lasting CNS dysfunctions. 4 Specifically, patients with fetal alcohol exposure (FAE) have marked cognitive deficits, including difficulty focusing and sustaining attention, 5 and place learning deficits in a virtual Morris water task. 6 Attention deficit hyperactivity disorder (ADHD) is frequently diagnosed in FAE children. These neurocognitive and behavioral characteristics differ between FAE children and those with a primary diagnosis of ADHD, as FAE children have difficulties primarily in the encoding and retrieval of information. 7 A significantly increased prevalence of depression is also found in children 8 and adults 9 prenatally exposed to alcohol. It is important to note that, in contrast to the higher female prevalence of depressive disorders in the general population, the rate of depression found in adults with prenatal alcohol exposure was nearly equal among men and women. 9 Fetal alcohol effects qualitatively similar to those described in children with a history of gestational alcohol exposure have been detected with animal models. 10 Cognitive deficits have been found in FAE animal models...

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Section: Methodssupporting

confidence: 80%

Section: Animalsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

et al. 2005

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“…There are many examples in the scientific literature of prenatal and early postnatal life experiences that attribute the risk of developing a sex-biased metabolic disease in later life to sex hormones (17,58,(67)(68)(69)(70)(71) . All tissues exhibit sexual dimorphism for a substantial proportion of the genes they express (58,72) .…”

Section: Transduction Of Environmental Signals To the Epigenetic Machmentioning

confidence: 99%

Nutritional developmental epigenomics: immediate and long-lasting effects

2010

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The phenotype of an individual is the result of complex interactions between genome, epigenome and current, past and ancestral environment leading to a lifelong remodelling of the epigenomes. The genetic information expression contained in the genome is controlled by labile chromatin-associated epigenetic marks. Epigenetic misprogramming during development is widely thought to have a persistent effect on the health of the offspring and may even be transmitted to the next generation. The epigenome serves as an interface between the environment and the genome. Dietary factors, including folate involved in C 1 metabolism, and other social and lifestyle exposures have a profound effect on many aspects of health including ageing and do so, at least partly, through interactions with the genome, which result in altered gene expression with consequences for cell function and health throughout the life course. Depending on the nature and intensity of the environmental insult, the critical spatiotemporal windows and developmental or lifelong processes involved, epigenetic alterations can lead to permanent changes in tissue and organ structure and function or to phenotypic changes that can (or cannot) be reversed using appropriate epigenetic tools. Moreover, the flexibility of epigenetic marks may make it possible for environmental, nutritional and hormonal factors or endocrine disruptors to alter, during a particular spatiotemporal window in a sex-specific manner, the sex-specific methylation or demethylation of specific CpG and/or histone modifications underlying sex-specific expression of a substantial proportion of genes. Moreover, genetic factors, the environment and stochastic events change the epigenetic landscape during the lifetime of an individual. Epigenetic alterations leading to gene expression dysregulation accumulate during ageing and are important in tumorigenesis and age-related diseases. Several encouraging trials suggest that prevention and therapy of age-and lifestyle-related diseases by individualised tailoring to optimal epigenetic diets or drugs are conceivable. However, these interventions will require intense efforts to unravel the complexity of these epigenetic, genetic and environment interactions and to evaluate their potential reversibility with minimal side effects.

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Enamel hypoplasia and early mortality: Bioarcheological support for the Barker hypothesis

Armelagos

Goodman

Harper

et al. 2009

Evolutionary Anthropology

184

125

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The Barker hypothesis asserts that stressful events early in the life history of an individual have negative health consequences later in adulthood. The hypothesis initially focused on prenatal stressors as indicated by birth weight and related outcomes. This initial concern with the fetal phase of development led to its description as the “fetal programming” or “fetal origins” hypothesis. The realization that stressors in the postnatal phase had similar impacts on adult health has led to its latest characterization as the Developmental Origins of Health and Disease Hypothesis (DOHaD). In this paper, we review the history and evidence in support of the DOHaD hypothesis. We then introduce an untapped source of information on early life stress: enamel hypoplasias and other developmental defects of enamel. Enamel defects are nearly indelible records of physiological perturbations, or stress, to developing ameloblasts (enamel‐forming cells). Furthermore, the location of the defects translates to specific periods of growth, providing a permanent temporal record of early life stressors from in utero to approximately twelve years of age. As we discuss, a handful of studies of different populations reveals that individuals with enamel defects that developed in utero and early in infant‐childhood development tend to be subject to earlier adolescent or adult mortality.

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Prenatal programming of adult thyroid function by alcohol and thyroid hormones

Cited by 56 publications

References 69 publications

Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

Nutritional developmental epigenomics: immediate and long-lasting effects

Enamel hypoplasia and early mortality: Bioarcheological support for the Barker hypothesis

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