ArticleNutrition & diabetes2012
Chronic prenatal ethanol exposure increases adiposity and disrupts pancreatic morphology in adult guinea pig offspring.
Article in Nutrition & diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- From teratogens to trajectories: Integrating teratology and Developmental Origins of Health and Disease (DOHaD) frameworks for a new take on fetal alcohol spectrum disorders (FASD).Neurobiology of stress · 2026Article
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- Prenatal ethanol exposure and changes in fetal neuroendocrine metabolic programming.Biological research · 2023Review
- Prenatal alcohol exposure causes persistent microglial activation and age- and sex- specific effects on cognition and metabolic outcomes in an Alzheimer's Disease mouse model.The American journal of drug and alcohol abuse · 2023Article
- Aging-Related Behavioral, Adiposity, and Glucose Impairments and Their Association following Prenatal Alcohol Exposure in the C57BL/6J Mouse.Nutrients · 2022Article
- Epigenetics of the developing and aging brain: Mechanisms that regulate onset and outcomes of brain reorganization.Neuroscience and biobehavioral reviews · 2021Review
- Fetal alcohol spectrum disorder predisposes to metabolic abnormalities in adulthood.The Journal of clinical investigation · 2020Article
- Early-life Programming of Type 2 Diabetes Mellitus: Understanding the Association between Epigenetics/Genetics and Environmental Factors.Current genomics · 2019Review
- From conception to infancy - early risk factors for childhood obesity.Nature reviews. Endocrinology · 2019Review
- Epigenetic Modifications Induced by Nutrients in Early Life Phases: Gender Differences in Metabolic Alteration in Adulthood.Frontiers in genetics · 2019Review
- Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic.The Journal of physiology · 2018Article
- Does prenatal alcohol exposure cause a metabolic syndrome? (Non-)evidence from a mouse model of fetal alcohol spectrum disorder.PloS one · 2018Article
- Fetal Alcohol Exposure Alters Blood Flow and Neurological Responses to Transient Cerebral Ischemia in Adult Mice.Alcoholism, clinical and experimental research · 2017Article
- Alcohol-Induced Developmental Origins of Adult-Onset Diseases.Alcoholism, clinical and experimental research · 2016Review
- Alcoholic Beverage Consumption and Chronic Diseases.International journal of environmental research and public health · 2016Review
- Abnormal Eating Behaviors Are Common in Children with Fetal Alcohol Spectrum Disorder.The Journal of pediatrics · 2016Article
- Sex-specific increase in susceptibility to metabolic syndrome in adult offspring after prenatal ethanol exposure with post-weaning high-fat diet.Scientific reports · 2015Article
- Impact of Maternal Diet on the Epigenome during In Utero Life and the Developmental Programming of Diseases in Childhood and Adulthood.Nutrients · 2015Review
- Early-life exposure to substance abuse and risk of type 2 diabetes in adulthood.Current diabetes reports · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEthanol consumption during pregnancy can lead to a range of adverse developmental outcomes in children, termed fetal alcohol spectrum disorder (FASD). Central nervous system injury is a debilitating and widely studied manifestation of chronic prenatal ethanol exposure (CPEE). However, CPEE can also cause structural and functional deficits in metabolic pathways in offspring. OBJECTIVES AND
methodsThis study tested the hypothesis that CPEE increases whole-body adiposity and disrupts pancreatic structure in guinea pig offspring. Pregnant guinea pigs received ethanol (4 g kg(-1) maternal body weight per day) or isocaloric-sucrose/pair-feeding (control) for 5 days per week throughout gestation.
resultsMale and female CPEE offspring demonstrated growth restriction at birth, followed by a rapid period of catch-up growth before weaning (postnatal day (PD) 1-7). Whole-body magnetic resonance imaging (MRI) in young adult offspring (PD100-140) revealed increased visceral and subcutaneous adiposity produced by CPEE. At the time of killing (PD150-200), CPEE offspring also had increased pancreatic adipocyte area and decreased β-cell insulin-like immunopositive area, suggesting reduced insulin production and/or secretion from pancreatic islets.
conclusionCPEE causes increased adiposity and pancreatic dysmorphology in offspring, which may signify increased risk for the development of metabolic syndrome and type 2 diabetes mellitus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.