Fetal alcohol spectrum disorder predisposes to metabolic abnormalities in adulthood
| Autor: | Isaac M. Oderberg, Arkadi Schwartz, Paul J. Wrighton, Wolfram Goessling, Gabriel D. Bossé, Daan Kloosterman, Sebastian Akle, Isaac Adatto, Isabelle Iversen, Kyle A. LaBella, Pouneh K. Fazeli, Matthew L. Steinhauser, Yariv Houvras, Randall T. Peterson, Allison Tsomides, Sahar Tavakoli, Michael E. Charness, Olivia Weeks |
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| Rok vydání: | 2020 |
| Předmět: |
Adult
Male 0301 basic medicine Population Adipose tissue Physiology Mice Transgenic Type 2 diabetes Development Intra-Abdominal Fat Overweight Mice 03 medical and health sciences 0302 clinical medicine Pregnancy medicine Animals Humans Obesity Registries education Zebrafish education.field_of_study biology business.industry Organ dysfunction Infant Newborn General Medicine medicine.disease biology.organism_classification 3. Good health Metabolism 030104 developmental biology Diabetes Mellitus Type 2 Liver Fetal Alcohol Spectrum Disorders Prenatal Exposure Delayed Effects 030220 oncology & carcinogenesis Embryonic development Cohort Female medicine.symptom business Research Article |
| Zdroj: | The Journal of Clinical Investigation |
| ISSN: | 1558-8238 0021-9738 |
| Popis: | Prenatal alcohol exposure (PAE) affects at least 10% of newborns globally and leads to the development of fetal alcohol spectrum disorders (FASDs). Despite its high incidence, there is no consensus on the implications of PAE on metabolic disease risk in adults. Here, we describe a cohort of adults with FASDs that had an increased incidence of metabolic abnormalities, including type 2 diabetes, low HDL, high triglycerides, and female-specific overweight and obesity. Using a zebrafish model for PAE, we performed population studies to elucidate the metabolic disease seen in the clinical cohort. Embryonic alcohol exposure (EAE) in male zebrafish increased the propensity for diet-induced obesity and fasting hyperglycemia in adulthood. We identified several consequences of EAE that may contribute to these phenotypes, including a reduction in adult locomotor activity, alterations in visceral adipose tissue and hepatic development, and persistent diet-responsive transcriptional changes. Taken together, our findings define metabolic vulnerabilities due to EAE and provide evidence that behavioral changes and primary organ dysfunction contribute to resultant metabolic abnormalities. |
| Databáze: | OpenAIRE |
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