The distribution of maternally-derived glucose was determined in selected tissues of fetuses from ethanol-fed (EF) rats and from pair-fed (PF) and ad lib-fed (AF) controls. Maternal ethanol ingestion resulted in reduced fetal brain and liver weights and lower liver and lung glycogen levels compared to those of the PF or AF control groups. In addition, experimental fetuses exhibited reduced uptake of maternally-derived [3H] 2-deoxy-D-glucose (2-DG) by placenta and fetal brain. Fetal body, liver, lung, and brain weights correlated with fetal plasma 3H activity and with the fetal:maternal plasma 3H ratio, an indicator of the rate of placental glucose transfer. Brain weight correlated with 2-DG content per gram tissue weight. These observations suggest that reduced nutrient availability due to impaired placental transfer plays a role in the intrauterine growth retardation associated with maternal ethanol ingestion.
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http://dx.doi.org/10.1016/0892-0362(89)90061-5 | DOI Listing |
Int J Mol Sci
January 2025
Department of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.
Alcohol is the second-most misused substance after tobacco. It has been identified as a causal factor in more than 200 diseases and 5.3% of all deaths and is associated with significant behavioral, social, and economic difficulties.
View Article and Find Full Text PDFJ Dev Orig Health Dis
December 2024
Department of Physiology, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, Brazil.
It is known that adverse stimuli, such as altered diets during pregnancy and lactation can result in deleterious effects on the progeny. The aim of this study was to evaluate the possible gastrointestinal repercussions in the offspring of Wistar rats exposed to high-fat diets. Pregnant rats were divided into three groups: normolipidic diet (3.
View Article and Find Full Text PDFPhysiol Behav
December 2024
Molecular and Behavioral Neuroscience Laboratory, Pharmacology Department, Universidade Federal de São Paulo, Brazil.
Alcohol use disorder (AUD) is a condition with multifactorial causes, including biopsychosocial factors. Childhood exposure to stress may increase susceptibility to AUD in adulthood. Despite its significance, the interaction between stress and AUD remains unclear.
View Article and Find Full Text PDFPLoS One
November 2024
Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, Maryland, United States of America.
Neuroscience
January 2025
Molecular and Behavioral Neuroscience Laboratory, Pharmacology Department, Universidade Federal de São Paulo, São Paulo, Brazil. Electronic address:
Clinical and preclinical studies suggest that early life stress can increase the risk of developing ethanol use disorder later in life. Although the endocannabinoid (eCB) system plays a role in stress-related behaviors and ethanol consumption, it remains unclear whether the eCB system is affected in response to a combination of both factors. By using male and female adolescent C57BL/6J mice subjected to a maternal separation (MS) stress paradigm from postnatal day (PND) 1 to 14, we explored (1) the consequences of early life stress experiences on ethanol consumption in adolescent mice and (2) how these events affect the eCB system and neuronal activation in brain regions associated with the reward system.
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