Comment; Interesting study in rats demonstrating that low doses of pre-natal exposure to alcohol in the mother leads to future metabolic abnormalities in males and their future development–even a little hurts the offspring!
Tam M.T. NguyenSarah E. SteaneKaren M. MoritzLisa K. AkisonFirst published: 08 October 2019 https://doi.org/10.1113/JP278531
Edited by: Laura Bennet & Janna Morrison
This article was first published as a preprint: Nguyen TMT, Steane BT, Moritz KM and Akison LK (2019). Prenatal alcohol exposure programs offspring disease: Insulin resistance in adult males in a rat model of acute exposure. bioRxiv. https://doi.org/10.1101/684639.
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as https://doi.org/10.1113/JP278531PDFTOOLSSHARE
Abstract
Alcohol consumption is highly prevalent amongst women of reproductive age. Given that approximately 50% of pregnancies are unplanned, alcohol has the potential to affect fetal development and program chronic disease in offspring. We examined the effect of an acute but moderate prenatal alcohol exposure (PAE) on glucose metabolism, lipid levels and dietary preference in adolescent and/or adult rat offspring. Pregnant Sprague‐Dawley rats received an oral gavage of ethanol (1 g kg−1 maternal body weight, n = 9 dams) or an equivalent volume of saline (control, n = 8 dams) at embryonic days 13.5 and 14.5. PAE resulted in a blood alcohol concentration of 0.05‐0.06% 1 h post‐gavage in dams. Fasting blood glucose concentration was not affected by PAE in offspring at any age, nor were blood glucose levels during a glucose tolerance test (GTT) in 6‐month old offspring (P > 0.5). However, there was evidence of insulin resistance in PAE male offspring at 6 months of age, with significantly elevated fasting plasma insulin (P = 0.001), a tendency for increased first phase insulin secretion during the GTT and impaired glucose clearance following an insulin challenge (P = 0.007). This was accompanied by modest alterations in protein kinase B (AKT) signalling in adipose tissue. PAE also resulted in reduced calorie consumption by offspring compared to controls (P = 0.04). These data suggest that a relatively low‐level, acute PAE programs metabolic dysfunction in offspring in a sex‐specific manner. These results highlight that alcohol consumption during pregnancy has the potential to affect the long‐term health of offspring.
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