(PO16-39-22) Influence of Maternal Choline Supplementation on Metabolic Outcomes of Offspring With Prenatal and Postnatal Alcohol Exposures

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Presenting Author(s)

Xinyin Jiang, PhD., RD
– Associate Professor, Brooklyn College, Brooklyn, New York, United States

Co-Author(s)

IK

Ismail Kadam, B.S.
– CUNY - Brooklyn College, New York, New York, United States
ST

Steven Trasino, PhD
– Hunter College

Disclosure(s):

Xinyin Jiang, PhD., RD: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Prenatal alcohol exposure (PAE) affects cognitive development. However, it is unclear whether PAE influences metabolic health of offspring and whether postnatal alcohol intake would exacerbate metabolic deterioration resulting from PAE. Choline is a semi-essential nutrient that has been demonstrated to mitigate the cognitive impairment of PAE. This study investigated how maternal choline supplementation may modify metabolic health of offspring with prenatal and postnatal alcohol exposures.

Methods: C57BL/6J female mice were fed either a Lieber DeCarli liquid diet with 1.4% ethanol between embryonic day (E) 9.5 and E17.5 or a control Lieber DeCarli diet. Choline was supplemented to 4 x concentrations versus control throughout pregnancy. At postnatal week 7, offspring mice were exposed to 1.4% ethanol for females and 3.9% ethanol for males for 4 weeks.

Results: Postnatal alcohol exposure led to lower weight gain of offspring regardless of PAE status. There were no differences in glucose tolerance by pre or postnatal alcohol exposure, yet prenatal choline supplementation led to better glucose tolerance in male offspring. Postnatal alcohol exposure led to lower expression of carnitine palmitoyltransferase 1a (Cpt1a), an important enzyme that mediates fatty acid β-oxidation, but prenatal choline supplementation prevented this alteration.

Conclusions: In the current model, PAE does not seem to exacerbate metabolic differences triggered by postnatal alcohol exposure. Maternal choline supplementation has a modest effect on normalizing liver metabolic gene expression that is altered by alcohol exposure.

Funding Sources: PSC-CUNY