Fetal anemia and elevated hepcidin in a mouse model of fetal alcohol spectrum disorder.

ABSTRACT:

Introduction

Prenatal alcohol exposure (PAE) impairs offspring growth and cognition, and this is worsened by concurrent iron deficiency. Alcohol disrupts fetal iron metabolism and produces functional iron deficiency, even when maternal iron status is adequate. We used a mouse model of moderate PAE to investigate the mechanisms underlying this dysregulated iron status.

Methods

C57BL/6J female mice received 3 g/kg alcohol daily from embryonic day (E) 8.5-17.5 and were assessed at E17.5.

Results

Alcohol reduced fetal hemoglobin, hematocrit, and red blood cell counts, despite elevated erythropoietin production. Alcohol suppressed maternal hepcidin expression and the upstream iron-sensing BMP/SMAD pathway, consistent with its effects in the nonpregnant state. In contrast,

SUBMITTER: Helfrich KK 

PROVIDER: S-EPMC11878275 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature