Low maternal vitamin A intake increases the incidence of teratogen induced congenital diaphragmatic hernia in mice.

Background: Congenital diaphragmatic hernia (CDH) is a severe birth defect associated with high perinatal mortality and long-term morbidity. The etiology of CDH is poorly understood although abnormal retinoid signaling has been proposed to contribute to abnormal diaphragm development. Existing epidemiological data suggest that inadequate dietary vitamin A intake is a risk factor for developing CDH.

Correction: Gene ontology enrichment analysis of congenital diaphragmatic hernia-associated genes.

A correction to this paper has been published and can be accessed via a link at the top of the paper.

Gene ontology enrichment analysis of congenital diaphragmatic hernia-associated genes.

Congenital diaphragmatic hernia (CDH) is a commonly occurring major congenital anomaly with a profound impact on neonatal mortality. The etiology of CDH is poorly understood and is complicated by multiple clinical presentations, reflecting the location and type of diaphragm defect. With the increased power of genetic screening, more genes are being associated with CDH, creating a knowledge gap between CDH-associated genes and their contribution to diaphragm embryogenesis.

Chronic alcohol consumption decreases brown adipose tissue mass and disrupts thermoregulation: a possible role for altered retinoid signaling.

Retinoic acid, an active metabolite of dietary vitamin A, acts as a ligand for nuclear receptor transcription factors with more than 500 known target genes. It is becoming increasingly clear that alcohol has a significant impact on cellular retinoic acid metabolism, with resultant effects on its function. Here, we test the hypothesis that chronic alcohol consumption impairs retinoic acid signaling in brown adipose tissue (BAT), leading to impaired BAT function and thermoregulation.