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Cell Rep. 2013 Dec 12;5(5):1403-12. doi: 10.1016/j.celrep.2013.11.010. Epub 2013 Dec 5.

Delayed hepatic adaptation to weaning in ACBP-/- mice is caused by disruption of the epidermal barrier.

Author information

1
Department of Biochemistry and Molecular Biology, University of Southern Denmark, 5230 Odense M, Denmark.
2
Department of Biochemistry and Molecular Biology, University of Southern Denmark, 5230 Odense M, Denmark. Electronic address: s.mandrup@bmb.sdu.dk.

Abstract

We previously reported that mice deficient in acyl-CoA-binding protein (ACBP) display a delayed metabolic adaptation to weaning. This includes a delayed activation of the hepatic lipogenic gene program, which may result from hepatic accumulation of triacylglycerol and/or cholesteryl esters in the late suckling period. To further investigate the basis for this phenotype, we generated mice deficient in ACBP in hepatocytes (Alb-ACBP(-/-)) and keratinocytes (K14-ACBP(-/-)). Surprisingly, the delayed adaptation to weaning, including hepatic lipid accumulation, is caused by ACBP deficiency in the skin rather than in the liver. Similarly to ACBP(-/-) mice, K14-ACBP(-/-) mice exhibit an increased transepidermal water loss, and we show that the hepatic phenotype is caused specifically by the epidermal barrier defect, which leads to increased lipolysis in white adipose tissue. Our data demonstrate that an imperfect epidermal barrier leads to profound suppression of the hepatic SREBP gene program and lipid accumulation in the liver.

PMID:
24316079
DOI:
10.1016/j.celrep.2013.11.010
[Indexed for MEDLINE]
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