RGD Reference Report - Prenatal ethanol exposure programs an increased susceptibility of non-alcoholic fatty liver disease in female adult offspring rats. - Rat Genome Database

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Prenatal ethanol exposure programs an increased susceptibility of non-alcoholic fatty liver disease in female adult offspring rats.

Authors: Shen, Lang  Liu, Zhongfen  Gong, Jun  Zhang, Li  Wang, Linlong  Magdalou, Jacques  Chen, Liaobin  Wang, Hui 
Citation: Shen L, etal., Toxicol Appl Pharmacol. 2014 Jan 15;274(2):263-73. doi: 10.1016/j.taap.2013.11.009. Epub 2013 Nov 22.
RGD ID: 12904726
Pubmed: PMID:24275070   (View Abstract at PubMed)
DOI: DOI:10.1016/j.taap.2013.11.009   (Journal Full-text)

Prenatal ethanol exposure (PEE) induces dyslipidemia and hyperglycemia in fetus and adult offspring. However, whether PEE increases the susceptibility to non-alcoholic fatty liver disease (NAFLD) in offspring and its underlying mechanism remain unknown. This study aimed to demonstrate an increased susceptibility to high-fat diet (HFD)-induced NAFLD and its intrauterine programming mechanisms in female rat offspring with PEE. Rat model of intrauterine growth retardation (IUGR) was established by PEE, the female fetus and adult offspring that fed normal diet (ND) or HFD were sacrificed. The results showed that, in PEE+ND group, serum corticosterone (CORT) slightly decreased and insulin-like growth factor-1 (IGF-1) and glucose increased with partial catch-up growth; In PEE+HFD group, serum CORT decreased, while serum IGF-1, glucose and triglyceride (TG) increased, with notable catch-up growth, higher metabolic status and NAFLD formation. Enhanced liver expression of the IGF-1 pathway, gluconeogenesis, and lipid synthesis as well as reduced expression of lipid output were accompanied in PEE+HFD group. In PEE fetus, serum CORT increased while IGF-1 decreased, with low body weight, hyperglycemia, and hepatocyte ultrastructural changes. Hepatic IGF-1 expression as well as lipid output was down-regulated, while lipid synthesis significantly increased. Based on these findings, we propose a "two-programming" hypothesis for an increased susceptibility to HFD-induced NAFLD in female offspring of PEE. That is, the intrauterine programming of liver glucose and lipid metabolic function is "the first programming", and postnatal adaptive catch-up growth triggered by intrauterine programming of GC-IGF1 axis acts as "the second programming".

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
metabolic dysfunction-associated steatotic liver disease susceptibilityISOIgf1 (Rattus norvegicus)12904726; 12904726associated with Fetal Growth Retardation and mRNA:increased expression:liver (rat)RGD 
metabolic dysfunction-associated steatotic liver disease susceptibilityISOIgf1r (Rattus norvegicus)12904726; 12904726associated with Fetal Growth Retardation and mRNA:increased expression:liver (rat)RGD 
metabolic dysfunction-associated steatotic liver disease susceptibilityIEP 12904726; 12904726associated with Fetal Growth Retardation and mRNA:increased expression:liver (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Igf1  (insulin-like growth factor 1)
Igf1r  (insulin-like growth factor 1 receptor)

Genes (Mus musculus)
Igf1  (insulin-like growth factor 1)
Igf1r  (insulin-like growth factor I receptor)

Genes (Homo sapiens)
IGF1  (insulin like growth factor 1)
IGF1R  (insulin like growth factor 1 receptor)


Additional Information