| Autor: |
Gårdebjer EM; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Cuffe JSM; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Ward LC; School of Chemistry and Molecular Biosciences, The University of Queensland , St. Lucia, Queensland , Australia., Steane S; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Anderson ST; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Dorey ES; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Kalisch-Smith JI; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Pantaleon M; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia., Chong S; Mater Research Institute, University of Queensland , St. Lucia, Queensland , Australia., Yamada L; Mater Research Institute, University of Queensland , St. Lucia, Queensland , Australia., Wlodek ME; Department of Physiology, University of Melbourne , Parkville, Victoria , Australia., Bielefeldt-Ohmann H; School of Veterinary Science, The University of Queensland , St. Lucia, Queensland , Australia., Moritz KM; School of Biomedical Sciences, The University of Queensland , St. Lucia, Queensland , Australia.; Centre for Child Health Research, The University of Queensland , St. Lucia, Queensland , Australia. |
| Abstrakt: |
The effects of maternal alcohol consumption around the time of conception on offspring are largely unknown and difficult to determine in a human population. This study utilized a rodent model to examine if periconceptional alcohol (PC:EtOH) consumption, alone or in combination with a postnatal high-fat diet (HFD), resulted in obesity and liver dysfunction. Sprague-Dawley rats were fed a control or an ethanol-containing [12.5% (vol/vol) EtOH] liquid diet from 4 days before mating until 4 days of gestation ( n = 12/group). A subset of offspring was fed a HFD between 3 and 8 mo of age. In males, PC:EtOH and HFD increased total body fat mass ( P PC:EtOH < 0.05, P HFD < 0.0001); in females, only HFD increased fat mass ( P HFD < 0.0001). PC:EtOH increased microvesicular liver steatosis in male, but not female, offspring. Plasma triglycerides, HDL, and cholesterol were increased in PC:EtOH-exposed males ( P PC:EtOH < 0.05), and LDL, cholesterol, and leptin (Lep) were increased in PC:EtOH-exposed females ( P PC:EtOH < 0.05). mRNA levels of Tnf-α and Lep in visceral adipose tissue were increased by PC:EtOH in both sexes ( P PC:EtOH < 0.05), and Il-6 mRNA was increased in males ( P PC:EtOH < 0.05). These findings were associated with reduced expression of microRNA-26a, a known regulator of IL-6 and TNF-α. Alcohol exposure around conception increases obesity risk, alters plasma lipid and leptin profiles, and induces liver steatosis in a sex-specific manner. These programmed phenotypes were similar to those caused by a postnatal HFD, particularly in male offspring. These results have implications for the health of offspring whose mothers consumed alcohol around the time of conception. |
