Sandra Helinski

Moritz KM


The School of Biomedical Sciences, The University of Queensland, St Lucia, 4072, Australia.


The developmental programming of health and disease (DOHaD) hypothesis suggests early life events contribute to increased susceptibility to diseases in later life. Animal models have examined the effected of maternal undernutrition, glucocorticoid exposure and placental insufficiency but somewhat surprisingly, prenatal alcohol exposure has rarely been studied in the context of DOHaD.

We have developed rat models of alcohol consumption patterns during pregnancy and examined effects on fetal growth and long term renal, cardiovascular and metabolic outcomes. Rats were administered a liquid diet containing 6% ethanol throughout pregnancy (Low dose chronic ethanol exposure-LCE) or given a higher dose of ethanol around the time of conception (12%, periconceptional exposure- PCE).

Both models resulted in fetal growth restriction. Offspring from the LCE model developed impairments in glucose homeostasis and renal function as well as altered blood pressure responsiveness and lung fibrosis. The PCE model resulted in profound insulin resistance, impaired renal and cardiac function and sex specific increases in adiposity. These outcomes were  associated with alterations in implantation and placental development. Our results suggest alcohol can affect the developing embryo even prior to implantation.

These studies highlight that in addition to the well-known effects on the developing brain, alcohol exposure during pregnancy affects other developing organs and contributes to long term “programming” of adult disease.