Endocrine Abstracts

Although development is a highly organised and tightly regulated process, the developing embryo is sensitive to environmental influences, resulting in pathophysiological changes which may increase the risk of later cardio-metabolic, neurobehavioural and reproductive disorders. We have shown that prenatal overexposure to the synthetic glucocorticoid dexamethasone (Dex) in rats reduces birthweight in the first generation (F1) and leads to hypertension and insulin resistance in the offspring. Since we originally reported that these ‘programmed’ phenotypes could be transmitted to a second generation (F2), particularly through the male line, a growing number of studies have shown that the effects of early life exposure to environmental influences are not limited to the F1 generation, but may be transmitted to a second or further generations through non-genomic mechanisms. In this talk I will review the evidence for the transmission of programmed effects across generations and discuss potential mechanisms, including whether induced changes in DNA methylation, histone modifications or non-coding RNA may be transmissible through the gametes.