Studies using human populations and animal models have shown that adult cardiovascular and metabolic disease risk is closely associated with poor environmental conditions experienced during the earliest stages of life. While the association between maternal diet and offspring adult health has been studied in detail, our understanding of the impact of paternal diet on offspring health remains largely neglected.

Using the well characterised rodent low protein diet (LPD; 9 % protein) model, we observe that offspring from LPD fed male mice have significantly increased weight at birth and adult body fat levels, impaired glucose tolerance and cardiovascular dysfunction (indicative of obesity, type 2 diabetes and heart disease) when compared to offspring from control, normal protein diet (NPD: 18% protein) diet fed male mice.

Our recent studies have begun to define the underlying mechanisms linking paternal diet with perturbed offspring development and ultimately adult ill-health. During fetal development, we observe significant changes in embryonic metabolic status, fetal growth and skeletal formation and placental development and transport capacity. Our analysis of paternal and maternal tissues reveal genome wide paternal sperm DNA hypomethylation, altered testicular expression of epigenetic regulators and reduced maternal uterine signalling responses. These data indicate paternal diet may affect offspring development via sperm genomic and seminal fluid specific mechanisms. Out latest studies are aimed at defining the relative sperm and seminal fluid specific programming effects on offspring health and their persistence across generations.