Childhood obesity is closely linked to obesity in parents; both genetic and environmental factors have been shown to contribute. A direct link between maternal well being including her diet on offspring obesity and metabolic risk is established. Whether obese fathers and his diet also have a role have not been systematically explored. This led to development of a rat model in this thesis, using high fat diet (HF) to determine directly any non-genetic role of paternal obesity, in transmitting his phenotype to offspring. This thesis involved 2 experimental protocols. The first consisted of a simple HF vs. control father model, and the second, 3 groups of fathers with graded degrees of obesity, compared to lean controls. Two types of diet were used to induce obesity in fathers; commercially available high fat chow in the first, and Western cafeteria diet in the second project. HF fathers were obese, hyperleptinaemic, glucose intolerant and insulin resistant; their offspring consumed control diet. In the first protocol, female offspring of HF fathers had impaired glucose tolerance and insulin secretion as juveniles. The underlying mechanisms included a reduced beta-cell reserve due to lack of large-sized islets and altered pancreatic islet biomarkers. Altered epigenome via DNA methylation was demonstrated as one of the mechanisms underpinning this transmission. In contrast to the effects of maternal diet-induced obesity, no difference was observed in body weight, adiposity and energy intake of offspring from the first cohort. The second project set out to follow up on investigation on obesity and appetite programming in offspring using an extended model consisting of fathers with three planes of obesity, generated by combining effects of litter adjustment and HF exposure, compared with lean controls. A spectrum of differential effects of obese father on body weight trajectories and plasma leptin was observed, with greatest impact in offspring from the heaviest group of fathers. No difference was observed in hypothalamic appetite regulation and adiposity, in keeping with findings from the first cohort. This thesis showed that metabolic perturbations in fathers, induced by chronic HF exposure, is also passed on to offspring, thus extending the concept of developmental and adaptive plasticity to include a paternal role in the early life origins of disease and amplification of the obesity and diabetes epidemics.