Enhancing satiety may be a route to overcome excess food intake, a causative agent of the obesity epidemic effecting [sic] developed and developing nations. A theory has evolved that if food processing has been a major contributor to the obesity epidemic then food processing and manipulation could be the solution to the crisis. This could be by means of the manipulation of food to target regulatory mechanisms of the food-gut-brain axis to produce satiety from fewer calories. This thesis is an investigation, using the Sprague Dawley rat model, into possible interactions between macronutrient content and food structure in the regulation of satiation and satiety, and to provide evidence for possible enhanced satiation or satiety by protein crosslinking noted in human studies. Three principle studies were performed: 1) variation in macronutrient content of a base diet presented in a solid or liquid form; 2) gavage of a single macronutrient containing solutions directly to the stomach; and 3) using protein crosslinking to change food form without changing caloric density. Overall, the study found no evidence to support an interaction between macronutrient content and diet form, nor that protein is a more effective macronutrient for inducing satiation or prolonging satiety. The analysis did identify that liquid diets can increase satiation, but can result in negative homeostatic effects and excess food consumption. Research exploring the use of protein crosslinking to promote satiation is still at an early stage but the findings presented in this thesis identify utilisation as a potential tool for enhanced satiation. These studies suggest that while protein crosslinking may enhance satiation there is no translation into longer term satiety. Nevertheless, these findings serve as a basis for further research and could provide information to the food industry for the development of food products that increase the satiation and satiety properties of food.