In this thesis I investigated relationships between dietary carbohydrate quantity and quality and the development of obesity, the metabolic syndrome and type-2 diabetes. I explored associations between glycaemic index, glycaemic load, dietary fibre, or carbohydrate intake and components of the metabolic syndrome in two National Diet and Nutrition Surveys. Glycaemic index was directly associated with body mass index and waist circumference in adult males, but was not a significant predictor of lipoprotein concentrations. A high carbohydrate intake was inversely associated with anthropo.metric variables in both cohorts and was significantly related to lipid profile. Glucagon-like peptide-l (GLP-l) is an insulin secretagogue and has been implicated in appetite regulation, thus is potentially involved in type-2 diabetes and obesity pathogenesis. Fasting GLP-l concentrations were measured in a cohort of healthy subjects and individuals with type-2 diabetes, and found to be lower in healthy subjects. Regression analyses revealed that no carbohydrate-related variables were associated with HbAlc, inst:ffin sensitivity or GLP-l concentrations in either group. Carbohydrate intake was directly associated with glucose concentrations in individuals with type-2 diabetes. An intervention study revealed that a low compared to a high glycaemic index diet led to greater improvements in glycaemic control, particularly in individuals with type-2 diabetes. Postprandial GLP-l concentrations did not differ significantly between subject groups and the observed changes over the study period did not differ between dietary interventions. I went on to investigate the chronic effects of a high-fibre, lowfat diet versus a low-fibre, high-fat diet in healthy subjects; postprandial glucose, insulin and GLP-l concentrations did not differ significantly between diets. Finally I examined the acute effects of a low versus high glycaemic index preload on the metabolic response to a meal. Differences in the glycaemic response to. the preloads did not translate into differences in the glucose, insulin or GLP-l response over the total postprandial period.