Although hyperglycaemia alone does not indicate whether there is an insufficiency of insulin secretion [89], it is possible that its development observed in this study following a double hit of fructose in both male and female rats coupled with impaired glucose tolerance and IR suggests that the fructose that was administered in the neonatal period may have been effective in programming the neonatal rats for the development of hyperglycaemia, impaired glucose tolerance and IR or pancreatic β-cell dysfunction later in adulthood after exposure to a secondary dietary insult. The gene discussed is INS; the disease is Impaired glucose tolerance.