Chronic exposure to fructose causes hyperinsulinaemia and obesity through altered mechanisms that include the effect of fructose on ATP depletion and uric acid generation [33], increased circulating C-peptide levels that are often associated with insulin resistance [34], involvement of the fructose transporter GLUT5 that shows significantly higher expression levels in young Zucker obese rats compared to lean controls [35], and the hexosamine hypothesis, in which hexosamine flux is thought to be involved in regulating glucose pathways [36]. The gene discussed is SLC2A5; the disease is obesity due to melanocortin 4 receptor deficiency.