Furthermore, in db/db mice, a genetic obesity model due to a leptin receptor mutation, p.o. administration of d-allulose (1 g kg−1) suppressed food intake at 0.5–6 h in a similar manner to chow-fed and HFD-fed obese C57BL/6J mice (Fig. 4g vs. Figs. 1a and 4a). This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.