It is reported that intermittent access to a palatable sweet solution in food restricted mice produces binge-like overconsumption of the sweetener. In our previous study, food restricted mice (binge group) with daily 4-h access to 0.5 M sucrose solution for 10 days showed binge-like sugar overconsumption, but the same 4-h access to sucrose did not produce overconsumption in the control group presented with chow for 20-h a day. The number of c-Fos positive cells in the nucleus of the solitary tract and the parabrachial nucleus of binge group after intragastric infusion of 0.5 M sucrose solution were significantly less than those in the control group. Intraperitoneal injection of peptide YY (PYY), one of the anorectic peptides released from the small intestine, yielded smaller number of c-Fos positive cells in these nuclei in the binge group. Based on these findings, we hypothesized that the decreased responsiveness to postprandial feeding inhibition contributes to the development and expression of binge-like overconsumption. However, it remains unclear whether postprandial PYY levels are reduced in mice showing binge-like sugar overconsumption. In the present study, we examined plasma PYY levels after intragastric infusion of 0.5 M sucrose solution in the binge group and another mice with 4-h access to chow alone (food restricted (FR) group). Whole blood samples were collected from hearts and centrifuged to collect plasma. Plasma PYY levels were analyzed by the ELISA method. Mice in the binge group showed significant lowered plasma PYY levels after intragastric infusion of sugar compared to the FR group. The present result suggests that the reduced PYY secretion is correlated with the attenuation of feeding inhibition, resulting in binge-like sugar overconsumption.