Blood glucose is one of key factors to regulate food intake. It is demonstrated that several neural systems respond to changes in glucose levels and control food intake. Studies have shown that dietary manipulations affect the regulatory systems. Successive daily sugar access for several hours under food restriction induces sugar overconsumption. We assumed that the disturbance in the glucostatic control of food intake would be one of the causes of sugar overconsumption. To test this assumption, we examined whether the daily intermittent sugar access under food restriction alters glycemic, behavioral and neuronal responses to a systemic glucose injection. Mice under 20-h food restriction received 4-h access to chow with or without 0.5 M sucrose solution (FR/Suc and FR mice, respectively) for 24 days. FR/Suc mice exhibited overconsumption of the sucrose solution from Day 13 to Day 24. After the 24-day feeding protocol, the mice were food restricted overnight followed by an intraperitoneal glucose injection (2 g/kg). Then, blood was collected from the tail vein at 15, 30, 60, and 120 min and analyzed for glucose by a portable glucometer. FR/Suc mice showed less blood glucose elevation compared to that before the feeding protocol, while in FR mice there was no significant difference in glucose levels between before and after the feeding protocol. In another group of mice, food intake was measured at 30 min after the glucose injection. On the next day, the mice were perfused at 90 min after the glucose injection and their brains were processed for Fos-immunoreactivity. The glucose injection reduced food intake in FR but not FR/Suc mice. Fos positive cells in the area postrema of FR/Suc mice were smaller than those in FR mice. These findings demonstrated that the intermittent sucrose access under food restriction attenuated the anorexic effect of glucose and the neuronal responses to glucose injection in the area postrema. It is suggested that these physiological and neuronal changes contribute to sucrose overconsumption.