Mechanism of Onset of Hyperphagia in Obese Rats Figure 5. Altered neurochemical phenotype in DIO rats. Photomicrographs of sections of nodose ganglia to show immunoreactivity for Y2 (A), MCH1R (B), and CB1 (C) from fed and fasted Sprague Dawley rats after 8 weeks on respective diets. A) Y2 is barely detectable in nodose neurons of LF, DR, and DIO rats fasted 24 hours. Refeeding for 1 hour increased Y2 expression in LF and DR but not DIO rats. Quantification of positive Y2 cells as a percent of total cells. B) MCH1R and C) CB1 expression is elevated in fasted rats and is decreased by refeeding for 1 hour in LF and DR but not DIO rats. Quantification of positive MCH1R and CB1 cells as a percent of total cells. Representative images from experiments with four to six rats in each group are shown. Significant differences were represented as a,b,c between groups. doi:10.1371/journal.pone.0032967.g005 together, the data suggest that leptin resistance in VAN may account for the well known decrease in lipid- and CCK-induced satiation and hyperphagia following chronic HF feeding. Inaccu- rate monitoring of nutrients in the intestinal lumen may lead to a lack of satiety and contribute to diet-induced hyperphagia and obesity. PLoS ONE | www.plosone.org 6 March 2012 | Volume 7 | Issue 3 | e32967