Endocrine Abstracts

CCK, secreted from duodenal cells in response to nutrients is involved in the satiety mechanisms, via activation of nucleus tractus solitarius (NTS). The arcuate (ARC) and paraventricular nuclei (PVN), which receives projections from NTS, integrate the circuitry that controls food intake. Corticotrophin releasing factor (CRF) participates in the energy homeostasis, decreasing food intake.

To evaluate the effect of glucocorticoid on feeding and neuronal activation after CCK treatment, Wistar rats were subjected to Sham surgery, adrenalectomy without (ADX) or with corticosterone replacement (ADX+B). Animals fasted (day 6) for 16 h received ip injection of CCK 3.5 μg/kg or vehicle for determination of food intake and CRF and Fos imunohistochemistry.

Lower food intake was observed in Sham and ADX+B rats after CCK, compared to the respective vehicle-treated groups. However, this hipophagic response induced by CCK was not observed in ADX rats. CCK increased Fos expression in the NTS in Sham, ADX and ADX+B animals, with no difference among the three CCK-treated groups. We observed a higher number of Fos imunorreactive neurons in the ARC and Fos/CRF neurons in the PVN in ADX group, compared to Sham group, both after vehicle and CCK (P<0.05). We demonstrated that ADX abolishes the hypophagic response induced by CCK, however, NTS neuronal activation was not altered by glucocorticoid deficiency.

These data suggest that in the absence of glucocorticoids, other factors besides CCK participate in the satiety mechanisms, leading to a decrease of food intake. The increased activation of hypothalamic anorexigenic pathways during fasting, may contribute to the lower food intake observed with glucocorticoid deficiency.