The paradigm for the control of feeding behavior has changed significantly. In this review, we present evidence that the separation of function in which cholecystokinin (CCK) controls short-term food intake and leptin regulate long-term eating behavior and body weight become less clear. In addition to the hypothalamus, the vagus nerve is critically involved in the control of feeding by transmitting signals arising from the upper gut to the nucleus of the solitary tract. Among the peripheral mediators, CCK is the key peptide involved in generating the satiety signal via the vagus. Leptin receptors have also been identified in the vagus nerve. Studies in the rodents clearly indicate that leptin and CCK interact synergistically to induce short-term inhibition of food intake and long-term reduction of body weight. The synergistic interaction between vagal CCK-A receptor and leptin is mediated by the phosphorylation of signal transducer and activator of transcription3 (STAT3), which in turn, activates closure of K+ channels, leading to membrane depolarization and neuronal firing. This involves the interaction between CCK/SRC/phosphoinositide 3-kinase cascades and leptin/Janus kinase-2/phosphoinositide 3-kinase/STAT3 signaling pathways. It is conceivable that malfunctioning of these signaling molecules may result in eating disorders.
Appetite ; Body Weight ; Cholecystokinin ; Eating ; Feeding and Eating Disorders ; Feeding Behavior ; Fires ; Hypothalamus ; Leptin ; Membranes ; Neurons ; Nodose Ganglion ; Phosphorylation ; Receptor, Cholecystokinin A ; Receptors, Leptin ; Rodentia ; Signal Transduction ; Solitary Nucleus ; Transducers ; Vagus Nerve

Animals ; Mice ; Colitis, Ulcerative/metabolism* ; beta Catenin ; Carcinogenesis ; Probiotics ; Colitis/metabolism*