contd..
The levels of peripheral peptides such as leptin, cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) rise after meal signaling the brain to stop food intake. Postprandial cholecystokinin (CCK) level is low in individuals with binge eating. Binge eating is a state when one consumes larger amount of food in a discrete period of time and have a lack of control over this behaviour. Ghrelin is a gut peptide that is down-regulated by excess growth hormone. It increases our food intake. It rises before meal and falls after having it. High energy value meals lead to sharp decline in ghrelin. Under normal conditions, peripheral peptide such as ghrelin influences food intake. Its presence facilitates intake whereas decline terminates the intake process. Other peptides such as CCK, leptin, amylin and GLP-1 terminate food intake and rise after meals.
Cholecystokinin is a hormone that signals the brain processes for satiety function, thus helping us stop from eating any more. Decreased cholecystokinin level leads to increase in the amount of food eaten. It is also influences anxiety, depression, psychosis, cognition, nociception, and feeding behavior. There is a likelihood that the release of cholecystokinin is modulated neurotransmitters such as dopamine, serotonin, opioids, glutamate, and GABA receptor activation (Ghijsen et al., 2001). Cholecystokinin is present in the anterior cingulate cortex in abundance and plays significant role in the affective component of pain. It also modulates the nigrostriatal and mesolimbic dopaminergic pathways. As mesolimbic dopaminergic pathway is crucial for motivation and rewarding processes, it gets altered in depression, thus affecting mood disorders.