The second is more complex and involves an increase in chemical signals, including the release of peptides such as cholecystokinin
(CCK, Paulino, Darcel, Tome & Raybould, 2008; Savastano & Covaa, 2005), glucagon-like peptide 1 (GLP-1, Williams, Baskin, & Schwartz, 2009) and peptide YY (PYY, Batterham et al., 2002).
The overexpression of cholecystokinin
receptor subtype 2 (CCK2R) is involved in various malignancies, such as medullary thyroid carcinoma (MTC), small cell lung cancer (SCLC), and neuroendocrine tumours (NET) [3,4] and therefore represents an interesting target for peptide receptor radionuclide imaging and therapy.
Magnocellular neurons of the PVN and supraoptic nucleus of the hypothalamus also produce a number of anorexigenic neuropeptides, including CART, pituitary adenylate cyclase-activating polypeptide, cholecystokinin
(CCK), and nesfatin-1 (51), and are activated during feeding and by satiety peptides such as CCK and GLP1.
For example, the intake of fatty foods slows gastric emptying and causes a reduction in the basal pressure of the LES through a mechanism probably mediated by cholecystokinin
(CCK) that can directly act on the LES, or indirectly, by inhibiting the action of gastrin .
Protein triggers cholecystokinin
, a hormone that signals the brain to slow down the emptying of the stomach.
It also stimulates hormones secreted by gastrointestinal mucosa cells, such as gastrin, cholecystokinin
, and glucagon.
Food contents in the duodenum will stimulate the release of cholecystokinin
and causes contraction of gallbladder.
(CCK) is a peptide hormone secreted by the gastrointestinal tract, and its effects include gallbladder and pancreatic secretion, gastric and intestinal motor function, reduced food intake and stimulation of GH secretion (Canosa et al., 2007; Crespo et al., 2014; Micale et al., 2014; Dalmolin et al., 2015).
In addition, acidic environment of the gut stimulates the secretion of pepsin, gastrin and cholecystokinin
, playing an essential role in the feed utilization, and subsequently improving growth performance (Hayat et al., 2014).
(9-11) In addition, there is evidence that NOD1 responses are key factors in the development of pancreatitis as reflected in the experimental pancreatitis caused by cholecystokinin
Their findings was published last week in Neuron under the title "(http://www.cell.com/neuron/fulltext/S0896-6273(17)30596-2?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627317305962%3Fshowall%3Dtrue) Initiation of Behavioral Response to Antidepressants by Cholecystokinin
Neurons of the Dentate Gyrus ."
For example, cholecystokinin
(CCK) analogues cause pancreatitis in rodents in the absence of alcohol treatments only at doses much greater than those needed to activate known physiologic responses such as pancreatic enzyme secretion and gallbladder contraction (Lam et al.