Abstract
CCK was first described as a substance derived from the small intestines of dogs and cats and that induced gall bladder contractions in 1928. In vertebrates, different forms of CCK peptides (CCK-58, CCK-33, CCK-22, CCK-12, CCK-8, and CCK-4) contain the conserved C-terminal four amino acid sequence (Trp-Met-Asp-Phe-NH2). A sulfated tyrosine located at the seventh residue from the C-terminus is also conserved in vertebrates. In mammals, CCK is expressed in a wide range of tissues, including the digestive tract (duodenum and small intestine) and the central nervous system. Two CCK receptor subtypes, CCK1R and CCK2R, have been identified. Lipids and proteins induce CCK release from I-cells in the duodenum and small intestine. CCK stimulates gall bladder contraction and pancreatic enzyme release via CCK1R. In addition, CCK inhibits gastric emptying and food intake through the vagal afferent neurons. In the central nervous system, CCK is implicated in anxiogenesis, satiety, appetite, nociception, memory, and learning.
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