cholecystokinin (CCK)

Introduction

Cholecystokinin regulates gastrointestinal functions, including inhibition of gastric emptying and food intake through activation of CCK-1 receptors on vagal afferent fibers innervating the gut.
CCK is also important for secretion of pancreatic fluid and producing gastric acid, contracting the gallbladder, decreasing gastric emptying, and facilitating digestion.
Saturated fat, long-chain fatty acids, amino acids, and small peptides that result from protein digestion stimulate the release of CCK from the small intestine.
There are various biologically active forms of CCK, classified according to the number of amino acids they contain, i.e., CCK-5, CCK-8, CCK-22, and CCK-33.
- In neurons, CCK-8 is always the predominating form, whereas the endocrine gut cells contain a mixture of small and larger CCK peptides of which CCK-33 or CCK-22 often predominate.
CCK is also present in enteric vagal afferent neurons, in cerebral cortex, in the thalamus, hypothalamus, basal ganglia, and dorsal hindbrain, and functions as a neurotransmitter
CCK directly activates vagal afferent terminals in the NTS by increasing calcium release
there is substantial evidence that elevated levels of CCK induce feelings of anxiety
Leptin and CCK interact synergistically to induce short-term inhibition of food intake and long-term reduction of body weight
epithelial cells that respond to both ghrelin and leptin are located near the vagal mucosal endings and modulate the activity of vagal afferents, acting in concert to regulate food intake
activation of bitter taste receptors stimulate both the release of CCK (reducing hunger) and ghrelin (increasing hunger), and therefore affects the vagus nerve.