TABLE 1.

Physiology of the satiating effect of a high-protein diet¹

Agent	Location of synthesis	Mechanism of action	Satiating effect	Reference
CCK	Duodenum and ileal cells	Releases digestive enzymes and bile from the pancreas and gallbladder, respectively	Binds to specific receptors (CCK-1R) located on vagal sensory terminals transmitting to the NTS a sensation of fullness	11, 12
PYY3–36	L cells in the gut	Reduces caloric intake; concentration is positively correlated with the number of calories consumed	Acts at the hypothalamus via vagal pathways afferent to NTS; effect is mediated by excitement of POMC neurons and activation of anorexigenic circuits	13, 14
GLP-1	Ileum	Delays gastric emptying and accentuates glucose-induced stimulation of insulin synthesis and secretion, suppressing glucagon secretion	Activates the vagus nerve, conveying satiety signals through afferent fibers to the NTS	15–17
Neuropeptides and amino acid precursors	Ventral tegmental area; accumbens nucleus	High-protein diet reduces reward-driven eating behavior through the activation of specific brain regions in the corticolimbic system	Serotonergic pathways and transmitters are involved in the reward circuit, influencing the brain availability of their amino acid precursors; a high-protein diet promotes a reduction in brain activation responses to food stimuli in the limbic regions related to food motivation (i.e., hippocampus, amygdala, anterior cingulated, and parahippocampus)	10, 20, 21

¹CCK, cholecystokinin; GLP-1, glucagon-like peptide 1; NTS, nucleus tractus solitarius; POMC, pro-opiomelanocortin; PYY, peptide YY.