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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Trends Endocrinol Metab. 2015 Mar 11;26(5):256–262. doi: 10.1016/j.tem.2015.02.008

Figure 1. Mechanisms through which changes in dietary protein intake are detected and communicated to the brain.

Figure 1

Dietary protein within the GI tract activates both endocrine and vagal signals, which act in a primarily anorexigenic fashion in the hypothalamus and brainstem. Absorbed amino acids are delivered to the liver via the hepatic portal vein. Reduced amino acid supply to the liver increases hepatic FGF21 secretion, which acts in the brain to increase both food intake and energy expenditure, likely via effects in the hypothalamus. Amino acids are transported out of the liver and into the general circulation, and circulating amino acids can act in both the hypothalamus and brainstem to suppress food intake. Finally, imbalances in dietary or circulating amino acid concentrations are detected in the anterior piriform cortex (APC), with activation of the APC reducing food intake. These various mechanisms allow animals to detect and adaptively respond to diets that are high, low or imbalanced in amino acid content.