Study on the Mechanism of Dietary Fat Palatability

(Young Investigator Award of JSNFS (2018))

Abstract

Dietary fat is an attractive food component. Recent studies have suggested that chemical perception of fatty acid plays a role in the high palatability of fatty foods. Previously, we have found that the fatty acid transporter, CD36, is expressed in rodent taste bud cells, and recently we discovered that G-protein coupled receptor 120 (GPR120) is also expressed in taste cells. GPR120 is known to be a receptor for unsaturated fatty acid, and the mouse is a species known to have a marked preference for unsaturated fatty acids. These findings suggest that GPR120 might function as a sensor for dietary fat. It is well known that intake of palatable food stimulates β-endorphin release in the brain. We have found that dietary fat ingestion activates β-endorphin neurons in the hypothalamus via activation of taste nerves. Taste nerve transection surgery suppressed the activation of β-endorphin neurons resulting from dietary fat ingestion. Taken together, our present findings indicate that dietary fat may stimulate taste cells on the tongue through CD36 and GPR120, thus activating β-endorphin neurons in the brain. It is speculated that activated β-endorphin neurons release β-endorphin to promote consummatory behavior involving fatty foods.