Study on the Mechanism of Dietary Fat Palatability

Abstract

Dietary fat is an attractive food component. Recent studies have suggested that chemical percep- tion 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 re- ceptor 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 neu- rons in the hypothalamus via activation of taste nerves. Taste nerve transection surgery suppressed the activa- tion 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 con- summatory behavior involving fatty foods. Key