Oral fatty acid signaling and intestinal lipid processing: Support and supposition

There is increasing recognition that specialized processes once thought to be relatively isolated to the oral cavity (e.g., taste) and intestine (e.g., nutrient absorption) are better characterized as common and continuous. This is exemplified by accumulating evidence linking oral detection of dietary fats to their intestinal processing. This review first summarizes this literature focusing on purported gustatory signaling by free fatty acid stimulation and enterocyte lipid storage and mobilization in humans. It then willfully speculates on the possible functions of this integrated system. It is proposed that it may aid absorption of fat soluble nutrients, enhance acute energy intake, sustain intestinal function during long inter-meal intervals, modulate appetite and/or detoxify ingested compounds including free fatty acids.

► Free fatty acids are effective signaling molecules in the oral cavity of humans though there is marked inter-individual variability in sensitivity. They are ligands for an array of putative fat receptors on taste receptor cells, but may also activate olfactory and trigeminal neurons.
► Oral fat detection influences lipid metabolism. It promotes a rapid rise in serum triacylglycerol, possibly by mobilizing lipid stored in the enterocyte from the previous eating event as well as by reducing the clearance rate through reduced adipocyte lipoprotein lipase activity.
► Oral (taste) detection thresholds for free fatty acids are not related to BMI, but there is a positive association between BMI and the post-stimulation serum triacylglycerol concentration for full-fat stimuli. This is less robust for fat-free versions of the same food.
► The functions of oral fat detection are poorly characterized, but may include, modulation of lipid trafficking in the enterocyte, detoxification of lipophilic cytotoxic compounds, appetite, energy intake and/or fat soluble nutrient absorption.