Figure 2

Schematic representation of fatty acid chemoreception in the oral cavity and gastrointestinal tract (alimentary canal) in lean (left) and obese (right) individuals. (1) Fat is present in foods in the form of TAG; free fatty acids are generated during the breakdown of fats and by lipase enzymes in the oral cavity. (2) Fatty acids access putative receptors (CD36, GPCR40, GPCR41, GPCR43, GPCR120 and delayed rectifying potassium (DRK) channels) within taste cells; lean individuals have greater quantities of these receptors compared to obese individuals. The receptors elicit the release of intracellular Ca²⁺ that in turn activates neurotransmitters and hormones associated with the cephalic response. (3) Following fat ingestion, gastric and pancreatic lipase plays a further role in the hydrolysis of fats enabling access to fatty acid receptors on enteroendocrine cells, stimulating satiety hormones and uptake of fatty acids. As a consequence, sensitivity to ghrelin, which is responsible for hunger stimulation, is inhibited, while the satiety-inducing hormone leptin is released as are the hormones CCK, PYY and GLP-1. (4) In a lean individual, expression of fatty acid receptors is greater, therefore increasing fat sensing ability through the alimentary canal and thereby decreasing energy intake. (5) In comparison, obese individuals have decreased expression of fatty acid receptors, attenuating fat sensing ability and increasing energy intake. Reproduced from [52].