Stewart, J.S., Golding, M., Delahunty, C. and Keast, R.S.J. 2008, The role of fatty acids in satiation and satiety, in NSA 2008 : Proceedings of the Nutrition Society of Australia Annual Scientific Meeting, HEC Press, Adelaide, S.Aust..
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NSA 2008 : Proceedings of the Nutrition Society of Australia Annual Scientific Meeting
Place of publication
Background – Satiation and satiety describe the events which lead to meal termination and the maintenance of hunger induced by physical and metabolic events following food ingestion. Fatty acids, components of dietary fat (triglyceride) may be important, if not essential components of satiation and satiety. Emerging evidence suggests fatty acid now constitutes a sixth taste modality and orally sensed fatty acids mediate unique cephalic and hormonal responses priming the body for fat digestion, and may contribute to sensory specific satiety. Once ingested, fatty acids are sensed in the gastrointestinal tract (GIT) where they cause the release of hormones, stimulate the vagus and enter the blood stream where they act a number of organs (brain, liver) to influence satiety. Objective – To review the role of fatty acids in sensory and metabolic satiation and satiety. Design
– Literature search and review of papers from the past decade on satiety, satiation, fat taste and fatty acids. Outcomes – The physiological significance of gustatory fat detection is still unclear, but it may signal the nutritious content of fat similar to the tastes of sweet or umami which signal the presence of carbohydrate or proteins. Like other tastants, fatty acid taste sensitivity is thought to vary in the population and differences in sensitivity may influence dietary choice and fat intake. Fatty acid taste may contribute to sensory specific satiety as foods are eaten. Animal models have observed an inverse relationship between oral fatty acid sensitivity and fat consumption, which leads to obesity. Observations that the obese have heightened preferences for, and consume more fat than lean individuals questions whether such a relationship may also be apparent in humans. At the GIT, fatty acids are sensed by
enterocytes and bind to receptors, transporters or ion channels where they initiate gut-brain communication over nutrient status through the vagus and cause the release of satiety hormones which lead to meal termination. Inefficient fatty acid sensing at either or both locations is thought to accompany the aetiology of obesity. Conclusion – Variations in sensitivity to fatty acids may alter preferences and consumption of fats or hormonal responses to fat ingestion which influence sensory-specific, metabolic and subjective satiety.
Field of Research
170112 Sensory Processes, Perception and Performance