Satiety, Taste and the Cephalic Phase: A Crossover Designed Pilot Study into Taste and Glucose Response
Thanyathorn Sae Iab1, Robin Dando1
1Department of Food Science, Cornell University, Ithaca, NY 14853, USA.
Abstract:
The glycemic response produced by a food depends on both the glycemic index of the food itself, and on how the body reacts to the food as it is consumed and digested, in turn dependent on sensory cues. Research suggests that taste stimulation can induce the cephalic phase insulin response before food has reached the digestion, priming the body for an incoming glucose load. This glycemic response can consequently affect the amount of food consumed in a subsequent meal. The aim of this study was to investigate the effects on satiety of four preloads that differed in caloric content and sensory properties, in a small group of female and male participants (n = 10). Water, sucrose, sucralose, and maltodextrin were used to represent 4 different conditions of the preload, with or without energy, and with or without sweet taste. Individual plasma glucose concentrations were sampled at baseline, 45 min after consuming the preload, and after consuming an ad-libitum test meal. Hunger, fullness, desire to eat, and thoughts of food feeling were assessed every 15 min using visual analog scales. Results in male participants when comparing two solutions of equal caloric content, maltodextrin and sucrose, showed that plasma glucose concentration spiked in the absence of taste input (p = 0.011). Maltodextrin, while providing calories does not have the sweet taste that can serve to trigger cephalic phase insulin release to attenuate an incoming glucose load, and was accompanied by significantly greater change in feelings of satiety than with the other preloads. Despite the difference in postprandial blood glucose, the energy consumed in the test meal across the treatments was not significantly different in either males or females. Results highlight the importance of taste in stimulating the body for the efficient and effective glucose homeostasis.
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