What is the mechanism for the postingestive anorectic effect of aspartame?
2013
Rogers, P.J.
The dipeptide intense sweetener aspartame reduces food intake when consumed in a capsule (i.e., without tasting) in amounts as small as those contained in 1–2 servings of a ‘diet’ soft drink (Rogers et al., Physiol Behav 57, 489). This cross-over study (n=17, 7 women, DEBQ restraint ⩽2.5) tested indirectly the possibility that the mechanism underlying this effect involves the stimulation of sweet taste receptors in the gut (Sclafani, PNAS 104, 14887). Four structurally unrelated intense sweeteners, aspartame (500mg), acesulfame-K (450mg), saccharin (330mg) and sucralose (150mg) (amounts determined by their relative tasted sweetness intensity), were compared with placebo (500mg cornflour) for their effects on lunchtime food intake. These capsulated treatments were consumed 1h before the meal. Mean food intake after placebo was 1045kcal and 948kcal after aspartame (p=.033, one-tail). The next lowest intake was after sucralose (1022kcal, p=.638 versus placebo). The effect size for aspartame is consistent with previous observations. The results for the other sweeteners make it unlikely that sweet taste signalling in the gut mediates the anorectic effect of aspartame. Other findings show that the reduction in appetite after ingestion of aspartame, and after ingestion of its constituent amino acids (phenylalanine and aspartic acid) together, is related to the spike in blood phenylalanine concentration that also occurs after these treatments (Hall et al., Physiol Behav 78, 557). Perhaps, then, the mechanism involves central detection of this change in blood phenylalanine concentration and ensuing activation of neural circuitry controlling satiety.
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