Exercise is associated with transient suppression of appetite which previously has been attributed to induction of appetite-regulatory hormone such as GLP-11 or the increase in circulating metabolites including L-lactate2. A targeted metabolomics approach with blood samples from two independent human exercise studies resulted in the identification of N-lactoyl-phenylalanine (Lac-Phe, 183241-73-8) as a highly upregulated circulating metabolite following exercise.3 Lac-Phe was shown, using pharmacological and genetic methods, to be an exercise-inducible metabolite that suppresses feeding and obesity. A single injection of Lac-Phe was demonstrated to reduce food intake by ~50% in diet-induced obese mice. However, Lac-Phe is completely inactive when administered orally.4
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