Peptide YY

Abstract

Purpose of review Peptide YY, released from the gastrointestinal tract, has been shown to reduce food intake and bodyweight in rodents and to reduce food intake after intravenous infusion in humans. The purpose of this review is to highlight recent advances in the peptide YY field with regard to energy balance in both rodent and human models. Recent findings The anorexigenic effect of peripherally administered peptide YY3–36 in rodents has been confirmed by others. A number of groups have been unable to reproduce these original findings. Recent studies have suggested that the failure of an anorexigenic response to peptide YY3–36 may be explained, at least partly, by interference by incidental extraneous experimental stress. Peptide YY3–36 was initially hypothesized to alter food intake inhibiting neuropeptide Y appetite-stimulating pathways in the hypothalamus. If these pathways were already inhibited by incidental stress, peptide YY3–36 would have nothing further to inhibit. There is conflicting evidence as to whether peptide YY3–36 alters food intake via a direct circulation/hypothalamic interaction or via the vagal pathway. Recent studies have found that plasma peptide YY levels are elevated post-gastric bypass in obese individuals, which may be the cause of the resulting appetite loss post-surgery. Finally, peptide YY, when administered in combination with glucagon-like peptide-1, reduces food intake to a greater extent than either alone in rodent and human models, suggesting a possible combination therapy for reducing bodyweight. Summary Peptide YY reduces food intake in rodent and human models and plays a role in the homeostatic mechanisms underpinning energy balance.