Altered ghrelin and peptide YY responses to meals in bulimia nervosa

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Abstract
Objective In recent years great advances have been made in our understanding of the peripheral signals produced within the gastrointestinal tract that regulate appetite, such as ghrelin and peptide YY (PYY). While ghrelin elicites hunger signals, PYY elicites satiety. Therefore, alterations in hormone physiology may play a role in the pathogenesis of bulimia nervosa (BN). In this study, we investigated the postprandial profile of ghrelin and PYY levels in patients with BN. Design and patients Postprandial plasma ghrelin and PYY levels and insulin and glucose responses were measured in 10 patients with BN and 12 control patients in response to a standard 400 kcal meal. Results Basal ghrelin levels present in BN subjects (265·0 ± 25·5 pmol/l) were significantly higher than those in healthy controls (199·3 ± 18·4 pmol/l, P < 0·05), while basal PYY levels were equivalent in BN (14·6 ± 1·3 pmol/l) and control (12·8 ± 1·1 pmol/l, P = 0·30) subjects. Postprandial ghrelin suppression (decremental ghrelin area under the curve) was significantly attenuated in BN patients, compared to controls (−96·3 ± 26·8 pmol/l × 3 h vs. −178·2 ± 25·7 pmol/l × 3 h, P < 0·05). After a meal, the incremental PYY area under the curve in BN patients was significantly blunted from that observed in controls (9·2 ± 2·6 pmol/l × 3 h vs. 26·8 ± 3·2 pmol/l × 3 h, P < 0·01).Glucose and insulin responses to meals were similar between the two groups. Conclusions BN patients exhibit elevated ghrelin levels before meals with reduced ghrelin suppression after eating. In bulimia nervosa subjects, the rise in PYY levels after meals is also blunted. A gut–hypothalamic pathway involving peripheral signals, such as ghrelin and PYY, may be involved in the pathophysiology of BN.