We appreciate the interest of Jordan and Birkenfeld (1) on our recent publication in Diabetes (2). In this article, we showed that intravenous infusion of B-type natriuretic peptide (BNP) decreases hunger and increases satiety in healthy men and lowers circulating concentrations of ghrelin and acylated ghrelin in the absence of changes in other appetite-regulating hormones (2).
Jordan and Birkenfeld discuss the impact of elevated BNP concentrations on food intake and potential mechanisms underlying the anorectic effects of BNP (1). We have clearly written in both the abstract and the article that our study was performed in fasted individuals, and we neither studied nor commented on BNP effects on food intake (2). The anorectic and ghrelin-lowering effects of BNP during fasting were observed in the absence of changes in both plasma glucose (P = 0.127; repeated-measures ANOVA, time × treatment) and circulating free fatty acid concentrations (P = 0.563; repeated-measures ANOVA, time × treatment). Furthermore, in a previous interventional study in men we also excluded direct BNP effects on β-cell function and insulin sensitivity (3,4). All our BNP interventions in men were performed in supine position in order to avoid changes in blood pressure and subsequent counterregulatory mechanisms that might indirectly affect study outcomes (2,3).
In summary, anorectic BNP effects reported in men while fasting cannot be related to changes in nutrients and insulin, and the postulation of a heart-gut-brain communication is supported by the data presented in the article (2). The link between BNP, ghrelin, and appetite might represent an important physiological axis participating in the complex interrelated central and peripheral mechanisms regulating appetite in humans.
ACKNOWLEDGMENTS
No potential conflicts of interest relevant to this article were reported.
