Systematic review and meta-analysis of the effect of meal intake on postprandial appetite-related gastrointestinal hormones in obese children.

UNLABELLED: Understanding the physiological response to meal intake, of gut-derived appetite and satiety hormone signals, in obese compared with healthy-weight children may assist with informing strategies to help curtail the obesity epidemic. A systematic review and meta-analysis of studies investigating the acute postprandial response of gastrointestinal appetite hormones to meal intake in obese children was undertaken. Systematic searches of databases EMBASE, CINAHL Plus, OVID Medline and the Cochrane Library were performed. INCLUSION CRITERIA: a randomised controlled trial or experimental cross-sectional study following an acute test meal protocol with pre- and postprandial analysis of plasma or serum gastrointestinal hormone concentrations. Database searching retrieved 1001 papers for review. Nine studies met the inclusion criteria, collectively reporting on six appetite hormones yielding a total of 32 test meal-hormone comparisons. Meta-analyses compared the pooled estimate of the mean difference of the postprandial change in total ghrelin and total peptide YY (PYY). Obese compared with healthy-weight children had an attenuated change in ghrelin at 60 min (N=5 studies; n=129 participants) and 120 min postprandial (N=4 studies; n=100 participants) (P<0.05 for both time points). Obese compared with healthy-weight children also had an attenuated PYY response at 60 min (N=5 studies; n=128 participants) and 120 min postprandial (N=4 studies; n=100 participants). Insufficient studies reported on the postprandial time course of other appetite-related hormones, precluding a meta-analysis. Limited evidence notwithstanding, these findings indicate that PYY and ghrelin responses to a meal may be altered in obese children. This review has also identified a major gap in knowledge of hormonal appetite responses in childhood obesity. More comprehensive investigations of the homoeostatic regulation of gut-derived appetite and satiety hormone signals with behavioural and clinical outcomes are warranted to understand if there are consequences of these differences.