Abstract
<jats:p>The satiety cascade includes post-prandial increases in plasma glucose and insulin, and changes in appetitive gut hormones, including decreases in orexigenic stomach-derived ghrelin, and increases in liver-foregut-derived LEAP2 hormone, a ghrelin antagonist. However, which contribute to post-prandial attenuation of eating behaviour with increasing preload meal size is unclear. In a randomised, single-blinded study, adults without obesity attended four visits, consuming 750mL liquid preloads 0, 600, 900, 1200 kcal, with assay of plasma glucose, acyl ghrelin (AG), LEAP2 and serum insulin over 0-3h with appetite ratings (n=17, 65 visits). At 2h a virtual portion size creation task measured desired food intake (n=15, 58 visits, after data exclusion), and at 3h an ad libitum meal measured actual food intake (n=11, 43 visits). The greater the pre-load meal size, the greater the post-prandial increase in plasma glucose and serum insulin, and greater the decrease in plasma AG and AG/LEAP2 ratio, associated with greater attenuation of eating behaviour (appetite ratings, desired/actual food intake). The strongest correlations of eating behaviour with blood measures were for serum insulin, plasma AG and AG/LEAP2 ratio, with weaker results for plasma glucose. Although there was a weak correlation of post-prandial plasma LEAP2 with pre-load meal size but not with eating behaviour. Post-prandial increases in serum insulin and decreases in plasma AG and AG/LEAP2 ratio appear part of the satiety cascade related to preload meal size in adults without obesity. Future studies should investigate potential mediation of satiety in this context via other appetitive gut hormones, and in obesity.</jats:p>