Poster Presentation ANZOS-OSSANZ-AOCO Joint Annual Scientific Meeting 2017

Evaluating gastrointestinal (GI) peptides as markers of satiety in dietary intervention studies: how informative are the ‘satiety’ peptides? (#233)

Jia Jiet Lim 1 2 , Sally D Poppitt 1 2
  1. Human Nutrition Unit, School of Biological Sciences, University of Auckland, Auckland, New Zealand
  2. Riddet Centre of Research Excellence (CoRE), Palmerston North, New Zealand

Multiple mechanical or chemical stimuli originating in the gastrointestinal (GI) tract are involved in the regulation of satiety and food intake. Arrival of nutrients into the gut results in the release of peptides which, along with the activation of neural signals, have long been hypothesized to alter appetite-related sensations and eating behaviour1,2. While these peptides have specific roles in digestion, absorption and metabolic fate of nutrients the physiological role they play in regulation of ingestion and eating behaviour is less well understood and the causative relationship has been challenged3. A literature research was conducted evaluating change in circulating CCK, GLP-1, PYY and satiety following endogenous (changes caused by diet) and exogenous (changes caused by pharmaceutical infusion) interventions. Relative changes in peptide concentrations were compared to identify the physiological relevance of these ‘satiety’ peptides.

Online literature search retrieved 128 dietary interventions from 44 published articles reporting baseline and postprandial peptide concentrations, and 38 pharmaceutical (infusion) interventions from 20 published articles. Baseline concentration of CCK and GLP-1 were similar between both study groups, whilst PYY had a wider range reported in the dietary studies. Peak hormone concentration (Cmax) was significantly lower following diet intervention for all peptides when calculated both as maximum value (mean ± SEM pM, GLP-1: diet 16.9±0.5, drug 36.2±3.0; PYY: diet 47.3±1.4, drug 78.2±3.1; CCK: diet 3.23±0.1, drug 17.8±1.3; P<0.001, all); and as fold increase above baseline (fold change, GLP-1: diet 1.9±0.01, drug 6.3±0.3; PYY: diet 1.9±0.03, drug 4.7±0.2; CCK: diet 3.0±0.1, drug 11.0±1.2; P<0.001, all). Whilst there was overlap in range of response between diet- and pharmaceutical-induced levels of all three peptides, diet studies consistently resulted in lower concentrations. Inability to attain a satiety-associated ‘threshold’ may explain the lack or variable response to a meal in many diet studies investigating appetite response.

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