Page 8 - Nutrinsight-4

NutrInsight • Satiety: from appetite sciences to food application
1.4 The prevailing model for Appetite Control:
the central role of adipose tissue and “satiety peptides”
A model for appetite control, developed mainly from animal studies, highlights the key influence of gastro- intestinal signals [Badman & Flier, 2005]. This model shows how the daily meal pattern and meal size are organised by the brain under the influence of numerous physiological signals from the periphery of the organism. Satiety signals can be neural, when the nutrient chemoreceptors and stretch receptors in the gastro-intestinal tract send messages to the brain via vagal afferent fibres. Hormonal signals, such as leptin, released by the adipose tissue, insulin, secreted by the pancreas in response to a meal, or ghrelin whose high level in the stomach before eating drops to low levels after the meal, are important modulators of appetite and satiety. Numerous “satiety peptides” and hormones are secreted by the gastro-intestinal tract following the intake of foods (cholescystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), among others). Gastro-intestinal peptides appear to constitute a bridge between physiology (the response to food) and the changes in appetite expressed by behaviour. It is then tempting to examine the particular influence of a given peptide, or a pattern of peptides, on the behavioural expression of satiety.
Gastro-intestinal hormones (including GLP-1, PYY, insulin, CCK, and ghrelin) have recently been studied in usual feeding circumstances in humans [Gibbons et al., 2013]. This research has shown that gastro-intestinal peptides respond sensitively and selectively to the nutrient composition of the food eaten. For example, post-ingestive changes in the blood levels of the hormone ghrelin are sensitive to the nutrient composition of the meal (Figure 2). Ghrelin levels decrease progressively in the early phase of satiety following a meal (first hour), while hunger feelings are totally suppressed. The levels of ghrelin then rise over the following hours, in parallel with the progressive return of hunger. While different peptides can contribute to satiety, there is no unique satiety peptide and different profiles of peptides can produce the same suppression of hunger [Gibbons et al., 2013].
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Ghrelin HF Ghrelin HCHO
Hunger HF
Hunger HCHO
0 30 60 90 120 150 180 210
CH
LUN
-50 -100 -150 -200 -250
-10
-20 -30 -40 -50
Time (minutes) -60
PHASE 1
EARLY SATIETY
PHASE 2
LATE SATIETY
PHASE 3
SATIATION
GHRELIN
HUNGER
Figure 2: ghrelin and hunger fluctuations following high fat/low carbohydrate (HF) and high carbohydrate/low fat (HCHo) test meals
Source: Adapted from Gibbons et al., 2013
In addition, while the contribution of gastro-intestinal peptides to satiety is likely in many circumstances, the mechanisms that account for the satiety effects observed over the satiety cascade are more complex than the influence of gastro-intestinal factors. In recent years, the potential influence of the gut microbiota has attracted much scientific attention. The chapter 4 by Pr. Nathalie Delzenne reviews key concepts in this field.
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Ghrelin change from baseline (pg/ml)
Hunger change from baseline (mm)