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About the value of controlling appetite • NutrInsight
2.2 Physiological markers of satiation and satiety
In parallel with behavioural measures, the use of biomarkers such as blood glucose or the levels of the hormones implicated in the long-term regulation of the energy balance also provides objective indications with regard to the satiation/satiety status of the individual. The same is true of brain imaging.
Hormonal markers
Examples of markers of the short-term regulation of appetite
Plasma cholecystokinin (CCK)
Cholecystokinin (CCK) is a hormone produced by the endocrine cells of the intestine (see Table 1, page 13). Next to the endocrine cells, a small proportion of CCK is produced by neurons in the gastro-intestinal tract and nervous system (24). The arrival of proteins or lipids in the intestine stimulates its secretion into the lumen and, in some cases, into the bloodstream where its concentration may remain high for up to 5h after eating. CCK causes gallbladder contraction and stimulates the release of digestive enzymes by the pancreas (amylase, peptidade, lipase). CCK has been subjected to very numerous studies, and nearly all of them have demonstrated its ability to reduce the food intake and/or subjective appetite (22). Its satiating potential appears to be potentiated by the distension of the stomach (25) or by the secretion of leptin (26). Furthermore, as indicated by its interaction with signals of adiposity, such as leptin, CCK may have a longer- term effect on the regulation of bodyweight (27;28). CCK is therefore found to be a short-term marker of appetite and, potentially, a long-term marker of bodyweight.
Glucagon-Like Peptide 1 (GLP-1)
Glucagon-Like Peptide 1 (GLP-1) is produced in the ileum (29) in response to the arrival of nutrients in the intestine (30;31). Its actions include potentiating the synthesis of insulin (32). GLP-1 is thought to affect the brain, from its peripheral secretion. Several GLP-1 receptors have been located in the hypothalamus, and can be activated by peripheral GLP-1 (33;34). Indirect evidence (obtained during studies of the effects of exogenous GLP-1) suggests that the active form of GLP-1 (GLP-17-36 amide ) reduces the food intake and subjective appetite in the short-term in normal, obese and diabetic individuals (35;36). This effect may be linked to its ability to modulate the motility of the stomach and intestine during and after eating, by being involved in the so called “ileal brake” mechanism (37). Despite the limited number of studies of the effect of endogenous GLP-1 7-36 amide , its use as a marker of the short-term regulation of appetite has been shown to be pertinent. In contrast, it is currently difficult to provide evidence of its value as a marker of long-term regulation.
Ghrelin
Ghrelin is a peptide most of which is synthesized by the stomach, even though it occurs throughout the entire digestive tract (38) (see Table 1). Its level in the bloodstream is high in the fasting subject, and it peaks just before a meal that the subject hopes to eat. Its concentration falls soon after ingesting food and proportionally to the energy consumed (39;40;41), but also to its content of certain macronutrients, proteins producing a greater inhibition of its secretion than carbohydrates (42). These observations were the first to suggest that ghrelin acts as a factor that triggers eating, and have been supported by
[ CCK and GLP-1:
two hormones that both reduce appetite.
Ghrelin, the only hormone that stimulates appetite.]
various studies of exogenous ghrelin that have revealed its
stimulating effect on eating and on the subjective appetite
(43;44;45). However, a recent study contradicts this hypothesis and suggests instead that the postprandial concentration of ghrelin is not a determining factor in initiating eating (40). However, data are circumstantial and additional proofs (as definitive loss-of-function experiments) are required to disprove the hypothesis.
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