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NutrInsight • About the value of controlling appetite
The action of ghrelin has also been shown to be dependent of the endocrine environment. For example, ghrelin reduces both the secretion and the anorexigenic action of leptin, in the same way that leptin reduces the secretion and anorexigenic action of ghrelin. This phenomenon has been designated the «ghrelin-leptin tango» (46). Finally, it appears that ghrelin can also interact with CCK (47). Ghrelin therefore appears to be one of the markers of hunger and of the initiation of eating, but its mechanism of action remains complex.
Examples of markers of the long-term regulation of appetite
Leptin
Leptin, a hormone produced mainly by the adipose tissue, is secreted into the blood stream via which it reaches the brain after crossing the blood/brain barrier (48).
The concentration of leptin in the bloodstream reflects both the energy reserves of the body (its basal concentration is positively correlated to the adipose mass) and with eating (49).
Animal studies have demonstrated that leptin has the effect on reducing both bodyweight and food intake. However, in a person in a situation of energy equilibrium, the correlation between the concentration of leptin and appetite is not clear. It is true that the concentration of leptin does not change immediately (3-4h) in response to eating a meal, and many studies do not show any relationship between the concentrations of leptin and the subjective appetite before and after a meal (50;51). In contrast, the concentration of leptin in the bloodstream is strongly correlated to appetite, when the subjects are in a situation of energy imbalance. Thus, leptin cannot be used as a biomarker of short-term satiety, but could be used as a biomarker of long-term satiety in subjects in a situation of energy imbalance (5;36).
Peptide tyrosine-tyrosine (PYY)
Peptide tyrosine-tyrosine (PYY) is secreted by the digestive tract (distal ileum and colon) in response to food intake and its concentration remains high for 6 h after the meal (52). Its release into the bloodstream is influenced by the calorie density and composition of the alimentary bolus (lipids producing the greatest stimulus just after the meal while proteins producing a higher signal after two hours (53)), or in the presence of other hormones (CCK seems to increase the concentration of PYY, whereas GLP-1 seems to reduce it). Several studies of the effect of exogenous PYY suggest that the secretion of PYY has the effect of inhibiting the food intake and the subjective appetite, perhaps, in part at least, by inhibiting the secretion of ghrelin (54;55;56). However, in view of the limited evidence for the role of endogenous PYY, it is not yet possible to say whether this can be used as a biomarker of appetite regulation.
Other biomarkers in appetite control... Perspectives
Insulin, a hormone produced by the pancreas, is involved in regulating the blood sugar level and the use of energy substrates. Its plasma concentration varies over the course of the day and increases mainly after a meal containing carbohydrates (57). Its role in the appetite regulation at central level is debated (5;36). Other pancreatic peptides, as namely pancreatic peptide (PP) and amylin could play a role in food intake regulation (58). Recent data suggest that the dietary modulation of gut microbiota could participate to the satiety regulation. The metabolic activity of the intestinal flora (by producing short chain fatty acids and some peptides) could become a new physiological target to take into account in appetite regulation (59).
The cannabinoid system, including fatty acids derivatives, appears as a complex but integrative system which seems to be involved in the control of food intake (60).
[ PYY and insulin, contested markers of satiety. ]
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