Biomarkers of satiation and satiety

Abstract

This review's objective is to give a critical summary of studies that focused on physiologic measures relating to subjectively rated appetite, actual food intake, or both. Biomarkers of satiation and satiety may be used as a tool for assessing the satiating efficiency of foods and for understanding the regulation of food intake and energy balance. We made a distinction between biomarkers of satiation or meal termination and those of meal initiation related to satiety and between markers in the brain [central nervous system (CNS)] and those related to signals from the periphery to the CNS. Various studies showed that physicochemical measures related to stomach distension and blood concentrations of cholecystokinin and glucagon-like peptide 1 are peripheral biomarkers associated with meal termination. CNS biomarkers related to meal termination identified by functional magnetic resonance imaging and positron emission tomography are indicators of neural activity related to sensory-specific satiety. These measures cannot yet serve as a tool for assessing the satiating effect of foods, because they are not yet feasible. CNS biomarkers related to satiety are not yet specific enough to serve as biomarkers, although they can distinguish between extreme hunger and fullness. Three currently available biomarkers for satiety are decreases in blood glucose in the short term (<5 min), which have been shown to be involved in meal initiation; leptin changes during longer-term (>2-4 d) negative energy balance; and ghrelin concentrations, which have been implicated in both short-term and long-term energy balance. The next challenge in this research area is to identify food ingredients that have an effect on biomarkers of satiation, satiety, or both. These ingredients may help consumers to maintain their energy intake at a level consistent with a healthy body weight.

Response of appetite and potential appetite regulators following intake of high energy nutritional supplements

“…We found that within participant relations between responses of appetite scores and responses of hormones showed significant correlations with regards to PYY and insulin, but not CCK. Thus, our findings contribute to the debate about whether appetite hormones act as biomarkers of appetite (De Graaf et al, 2004;A. Flint et al, 2007;Lemmens et al, 2011) and support the notion of the subjective appetite measures being better correlates of energy intake than circulating levels of individually considered appetite hormones (Doucet et al, 2008).…”

“…Even though the enhanced satiety and reduced hunger measured for 60 min (pre-breakfast period) after HENSD supplementation coincided with significantly higher plasma concentrations of PYY, CCK and insulin, during the pre-lunch period there was dissociation between appetite measures and expected action of hormonal appetite regulators, a phenomenon also found in some other studies (De Graaf, Blom, Smeets, Stafleu, & Hendriks, 2004;Doucet et al, 2008;Gielkens, Verkijk, Lam, Lamers, & Masclee, 1998). For further understanding of relations between responses of appetite scores and hormone responses we used a statistical approach that focuses on within participant relations between changes in appetite scores and changes in hormone concentrations (Lemmens et al, 2011) and obtained regression slopes and R 2 values for the regression of appetite scores on each of the measured appetite hormones.…”

Brain Activation by Visual Food-Related Stimuli and Correlations with Metabolic and Hormonal Parameters: A fMRI Study

“…Several hormones, for example ghrelin, leptin and insulin, have been shown to be involved in the central regulation of appetite, hunger and satiation [11][12][13]. Receptors for these hormones have been found in the hypothalamus, and the involvement of these hormones in the energy homeostasis and food intake has widely been hypothesized [14][15][16].…”

Breast Milk Hormones and Their Protective Effect on Obesity

“…It reduces appetite and increases energy expenditure by acting on the arcuate nucleus in the hypothalamus through its receptor (Ob-R) [10]. Circulating leptin levels correlate with fat mass in adults and children [11].…”