No abstract

ScopeIncreasing the intake of satiety‐enhancing food compounds represents a promising strategy for maintaining a healthy body weight. Recently, satiating effects for the capsaicinoid nonivamide have been demonstrated. As various proteins and amino acids have also been demonstrated to decrease energy intake, oral glucose tolerance test (oGTT)‐based bolus interventions of 75 g glucose + 0.15 mg nonivamide (NV control) are tested with/without combination of a wheat protein hydrolysate (WPH: 2 g) and/or l‐arginine (ARG: 3.2 g) for their satiating effects in 27 moderately overweight male subjects.Methods and ResultsCompared to NV control intervention, ARG and WPH + ARG treatment both reduce (p < 0.01) total calorie intake from a standardized breakfast by –5.9 ± 4.15% and –6.07 ± 4.38%, respectively. For the WPH + ARG intervention, increased mean plasma serotonin concentrations (AUC: 350 ± 218), quantitated by ELISA, and delayed gastric emptying, assessed by 13C‐Na‐acetate breath test (−2.10 ± 0.51%, p < 0.05), are demonstrated compared to NV control. Correlation analysis between plasma serotonin and gastric emptying reveals a significant association after WPH ± ARG intervention (r = –0.396, p = 0.045).ConclusionCombination of WPH and ARG enhances the satiating effect of nonivamide, providing opportunities to optimize satiating food formulations by low amounts of the individual food constituents.

Knowledge regarding the involvement of sweetness perception on energy intake is scarce. Here, the impact of glucose and sucrose sweetness, beyond their caloric load, on subsequent food intake and biomarkers of satiation was evaluated by co-administration of the sweet taste receptor inhibitor lactisole. A total of 27 healthy, male subjects received solutions of either 10% glucose w/o 60 ppm lactisole or 10% sucrose w/o 60 ppm lactisole. Subsequent food intake from a standardized breakfast was evaluated 2 h after receiving the respective test solution. Changes in postprandial plasma concentrations of cholecystokinin, ghrelin, and serotonin were determined over a period of 120 min, as was the body temperature. Administration of lactisole to the sucrose solution increased the energy intake from the subsequent standardized breakfast by 12.9 ± 5.8% (p = 0.04), led to a decreased Δ AUC of the body core temperature by 46 ± 20% (p = 0.01), and time-dependently reduced Δ serotonin plasma concentrations (−16.9 ± 6.06 ng/mL vs. −0.56 ± 3.7 ng/mL after sucrose administration, p = 0.03). The present study shows that lactisole increases energy intake and decreases plasma serotonin concentrations as well as body core temperature induced by sucrose, but not glucose. This finding may be associated with the different binding affinities of sucrose and glucose to the sweet taste receptor.

Among mammals, serotonin is predominantly found in the gastrointestinal tract, where it has been shown to participate in pathway-regulating satiation. For the stomach, vascular serotonin release induced by gastric distension is thought to chiefly contribute to satiation after food intake. However, little information is available on the capability of gastric cells to synthesize, release and respond to serotonin by functional changes of mechanisms regulating gastric acid secretion. We investigated whether human gastric cells are capable of serotonin synthesis and release. First, HGT-1 cells, derived from a human adenocarcinoma of the stomach, and human stomach specimens were immunostained positive for serotonin. In HGT-1 cells, incubation with the tryptophan hydroxylase inhibitor p-chlorophenylalanine reduced the mean serotonin-induced fluorescence signal intensity by 27%. Serotonin release of 147 ± 18%, compared to control HGT-1 cells (set to 100%) was demonstrated after treatment with 30 mM of the satiating amino acid L-Arg. Granisetron, a 5-HT3 receptor antagonist, reduced this L-Arg-induced serotonin release, as well as L-Arg-induced proton secretion. Similarly to the in vitro experiment, human antrum samples released serotonin upon incubation with 10 mM L-Arg. Overall, our data suggest that human parietal cells in culture, as well as from the gastric antrum, synthesize serotonin and release it after treatment with L-Arg via an HTR3-related mechanism. Moreover, we suggest not only gastric distension but also gastric acid secretion to result in peripheral serotonin release.