Our objective was to study the relationship between the satiety induced by high-protein meals and the activation of brain areas involved in the onset of satiety. In rats, we used immunohistochemistry to monitor brain centers activated by a meal by receiving information from the gastrointestinal tract or via humoral pathways. In the nucleus of the solitary tract (NTS), the acute or chronic intake of high-protein meals led to increased activation of the noradrenergic/adrenergic neurons involved in cholecystokinin-induced satiety. In the arcuate nucleus of the hypothalamus, the melanocortin pathway was also more strongly activated after the acute or chronic intake of high-protein meals. Moreover, the glucagon-like peptide 1 pathway arising from the NTS, which is triggered, among other behaviors, during nonphysiological anorexia, was not activated by high-protein meals, supporting the lack of aversive behavior associated with this diet. Taken together, these results show that the ability of high-protein meals to inhibit food intake occurs alongside the activation, in nutrient-sensitive brain areas, of several specific neuronal populations involved in satiety.
This study was designed to characterize the suppressant effect of yeast protein and purified peptides on energy intake. For this purpose, 5 experiments were carried out using adult male Wistar rats. Rats that consumed ad libitum a standard yeast protein diet ate significantly less and were leaner over 21 d than rats that consumed ad libitum a standard milk protein diet (Expt. 1). Moreover, rats fed a high yeast protein load reduced their next meal and daily energy intake more than rats fed any other well-balanced, amino acid, high protein load (soy, total milk protein, or wheat gluten) and more than those fed a wheat starch diet (Expt. 2). Purified peptides from the yeast protein extract produced similar effects on subsequent energy intake (Expt. 3). Study of the behavioral satiety sequence showed that rats consuming P14-y or P55-y diets ad libitum did not acquire a conditioned food aversion (Expt. 4). Finally, a preliminary study of gastric emptying in rats fed yeast protein loads showed that yeast protein was emptied more rapidly through the pylorus than total milk protein during a meal, which may induce satiety (Expt. 5). Taken together, these experiments show that yeast proteins enhance satiety in rats more than other proteins.
Yeast‐derived peptides were previously shown to display a high satiating effect. This work evaluate their effect i) on food intake in rats as well as in humans, and ii) on the activation of brain neuronal pathways involved in food intake including the Nucleus of the Tractus Solitary (NTS) and the Arcuate Nucleus of the Hypothalamus (Arc). Food intake in rats and humans: The ingestion of a daily load of yeast peptides induced a decrease in daily food intake in rats and in humans after a two‐week habituation period. This decrease did not occurred during the meal following the load (lunch in humans) but several hours later in rats (−16% of control group daily intake) and during the diner in humans (−13% of control group daily intake). Activation of neuronal pathways in rats: After habituation period, yeast protein loads induced an increase in melanocortin pathway within the Arc, which regulates long‐term energy intake, whereas activation of the Glucagon Like Peptide‐1 (GLP‐1) pathway within the NTS, which is triggered during aversive‐induced anorexia, was not increased.
Conclusion: Yeast peptides induced a strong food intake suppressing effect in rats and in humans. This effect was not compensated during the rest of the day and did not disappear after habituation. It did not result from a conditioned taste aversion and might be related to a stronger activation of arcuate melanocortin pathway.
The relationship between the satiety induced by high protein meals and activation of brain areas involved in satiety onset remains incompletely understood. We monitored neuronal pathways in brain centres known to be activated by a meal including the Nucleus of the Tractus Solitary (NTS) and the Arcuate Nucleus of the Hypothalamus (Arc) receiving information from gastrointestinal tract and from the blood, respectively. In the NTS, compared to a normal protein diet, acute or chronic intake of a high protein diet increased activation of the noradrenergic/adrenergic pathway known to be involved in cholecystokinin (CCK) induced satiety, but not the Glucagon Like Peptide 1 (GLP‐1) pathway, which is triggered during aversive‐induced anorexia. In the ARC, the melanocortin pathway also presented a greater activation after acute or chronic intake of high protein meals. Taken together, these results indicated that the potency of high protein meals in inhibiting food intake was occurring along with the activation of several specific brain neural pathways involved in satiety and not in aversive behaviour.
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