Flavonoids stimulate cholecystokinin peptide secretion from the enteroendocrine STC-1 cells.

Animal experiments showed that flavonoids might have the potential for an anti-obesity effect by reducing weight and food intake. However, the exact mechanisms that could be involved in these proposed effects are still under investigation. The complex process of food intake is partially regulated by gastrointestinal hormones.

Analysis of interaction of phenolic compounds with the cholecystokinin signaling pathway to explain effects on reducing food intake.

Previous animal experiments demonstrated that phenolic compounds can reduce weight and food intake, but the exact mechanism(s) behind these effects remain unknown. For regulation of food intake, the cholecystokinin (CCK) hormone signaling pathway plays an important role as it induces satiety by binding on its specific receptor (CCK1R), hereby reducing food intake. In this study, we investigated the possible interactions of eight phenolic compounds of different classes (tannic acid, gallic acid, benzoic acid, hydroxybenzoic acid, protocatechuic acid, quercetin, kaempferol and resveratrol) with the CCK1R signaling pathway.

Angiotensin-converting enzyme inhibitory effects by plant phenolic compounds: a study of structure activity relationships.

In this study, 22 phenolic compounds were investigated to inhibit the angiotensin-converting enzyme (ACE). Tannic acid showed the highest activity (IC50 = 230 μM). The IC50 values obtained for phenolic acids and flavonoids ranged between 0.

Screening of soy and milk protein hydrolysates for their ability to activate the CCK1 receptor.

The cholecystokinin receptor-type 1 (CCK1R) is a G-protein coupled receptor localized in the animal gastrointestinal tract. Receptor activation by the natural peptide ligand CCK leads to a feeling of satiety. In this study, hydrolysates from soy and milk proteins were evaluated for their potential to activate the CCK1R, assuming that bioactive peptides with a satiogenic effect can be used as an effective therapeutic strategy for obesity.