| First Author | Nässl AM | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 10 | Pages | e26407 |
| PubMed ID | 22031831 | Mgi Jnum | J:179757 |
| Mgi Id | MGI:5303018 | Doi | 10.1371/journal.pone.0026407 |
| Citation | Nassl AM, et al. (2011) The intestinal peptide transporter PEPT1 is involved in food intake regulation in mice fed a high-protein diet. PLoS One 6(10):e26407 |
| abstractText | High-protein diets are effective in achieving weight loss which is mainly explained by increased satiety and thermogenic effects. Recent studies suggest that the effects of protein-rich diets on satiety could be mediated by amino acids like leucine or arginine. Although high-protein diets require increased intestinal amino acid absorption, amino acid and peptide absorption has not yet been considered to contribute to satiety effects. We here demonstrate a novel finding that links intestinal peptide transport processes to food intake, but only when a protein-rich diet is provided. When mice lacking the intestinal peptide transporter PEPT1 were fed diets containing 8 or 21 energy% of protein, no differences in food intake and weight gain were observed. However, upon feeding a high-protein (45 energy%) diet, Pept1(-/-) mice reduced food intake much more pronounced than control animals. Although there was a regain in food consumption after a few days, no weight gain was observed which was associated with a reduced intestinal energy assimilation and increased fecal energy losses. Pept1(-/-) mice on high-protein diet displayed markedly reduced plasma leptin levels during the period of very low food intake, suggesting a failure of leptin signaling to increase energy intake. This together with an almost two-fold elevated plasma arginine level in Pept1(-/-) but not wildtype mice, suggests that a cross-talk of arginine with leptin signaling in brain, as described previously, could cause these striking effects on food intake. |
