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The intestinal peptide transporter PEPT1 is involved in food intake regulation in mice fed a high-protein diet.

Nässl AM, Rubio-Aliaga I, Sailer M, Daniel H - PLoS ONE (2011)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: ZIEL Research Center of Nutrition and Food Sciences, Abteilung Biochemie, Technische Universität München, Freising, Germany.

ABSTRACT
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.

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Analysis of plasma hormone levels reveals lower leptin concentrations in Pept1−/− animals.Plasma samples of fasted (6 h fasting period) and non-fasted Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) diet or a high-protein (HP = 45% protein energy) diet were analysed after 24 h for changes in ghrelin, leptin and insulin levels (n = 6 animals). Data are presented as mean±SD. (•) indicate outliers. *P<0.05, $P<0.01, §P<0.001.
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pone-0026407-g005: Analysis of plasma hormone levels reveals lower leptin concentrations in Pept1−/− animals.Plasma samples of fasted (6 h fasting period) and non-fasted Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) diet or a high-protein (HP = 45% protein energy) diet were analysed after 24 h for changes in ghrelin, leptin and insulin levels (n = 6 animals). Data are presented as mean±SD. (•) indicate outliers. *P<0.05, $P<0.01, §P<0.001.

Mentions: To assess whether selected hormones or adipokines revealed changes that could be associated with the differences in food intake, ghrelin, insulin and leptin levels were determined. As shown in Figure 5, neither ghrelin nor insulin levels changed, whereas leptin levels differed significantly between Pept1+/+ and Pept1−/− mice. Plasma leptin levels dropped significantly in PEPT1-deficient animals on the HP diet after 24 h to 2.2±1.4 ng/ml as compared to wildtype animals with 7.6±2.4 ng/ml (P = 0.001). This effect, yet not reaching significance was also observed on control diet in both, the fed (ko: 2.6± 2.1 ng/ml vs. wt: 5.6±1.6 ng/ml) and the fasted state (ko: 2.5±1.7 ng/ml vs. wt: 5.7±2.4 ng/ml).


The intestinal peptide transporter PEPT1 is involved in food intake regulation in mice fed a high-protein diet.

Nässl AM, Rubio-Aliaga I, Sailer M, Daniel H - PLoS ONE (2011)

Analysis of plasma hormone levels reveals lower leptin concentrations in Pept1−/− animals.Plasma samples of fasted (6 h fasting period) and non-fasted Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) diet or a high-protein (HP = 45% protein energy) diet were analysed after 24 h for changes in ghrelin, leptin and insulin levels (n = 6 animals). Data are presented as mean±SD. (•) indicate outliers. *P<0.05, $P<0.01, §P<0.001.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3198773&req=5

pone-0026407-g005: Analysis of plasma hormone levels reveals lower leptin concentrations in Pept1−/− animals.Plasma samples of fasted (6 h fasting period) and non-fasted Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) diet or a high-protein (HP = 45% protein energy) diet were analysed after 24 h for changes in ghrelin, leptin and insulin levels (n = 6 animals). Data are presented as mean±SD. (•) indicate outliers. *P<0.05, $P<0.01, §P<0.001.
Mentions: To assess whether selected hormones or adipokines revealed changes that could be associated with the differences in food intake, ghrelin, insulin and leptin levels were determined. As shown in Figure 5, neither ghrelin nor insulin levels changed, whereas leptin levels differed significantly between Pept1+/+ and Pept1−/− mice. Plasma leptin levels dropped significantly in PEPT1-deficient animals on the HP diet after 24 h to 2.2±1.4 ng/ml as compared to wildtype animals with 7.6±2.4 ng/ml (P = 0.001). This effect, yet not reaching significance was also observed on control diet in both, the fed (ko: 2.6± 2.1 ng/ml vs. wt: 5.6±1.6 ng/ml) and the fasted state (ko: 2.5±1.7 ng/ml vs. wt: 5.7±2.4 ng/ml).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: ZIEL Research Center of Nutrition and Food Sciences, Abteilung Biochemie, Technische Universität München, Freising, Germany.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus