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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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Decreased activities of enzymes and glucose in plasma of Pept1−/− animals.Enzyme and metabolite activities in plasma of Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) or high-protein (HP = 45% protein energy) diet were analyzed. Alkaline phosphatase (ALP), amylase, glucose and blood urea nitrogen (BUN) were determined after 5 days on the high-protein diet (n = 10). Data are presented as mean±SD. (•) indicate outlier. *P<0.05, $P<0.01, §P<0.001.
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pone-0026407-g003: Decreased activities of enzymes and glucose in plasma of Pept1−/− animals.Enzyme and metabolite activities in plasma of Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) or high-protein (HP = 45% protein energy) diet were analyzed. Alkaline phosphatase (ALP), amylase, glucose and blood urea nitrogen (BUN) were determined after 5 days on the high-protein diet (n = 10). Data are presented as mean±SD. (•) indicate outlier. *P<0.05, $P<0.01, §P<0.001.

Mentions: Clinical chemistry data of mouse plasma collected after 5 days revealed lower alkaline phosphatase levels in Pept1−/− animals, both on C and HP diet. In addition Pept1−/− mice, when fed the HP diet displayed also significantly decreased levels of amylase and glucose. In contrast, wildtype animals on HP diet showed higher blood urea nitrogen levels when compared to mice on C diet (HP: 41.8±6.2 mg/dl vs. C: 31±4.1 mg/dl, P<0.001), whereas blood urea nitrogen levels in Pept1−/− animals on HP diet were comparable to those on C diet (HP: 31.8±5.6 mg/dl vs. C: 30.4±3.8 mg/dl; P<0.001). These data are summarized in Figure 3. When blood urea nitrogen levels were determined after 18 days, genotype effects were no longer detectable and enyzme activities did also not show any more differences (data not shown). Yet, independent of genotype, mice on the HP diet displayed significant elevated blood urea nitrogen concentrations (HP: 44±4.3 mg/dl; vs. C: 26±3.6, mg/dl; P<0.001).


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)

Decreased activities of enzymes and glucose in plasma of Pept1−/− animals.Enzyme and metabolite activities in plasma of Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) or high-protein (HP = 45% protein energy) diet were analyzed. Alkaline phosphatase (ALP), amylase, glucose and blood urea nitrogen (BUN) were determined after 5 days on the high-protein diet (n = 10). Data are presented as mean±SD. (•) indicate outlier. *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-g003: Decreased activities of enzymes and glucose in plasma of Pept1−/− animals.Enzyme and metabolite activities in plasma of Pept1+/+ (wt) and Pept1−/− (ko) animals fed a control (C = 21% protein energy) or high-protein (HP = 45% protein energy) diet were analyzed. Alkaline phosphatase (ALP), amylase, glucose and blood urea nitrogen (BUN) were determined after 5 days on the high-protein diet (n = 10). Data are presented as mean±SD. (•) indicate outlier. *P<0.05, $P<0.01, §P<0.001.
Mentions: Clinical chemistry data of mouse plasma collected after 5 days revealed lower alkaline phosphatase levels in Pept1−/− animals, both on C and HP diet. In addition Pept1−/− mice, when fed the HP diet displayed also significantly decreased levels of amylase and glucose. In contrast, wildtype animals on HP diet showed higher blood urea nitrogen levels when compared to mice on C diet (HP: 41.8±6.2 mg/dl vs. C: 31±4.1 mg/dl, P<0.001), whereas blood urea nitrogen levels in Pept1−/− animals on HP diet were comparable to those on C diet (HP: 31.8±5.6 mg/dl vs. C: 30.4±3.8 mg/dl; P<0.001). These data are summarized in Figure 3. When blood urea nitrogen levels were determined after 18 days, genotype effects were no longer detectable and enyzme activities did also not show any more differences (data not shown). Yet, independent of genotype, mice on the HP diet displayed significant elevated blood urea nitrogen concentrations (HP: 44±4.3 mg/dl; vs. C: 26±3.6, mg/dl; P<0.001).

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