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.
Highlights
Numerous studies have demonstrated that diets with a high protein content provide higher satiety levels than the other macronutrients [1,2]
Determination of food intake and body weight changes in Pept12/2 mice fed for 5 days a LP or C diet did not show any significant alterations when compared to wildtype animals
When animals were provided with a HP diet, food intake rates immediately declined in all animals but more pronounced in Pept12/2 animals (Figure 1)
Summary
Numerous studies have demonstrated that diets with a high protein content provide higher satiety levels (at least short term) than the other macronutrients [1,2]. Intake of dietary protein is sensed in the intestine with concomitant secretion of gastrointestinal hormones and activation of visceral processes that alter gastric motility, stimulate pancreatic secretion, mediate peripheral effects and contribute to satiety [3,4,5]. It was demonstrated that leucine contributes to food intake control via AMP-activated protein kinase and mammalian target of rapamycin when supplied to hypothalamic centers [13,14]. High-protein intake causes major adaptations in metabolic processes in intestine and liver associated with changes in plasma levels of a variety of amino acids [17]. Protein-rich diets challenge the digestive tract with large quantities of amino acids and short chain peptides for uptake into epithelial cells and into circulation, a contribution of intestinal transport processes to food intake control has never been anticipated
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