Abstract
Protein intake in early life influences metabolism, weight gain, and later obesity risk. As such, a better understanding of the effects of protein intake on the postprandial metabolism and its dynamics over time may elucidate underlying mechanisms. In a randomized crossover study, we observed fasted adults who consumed two isocaloric toddler milk formulas concentrated as meals of 480 kcal with 67 g of carbohydrates 30 g (HP) or 7 g (LP) protein, and 10 g or 20 g fat, respectively. Anthropometry and body plethysmography were assessed, and blood samples collected at baseline and over five hours. Time-specific concentrations, areas under concentration curves (AUC), and maximum values of metabolites were compared by paired t-tests to examine the effects of protein content of toddler milks on postprandial plasma concentrations of insulin, glucose, branched-chain amino acids (BCAA), urea and triglycerides. Twenty-seven men and women aged 26.7 ± 5.0 years (BMI: 22.2 ± 2.5 kg/m2) (mean ± SD) participated. BCAA AUC, and Cmax values were significantly higher with HP than LP (144,765 ± 21,221 vs. 97,089 ± 14,650 µmol·min/L, p < 0.001; 656 ± 120 vs. 407 ± 66 µmol/L, p < 0.001), as were insulin AUC and Cmax values (6674 ± 3013 vs. 5600 ± 2423 µmol·min/L, p = 0.005; 71 ± 37 vs. 55 ± 28 µmol/L, p = 0.001). Higher glucose, urea, and triglyceride concentrations occurred in the late postprandial phase (≥180 min) with HP. In conclusion, we noted that higher milk protein intake induces increased postprandial BCAA concentrations for at least 5 h and led to higher initial insulin secretion. Gluconeogenesis due to an influx of amino acids and their degradation after HP meal might explain the late effects of protein intake on glucose and insulin.
Highlights
The early protein hypothesis suggests that a higher protein supply fed to infants with conventional infant formula, as compared with breastmilk, induces an increased early weight gain and an increased risk of obesity in later life [1,2,3,4]
Together with branched-chain amino acids (BCAA), insulin and IGF-1 activate the mammalian target of rapamycin signaling pathway, the mammalian target of the rapamycin complex 1, critical for adipogenesis and the maintenance of fat tissue [9,10]
As we found no association of concentration maximums (Cmax) or areas under concentration curves (AUC) of BCAAs with those of glucose or insulin, and time of maximum concentration (Tmax) for BCAAs was significantly later than for insulin, amino acids appear to have continuously cumulated after the initial insulin peak
Summary
The early protein hypothesis suggests that a higher protein supply fed to infants with conventional infant formula, as compared with breastmilk, induces an increased early weight gain and an increased risk of obesity in later life [1,2,3,4]. A large double-masked, randomized trial, the European Childhood Obesity Project (CHOP), provided evidence that higher milk protein intake in the first year of life markedly increased body mass index (BMI), body fatness, and the prevalence of obesity at ages 2 and 6 years [5,6,7]. Observational studies have suggested that the effect of protein intake on weight and BMI is not restricted to infancy but can be seen during toddlerhood— the available evidence is limited [11].
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