Nutritional Composition of Infant Cereal Prototypes Can Precisely Predict Their Glycemic Index.

Designing cereal-based products with appropriate metabolic responses is of high interest to the food industry in view of the potential health impact of the product. The objective of this study was to test whether a model that used the nutrient composition of breakfast cereals to predict their glycemic index (GI) and glycemic load (GL) could also accurately predict the GI and GL for complete (containing protein, reconstituted in water) infant cereal prototypes. Four independent studies measured the postprandial glucose response of 20 complete infant cereal prototypes (51−76 g/100 g glycemic carbohydrates) in healthy adults. The predictions were strongly correlated with the measured values for both the GI (r = 0.93, p-value < 0.01) and GL (r = 0.98, p-value < 0.01). The in vivo incremental area under the curve (iAUC) for glucose showed a strong linear relationship with the predicted GL (r = 0.99, p < 0.01). In summary, the model previously developed to predict the GI and GL of breakfast cereals was both accurate and precise for infant cereals and could be considered a simple tool to support nutritionally responsible product development.

Comparison of the acute metabolic effect of different infant formulas and human milk in healthy adults: a randomized trial.

BACKGROUND/OBJECTIVES: Different infant formulas, varying in protein type and quantity, are available for infants who are not breastfed or are partially breastfed. Postprandial insulinemic and glycemic responses to intact vs partially hydrolyzed protein in infant formula are unclear. To compare the effect of different forms (partially hydrolyzed vs non-hydrolyzed) and levels of protein in infant formula compared with a human milk reference subgroup on insulin response in adults. SUBJECTS/METHODS: In a randomized, double-blinded, cross-over study, 35 healthy adults consumed 600 ml of three different infant formulas: Intact protein-based formula (INTACT) (1.87 g protein/100 kcal; whey/casein ratio of 70/30; 63 kcal/100 ml), partially hydrolyzed whey-based formula (PHw) (1.96 g protein/100 kcal; 100% whey; 63 kcal/100 ml), a high-protein partially hydrolyzed whey-based formula (HPPHw) (2.79 g protein/100 kcal; 100%whey; 73 kcal/100 ml) and a subgroup also consumed human milk (HM) (n = 11). Lipid and carbohydrate (lactose) contents were similar (5.1-5.5 and 10.5-11.6 g/100 kcal, respectively). Venous blood samples were taken after overnight fasting and at different intervals for 180 min post-drink for insulin, glucose, blood lipids, GLP-1, glucagon, and C-peptide. RESULTS: Twenty-nine subjects (eight consuming HM) adhered to the protocol. INTACT and PHw groups had similar postprandial insulinemia and glycaemia (Cmax and iAUC) that were not different from those of the HM subgroup. HPPHw resulted in higher postprandial insulin responses (iAUC) relative to all other groups (p < 0.001, p < 0.001, p = 0.002 for the comparison with INTACT, PHw, HM, respectively). HPPHw resulted in a higher glucose response compared to INTACT and PHw (iAUC: p = 0.003, p = 0.001, respectively), but was not different from HM (p = 0.41). CONCLUSION: This study in adults demonstrates similar postprandial insulinemia and glycaemia between INTACT and PHw, close to that of HM, but lower than HPPHw, which had a higher protein content compared to the other test milks. The findings remain to be confirmed in infants. CLINICAL TRIAL REGISTRATION: This study is registered at clinicaltrials.gov, identifier NCT04332510.

Whey Versus Casein as a Protein Source during the Weaning Period: Impact on Growth and Later Adiposity and Glucose Homeostasis in a Rat Model of Intrauterine Growth Restriction.

The impact of early life protein source (whey vs. casein) on short- and long-term glucose homeostasis and adiposity is unknown and was investigated in this study. At the end of the suckling period, non-IUGR (intrauterine growth restriction) and IUGR pups were separated from dams and were randomized into four groups. From age 21-49 days, non-IUGR and IUGR pups were fed ad-libitum chow or a semi-synthetic diet (20% from protein; casein or whey) and from age 50-199 days, all groups were fed ad-libitum chow. Food intake, body composition, glucose, and insulin homeostasis were assessed. Among the chow groups, IUGR had slower growth and higher fasting glucose at age 42 days, as well as higher fasting and AUC glucose at age 192 days relative to non-IUGR. The whey IUGR group had a slower growth rate and higher fasting glycemia in early life (age 21-49 days) and higher HOMA-IR later in life (age 120-122 and 190-192 days) relative to casein IUGR. This study shows the potential advantage of casein relative to whey during weaning on short term energy intake, growth, and glucose homeostasis in an IUGR model and reveals, for the first time, its long term impact on insulin sensitivity, which may have implications for later metabolic health, particularly in small-for-gestational-age populations at risk of type 2 diabetes.

Dietary modulation of body composition and insulin sensitivity during catch-up growth in rats: effects of oils rich in n-6 or n-3 PUFA.

The present study investigates whether excessive fat accumulation and hyperinsulinaemia during catch-up growth on high-fat diets are altered by n-6 and n-3 PUFA derived from oils rich in either linoleic acid (LA), α-linolenic acid (ALA), arachidonic acid (AA) or DHA. It has been shown that, compared with food-restricted rats refed a high-fat (lard) diet low in PUFA, those refed isoenergetically on diets enriched in LA or ALA, independently of the n-6:n-3 ratio, show improved insulin sensitivity, lower fat mass and higher lean mass, the magnitude of which is related to the proportion of total PUFA precursors (LA+ALA) consumed. These relationships are best fitted by quadratic regression models (r2>0·8, P < 0·001), with threshold values for an impact on body composition corresponding to PUFA precursors contributing 25-30 % of energy intake. Isoenergetic refeeding on high-fat diets enriched in AA or DHA also led to improved body composition, with increases in lean mass as predicted by the quadratic model for PUFA precursors, but decreases in fat mass, which are disproportionately greater than predicted values; insulin sensitivity, however, was not improved. These findings pertaining to the impact of dietary intake of PUFA precursors (LA and ALA) and their elongated-desaturated products (AA and DHA), on body composition and insulin sensitivity, provide important insights into the search for diets aimed at counteracting the pathophysiological consequences of catch-up growth. In particular, diets enriched in essential fatty acids (LA and/or ALA) markedly improve insulin sensitivity and composition of weight regained, independently of the n-6:n-3 fatty acid ratio.

The fat:carbohydrate energy ratio of the weaning diet programs later susceptibility to obesity in male sprague dawley rats.

Dietary fat intake, which is high during suckling, is markedly reduced when food and drinks are introduced into the diet. We investigated whether alterations in the fat:carbohydrate (CHO) content of the weaning diet influenced the later development of adiposity and insulin sensitivity. Three groups of male rats (24/group) were fed from age 16-37 d (phase I) with weaning diets varying in their fat:CHO energy (E) ratios, 10:70 low-fat, high-CHO (LFHC); 30:50 medium-fat, medium-CHO (MFMC), and 60:30 high-fat, high-CHO (HFLC), on an isocaloric basis. Then, all groups consumed ad libitum first a low-fat diet (13% fat E) for 30 wk (phase II) and subsequently a high-fat diet (45% fat E) for another 18 wk (phase III). At the end of phase I, the group fed the HFLC diet demonstrated higher plasma glucose and insulin responses to an oral glucose tolerance test (P < 0.05), but this effect was transient and did not persist into adulthood (phases II and III). By contrast, when challenged with a high-fat diet later in life (age 35.3-53.3 wk), the LFHC group had greater gains in weight (as percent initial weight) and body fat (as absolute and percent body weight) than the other 2 groups that had been weaned with diets higher in fat (P < 0.04 for all). These results provide evidence that metabolic programming by altering the dietary fat:CHO ratio can occur during the weaning period and emphasizes the importance of the fat:CHO ratio of the complementary diet and its relation to the susceptibility to develop adiposity later in life.

Comparison of two models of intrauterine growth restriction for early catch-up growth and later development of glucose intolerance and obesity in rats.

Two models of intrauterine growth restriction, maternal food restriction (FR), and dexamethasone (DEX) exposure were compared for early postnatal catch-up growth and later development of glucose intolerance and obesity in Sprague-Dawley rats. Mated dams were randomly divided into three groups at 10 days gestational age. Group FR was food restricted (50% of nongestating rats) during the last 11 days of gestation; Group DEX received DEX injections during the last week of gestation, and Group CON, the control group, had no intervention. Birth weight, catch-up growth, body weight, and food intake were measured in male offspring for 22 wk. Body composition, blood glucose, and plasma insulin in response to a glucose load were assessed at 8, 16, and 22 wk. Pups from both FR and DEX dams had similarly lower birth weights than CON (22% and 25%, P < 0.0001), but catch-up growth, which occurred during the suckling period, was much more rapid in FR than DEX offspring (6 vs. 25 days, 95% CI). Postweaning, there were no significant differences between groups in food intake, body weight, body fat, and plasma insulin, but baseline plasma glucose at 22 wk and 2-h glucose area-under-the-curve at 8 and 22 wk were greater only in FR vs. CON offspring (P < 0.05), thereby contrasting with the lack of significant differences between DEX and CON. These results suggest that prenatal food restriction is a more sensitive model than DEX exposure for studies aimed at investigating the link between low birth weight, early postnatal catch-up growth, and later development of glucose intolerance.