Role of Amino Acids in Blood Glucose Changes in Young Adults Consuming Cereal with Milks Varying in Casein and Whey Concentrations and Their Ratio.

BACKGROUND: Increasing the total protein content and reducing the casein to whey ratio in milks consumed with breakfast cereal reduce postprandial blood glucose (BG). OBJECTIVES: We aimed to explore associations between plasma amino acids (AAs), BG, and glucoregulatory hormones. METHODS: In this repeated-measures design, 12 healthy adults consumed cereal (58 g) and milks (250 mL) with 3.1 wt% or high 9.3 wt% protein concentrations and with casein to whey ratios of either 80:20 or 40:60. Blood was collected at 0, 30, 60, 120, 140, 170, and 200 min for measurement of the primary outcome, BG, and for the exploratory outcomes such as plasma AA, gastric emptying, insulin (INS), and glucoregulatory hormones. Measures were made prior to and after an ad libitum lunch at 120 min. Exploratory correlations were conducted to determine associations between outcomes. RESULTS: Pre-lunch plasma AA groups [total (TAA), essential (EAA), BCAA, and nonessential (NEAA)] were higher after 9.3 wt% than 3.1 wt% milks by 12.7%, 21.4%, 20.9%, and 7.6%, respectively (P ≤ 0.05), while post-lunch AA groups were higher by 10.9%, 19.8%, 18.8%, and 6.0%, respectively (P ≤ 0.05). Except for NEAA, pre-lunch AAs were higher after 40:60 than 80:20 ratio milks by 4.5%, 8.3%, and 9.3% (P ≤ 0.05). When pooled by all treatments, pre-lunch AA groups associated negatively with BG (r/ρ ≥ -0.45, P ≤ 0.05), but post-lunch only TAA and NEAA correlated (r ≥ -0.37, P < 0.05). Pre-lunch BG was inversely associated with Leu, Ile, Lys, Met, Thr, Cys-Cys, Asn, and Gln (r/ρ ≥ -0.46, P ≤ 0.05), but post-lunch, only with Thr, Ala, and Gly (r ≥ -0.50, P ≤ 0.05). Pre-lunch associations between AA groups and INS were not found. CONCLUSIONS: Protein concentration and the ratio of casein to whey in milks consumed at breakfast with cereal affect plasma AA concentrations and their associations with decreased BG. The decrease in BG could be explained by INS-independent mechanisms. This trial was registered at www.clinicaltrials.gov as NCT02471092.

Correlating in vitro digestion viscosities and bioaccessible nutrients of milks containing enhanced protein concentration and normal or modified protein ratio to human trials.

This work compared in vitro and in vivo digestion of breakfast cereal with milks containing high protein concentration (9.3 wt%) and the normal protein ratio (80 casein : 20 whey) or a modified ratio (40 casein : 60 whey) and with a water-permeate control. The in vivo study indicated that high protein concentration and modified ratio in milks delays the postprandial appearance of blood glucose (BG) and amino acids due to delayed gastric emptying and hormonal responses. However, the role of viscosity and/or protein structure during digestion was not examined. Therefore, milks and the control were digested in vitro (oral (O, 2 min), gastric (G, 62 min) and duodenal (D, 92 min)) to determine viscosity, particle disintegration, protein solubility and hydrolysis, and the bioaccessibilities of sugars and total amino acids (TAA). The normal ratio (80 : 20) treatment demonstrated higher structural viscosity during digestion (P < 0.05) due to the formation of casein aggregates and interaction with cereal and greater TAA (mg per g protein of undigested breakfast) caused by gastric hydrolysis (DH%; P = 0.01). Overall, there were no treatment differences for disintegration, solubility and d-glucose. Protein-containing treatments inhibited amylolysis and lowered reducing sugars (mg g-1 available carbohydrates of undigested breakfast) compared to the control. Similar trends were observed between higher viscosity (Pa s) during gastric stage and slower in vivo gastric emptying (paracetamol, mmol L-1). Also, protein treatments inhibited amylolysis and lowered reducing sugar (mg g-1 of carbohydrates) and may have contributed to lowered BG (mmol L-1 g-1 of carbohydrates) after the duodenal phase. However, increased viscosity, elicited by higher proportions of casein, did not inhibit starch hydrolysis and appearance of BG. In vitro systems provide similar trends in biomarkers to in vivo studies and can be used to answer specific physiological questions.

Increased milk protein content and whey-to-casein ratio in milk served with breakfast cereal reduce postprandial glycemia in healthy adults: An examination of mechanisms of action.

This study describes the effects on glycemic response and the underlying mechanisms of action of increasing the protein concentration and decreasing the casein-to-whey ratio in milk when consumed with a high glycemic breakfast cereal. Twelve healthy men and women, aged 18 to 30 yr and with a body mass index of 20 to 24.9 kg/m2, consumed (in random order) milk beverages (250 mL) containing either 3.1 or 9.3% protein and casein-to-whey ratios of either 80:20 or 40:60. We measured postprandial appetite, glucose, regulatory hormones, and stomach emptying rate over 200 min, as well as food intake at an ad libitum meal at 120 min. Although pre-meal appetite was suppressed to a greater extent with milk beverages that had high (9.3%) compared with regular (3.1%) protein content, food intake was similar among all 4 treatments. Pre-meal mean blood glucose was lower with beverages that had high rather than regular milk protein content, with the lowest glucose peaks after the high milk protein treatment with the 40:60 casein-to-whey ratio. Pre-meal insulin and C-peptide levels were not affected by milk protein content or casein-to-whey ratio, but pre-meal glucagon-like peptide 1 was higher after the treatment containing high milk protein and the 40:60 casein-to-whey ratio, and pre-meal cholecystokinin was higher after the treatments containing high milk protein content. Plasma paracetamol response was also lower after the treatments containing high compared with regular milk protein content. When consumed with carbohydrate, milk beverages with high protein content and (to a lesser extent) a decreased casein-to-whey ratio lowered postprandial glycemia through insulin-independent mechanisms, primarily associated with delayed stomach emptying.