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  • Title: 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.
    Author: El Khoury D, Vien S, Sanchez-Hernandez D, Kung B, Wright A, Goff HD, Anderson GH.
    Journal: J Dairy Sci; 2019 Aug; 102(8):6766-6780. PubMed ID: 31229285.
    Abstract:
    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.
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