Abstract
Background: We tested whether ingestion of whey protein can induce greater post-prandial amino acid (AA) levels in the plasma and a higher beta-cell response than casein ingestion in type 2 diabetes mellitus patients. Methods: The study was designed as a double-blind, randomized, and controlled cross-over clinical trial. Twelve post-absorptive type 2 diabetic subjects who were withdrawn from their usual hypoglycemic therapy were studied. A medium calorie (≈6 kcal/kg BW), high protein (≈50% of total kcal) mixed meal, containing whey protein, casein, or a free amino acid (FREE AA) mixture matching the casein AA composition, was randomly administered on three different occasions. Results: Following ingestion of whey protein, plasma concentrations of total, branched chain, and essential AA were 25-50% greater than after ingestion of casein (p < 0.0001), and were similar to those observed after the FREE AA meal. With whey protein, C-peptide, insulin, and pro-insulin concentrations were greater by 12-40% (p < 0.02 or less) than with casein, and similar to those with FREE AA. Glucagon-like polypeptide 1 (GLP-1) response tended to be lower with casein than with whey protein. Glucose-dependent insulinotropic polypeptide (GIP) response was greater with either whey protein or casein than with FREE AA. Post-prandial glucose concentrations were similar after whey protein and casein ingestion, but lower after the FREE AA meal. Conclusions: In type 2 diabetes, the ingestion of a fast-absorbable protein results in a greater post-prandial aminoacidemia and a higher beta-cell secretion than the ingestion of a 'slow' protein. Whether these changes can be maintained chronically in combination with hypoglycemic therapy, possibly also resulting in better glycemic control, remains to be established. Copyright © 2006 John Wiley & Sons, Ltd.
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Tessari, P., Kiwanuka, E., Cristini, M., Zaramella, M., Enslen, M., Zurlo, C., & Garcia-Rodenas, C. (2007). Slow versus fast proteins in the stimulation of beta-cell response and the activation of the entero-insular axis in type 2 diabetes. Diabetes/Metabolism Research and Reviews, 23(5), 378–385. https://doi.org/10.1002/dmrr.698
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