The effects of feeding a sodium caseinate derived hydrolysate on glycaemic control and insulin sensitivity following an oral lipid load

Type Article

Journal Article


E. B. Kennedy; E. Meaney; L. A. Shakerdi; A. B. Nongonierma; R. J. Fitzgerald; C. W. Le Roux; H. M. Roche

Year of publication











Background and aims: Obesity with its associated state of chronic low‐grade inflammation with dysregulated metabolism is a major driver of insulin resistance (IR). Dysregulated postprandial insulin and glucose responses, which are hallmarks of IR, are among the main therapeutic targets. Intake of casein and casein derived hydrolysates are associated with increased insulin secretion and reduced glucose levels. Certain casein hydrolysates are also associated with reductions in metabolic inflammation and improvements in insulin signaling. The current study addressed the hypothesis that a sodium caseinate (NaCas) derived bioactive hydrolysate could improve glycaemic control in an obese insulin resistant cohort, using an oral lipid load combined with a hyperinsulinemic euglycaemic clamp technique, using an acute metabolic challenge approach. Materials and methods: Six obese male volunteers participated in this randomized cross‐over controlled trial. Following an overnight fast, participants received an oral lipid load (100 mL soyabean oil) to induce IR. After 2 hours volunteers completed a 4 hour hyperinsulinemic‐euglycaemic clamp (30 mU/m2/min) combined with either 12g sodium caseinate (NaCas), 12g NaCas derived bioactive hydrolysate or a water control (Figure 1). Glucose, insulin, triacylglycerol (TAG), non‐esterified fatty acids (NEFA), C‐peptide, GIP and GLP‐1 responses were determined after the oral lipid load, with or without oral administration of the NaCas derived hydrolysate versus NaCas control and water. Data analyzed by repeated measures ANOVA using SPSS statistical software. Results: Administration of the NaCas derived hydrolysate did not improve whole‐body insulin sensitivity following an oral lipid load, compared to the native NaCas or water controls. Consumption of the NaCas derived hydrolysate did not alter glucose metabolism as measured by glucose, insulin and C‐peptide concentrations, compared to NaCas or water controls. NEFA concentrations decreased by 36% following the NaCas derived hydrolysate while triglycerides increased by 30% compared to baseline, however this was not significantly different from the NaCas or water controls. Conclusion: Ingestion of 12g NaCas or NaCas derived hydrolysate did not improve insulin sensitivity compared to a water control in obese, insulin resistant males following an oral lipid load. Despite the promising finding that NaCas increases insulin secretion and improves insulin signaling this does extend to improved insulin sensitivity in the current study. (Figure Presented).