A Protein/Lipid Preload Attenuates Glucose-Induced Endothelial Dysfunction in Individuals with Abnormal Glucose Tolerance

Figures

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  Figure 1. Outline of the study protocol. Endothelial function was assessed by the reactive hyperemia index (RHI) using an EndoPAT device at fasting, 60 min and 120 min during two 75 g oral glucose tolerance tests (OGTTs) preceded by water or a protein/lipid preload. Plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, free fatty acids, and amino acids were measured.

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  Figure 2. Fasting endothelial function assessed by the reactive hyperemia index (RHI) and its percentage changes (Δ%) during two 75 g oral glucose tolerance tests preceded by water (CTRL) or a protein/lipid preload (PREL) in subjects with normal glucose tolerance (NGT) or abnormal glucose tolerance (AGT). Data are mean ± SEM. Baseline differences between the three groups were tested by Kruskal–Wallis test followed by post-hoc pairwise comparisons. In AGT, repeated measures were analyzed by mixed models including study (S), time (T), and an interaction term (S × T) as fixed effects and subject as random effect. p value for time effect is <0.05.

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  Figure 3. Plasma concentrations of glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), glucagon, free fatty acids (FFA), arginine, branched-chain amino acids (BCAA), and total amino acids during two 75 g oral glucose tolerance tests preceded by water (CTRL) or a protein/lipid preload (PREL) in subjects with normal glucose tolerance (NGT) or abnormal glucose tolerance (AGT). Data are mean ± SEM. In AGT, repeated measures were analyzed by mixed models including study (S), time, and an interaction term (S × T) as fixed effects and subject as random effect. P values are not shown for time effects (<0.05 for all variables).

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  Figure 4. Correlations between differences in RHI percentage changes at the end of the preload vs. control study (ΔRHIΔ%) and changes in the areas under the curve (AUC) of plasma glucose (ΔglucoseAUC), glucagon-like peptide-1 (ΔGLP-1AUC), and arginine (ΔarginineAUC) in subjects with abnormal glucose tolerance.

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  Figure 5. Fasting arterial stiffness assessed by the augmentation index (AI) and its change during two 75 g oral glucose tolerance tests preceded by water (CTRL) or a protein/lipid preload (PREL) in subjects with normal glucose tolerance (NGT) or abnormal glucose tolerance (AGT). Data are mean ± SEM. Baseline differences between the three groups were tested by Kruskal–Wallis test followed by post-hoc pairwise comparisons. In AGT, repeated measures were analyzed by mixed models including study (S), time (T), and an interaction term (S × T) as fixed effects and subject as random effect. p value for time effect is <0.05.