The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

Abstract

BackgroundPrevious studies have demonstrated that postprandial hyperglycemia attenuates brachial artery flow-mediated dilation (FMD) in prediabetic patients, in diabetic patients, and even in normal subjects. We have previously reported that postprandial hyperinsulinemia also attenuates FMD. In the present study we evaluated the relationship between different degrees of postprandial attenuation of FMD induced by postprandial hyperglycemia and hyperinsulinemia and differences in ingested carbohydrate content in non-diabetic individuals.MethodsThirty-seven healthy subjects with no family history of diabetes were divided into 3 groups: a 75-g oral glucose loading group (OG group) (n = 14), a test meal group (TM group) (n = 12; 400 kcal, carbohydrate content 40.7 g), and a control group (n = 11). The FMD was measured at preload (FMD0) and at 60 minutes (FMD60) and 120 (FMD120) minutes after loading. Plasma glucose (PG) and immunoreactive insulin (IRI) levels were determined at preload (PG0, IRI0) and at 30 (PG30, IRI30), 60 (PG60, IRI60), and 120 (PG120, IRI120) minutes after loading.ResultPercentage decreases from FMD0 to FMD60 were significantly greater in the TM group (−21.19% ± 17.90%; P < 0.001) and the OG group (−17.59% ± 26.64%) than in the control group (6.46% ± 9.17%; P < 0.01), whereas no significant difference was observed between the TM and OG groups. In contrast, the percentage decrease from FMD0 to FMD120 was significantly greater in the OG group (−18.91% ± 16.58%) than in the control group (6.78% ± 11.43%; P < 0.001) or the TM group (5.22% ± 37.22%; P < 0.05), but no significant difference was observed between the control and TM groups. The FMD60 was significantly correlated with HOMA-IR (r = −0.389; P < 0.05). In contrast, FMD120 was significantly correlated with IRI60 (r = −0.462; P < 0.05) and the AUC of IRI (r = −0.468; P < 0.05). Furthermore, the percentage change from FMD0 to FMD120 was significantly correlated with the CV of PG (r = 0.404; P < 0.05), IRI60 (r = 0.401; p < 0.05) and the AUC of IRI (r = 0.427; P < 0.05). No significant correlation was observed between any other FMDs and glucose metabolic variables.ConclusionDifferences in the attenuation of postprandial FMD induced by different postprandial insulin levels may occur a long time postprandially but not shortly after a meal.

Relationship between fluctuations in glucose levels measured by continuous glucose monitoring and vascular endothelial dysfunction in type 2 diabetes mellitus

“…In cases with normal glucose tolerance, vascular endothelial function correlates with postprandial glucose fluctuation, insulin resistance, and postprandial serum insulin level [25], and within the normoglycemic range, individuals whose 2-h plasma glucose levels did not return to their fasting plasma glucose levels during OGTT had elevated fasting insulin levels and increased incidence of coronary heart disease [26]. Patients with mild abnormalities in glucose metabolism are reported to suffer from endothelial dysfunction.…”

Glycemic variability is associated with subclinical atherosclerosis in Chinese type 2 diabetic patients

“…Meanwhile, as a major contributor to glycemic variability, postprandial blood glucose, especially the acute hyperglycemia after a meal or glucose load, was found to be strongly associated with endothelial function, carotid IMT and cardiovascular diseases [26,27]. Suzuki et al [28] found the attenuation of brachial artery flow-mediated dilation (FMD) in the postprandial state was correlated with postprandial glucose fluctuation and the postprandial serum insulin level in individuals with normal glucose tolerance. Esposito, et al [29] found that incremental glucose peak, the maximal incremental increase in blood glucose obtained at any point after the meal, was correlated with carotid IMT, suggesting postprandial glucose is involved in the process of subclinical atherosclerosis.…”

Beneficial effect of combination therapy with mitiglinide and voglibose on fasting and postprandial endothelial dysfunction in patients with type2 diabetes: a pilot study

“…Beneficial effect of combination therapy with mitiglinide and voglibose on fasting and postprandial endothelial dysfunction in patients with type2 diabetes: a pilot study We focused on the potential of the combination treatment to ameliorate endothelial dysfunction due to reducing the postprandial hyperglycemia [9,10], because previous studies showed that each monotherapy of glinide and α-glucosidase inhibitor ameliorated endothelial dysfunction [11,12]. In this context, we conducted this pilot study to investigate whether switching from SU to mitiglinide/ voglibose could reduce the fluctuation of blood glucose, eventually decreasing in the hypoglycemic episodes and amelioration of endothelial dysfunction in patients with type 2 diabetes.…”