Oral Glucose Load Acutely Impairs Endothelial Function and Arterial Stiffness in Healthy Subjects: an Effect Prevented by Short-Term Administration of Flavanol-Rich Dark Chocolate

Objective Impaired glucose metabolism and insulin sensitivity have been reported in patients with Gitelman syndrome (GS), but insulin secretion and the related mechanisms are not well understood. Design and methods The serum glucose levels, insulin secretion and insulin sensitivity were evaluated in patients with GS (n = 28), patients with type 2 diabetes mellitus (DM) and healthy individuals (n = 20 in both groups) using an oral glucose tolerance test. Serum and urine sodium, potassium and creatinine levels were measured at 0, 30, 60, 120 and 180 min after an oral glucose load was administered. Results The areas under the serum glucose curves were higher in the GS patients than those in the healthy controls (17.4 ± 5.1 mmol·h/L vs 14.5 ± 2.8 mmol·h/L, P = 0.02) but lower than those in the DM patients (24.8 ± 5.3 mmol·h/L, P < 0.001). The areas under the serum insulin curves and the insulin secretion indexes in GS patients were higher than those in DM patients and lower than those in healthy subjects. The insulin secretion-sensitivity index of GS patients was between that of healthy subjects and DM patients, but the insulin sensitivity indices were not different among the three groups. After one hour of glucose administration, the serum potassium level significantly decreased from baseline, and the urinary potassium-to-creatinine ratio increased gradually and peaked at 2 h. Conclusions Glucose metabolism and insulin secretion were impaired in GS patients, but insulin sensitivity was comparable between GS patients and patients with type 2 DM. After administration of an oral glucose load, the plasma potassium level decreased in GS patients due to the increased excretion of potassium in the urine.

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An Oral Glucose Load Decreases Postprandial Extracellular Vesicles in Obese Adults with and without Prediabetes

Nutrients ◽

10.3390/nu11030580 ◽

2019 ◽

Vol 11 (3) ◽

pp. 580 ◽

Cited By ~ 1

Author(s):

Natalie Z. M. Eichner ◽

Nicole M. Gilbertson ◽

Luca Musante ◽

Sabrina La Salvia ◽

Arthur Weltman ◽

...

Keyword(s):

Arterial Stiffness ◽

Glucose Tolerance ◽

Extracellular Vesicles ◽

Augmentation Index ◽

Annexin V ◽

Oral Glucose ◽

Oral Glucose Load ◽

Glucose Load ◽

Cvd Risk ◽

Obese Adults

Although extracellular vesicles (EVs) are a novel biomediator of type 2 diabetes (T2D) and cardiovascular disease (CVD), the effects of hyperglycemia on EVs in humans is unknown. We tested the hypothesis that a 75-g oral glucose tolerance test (OGTT) would promote changes in EVs in relation to CVD risk. Twenty-five obese adults (Age: 52.4 ± 3.2 year, BMI: 32.5 ± 1.2 kg/m2) were screened for normal glucose tolerance (NGT, n = 8) and prediabetes (PD, n = 17) using American Diabetes Association criteria (75 g OGTT and/or HbA1c). Body composition (bioelectrical impedance) and fitness (VO2peak) were measured. Arterial stiffness (augmentation index; AIx) was measured at 0, 60- and 120-min while insulin, glucose, and free fatty acids were evaluated every 30 min during the OGTT to assess CVD risk. Annexin V positive (AV+) and Annexin V negative (AV-) total EVs, platelet EVs (CD31+/CD41+; CD41+), leukocyte EVs (CD45+; CD45+/CD41−), platelet endothelial cell adhesion molecule (PECAM) (CD31+) and endothelial EVs (CD 31+/CD41−; CD105+) were collected at 0 and 120 min. There were no differences in age, BMI, or body fat between NGT and PD (all P > 0.63). Total EVs, AV+ CD31+ (PECAM), and AV+ CD31+/CD41- (endothelial) EVs decreased after the OGTT (P ≤ 0.04). Circulating insulin at 2-h correlated with elevated post-prandial AV- CD45+ (r = 0.48, P = 0.04) while arterial stiffness related to reduced total EVs (r = −0.49, P = 0.03) and AV+CD41+ (platelet) (r = −0.52, P = 0.02). An oral glucose load lowers post-prandial total, platelet, and endothelial EVs in obese adults with NGT and prediabetes in relation to CVD risk.

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The Disposal of an Oral Glucose Load in Healthy Subjects: A Quantitative Study

Diabetes ◽

10.2337/diab.34.6.580 ◽

1985 ◽

Vol 34 (6) ◽

pp. 580-588 ◽

Cited By ~ 197

Author(s):

E. Ferrannini ◽

O. Bjorkman ◽

G. A. Reichard ◽

A. Pilo ◽

M. Olsson ◽

...

Keyword(s):

Quantitative Study ◽

Healthy Subjects ◽

Oral Glucose ◽

Oral Glucose Load ◽

Glucose Load

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Effects of Oral Glucose Load on Endothelial Function and on Insulin and Glucose Fluctuations in Healthy Individuals

Experimental Diabetes Research ◽

10.1155/2008/672021 ◽

2008 ◽

Vol 2008 ◽

pp. 1-6 ◽

Cited By ~ 15

Author(s):

A. Major-Pedersen ◽

N. Ihlemann ◽

T. S. Hermann ◽

B. Christiansen ◽

H. Dominguez ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Endothelial Function ◽

Oral Glucose ◽

Flow Mediated Dilation ◽

Oral Glucose Load ◽

Glucose Load ◽

Healthy Individuals ◽

Insulin Resistant ◽

Postprandial State ◽

Glucose Fluctuations

Background/aims. Postprandial hyperglycemia, an independent risk factor for cardiovascular disease, is accompanied by endothelial dysfunction. We studied the effect of oral glucose load on insulin and glucose fluctuations, and on postprandial endothelial function in healthy individuals in order to better understand and cope with the postprandial state in insulin resistant individuals.Methods. We assessed post-oral glucose load endothelial function (flow mediated dilation), plasma insulin, and blood glucose in 9 healthy subjects.Results. The largest increases in delta FMD values (fasting FMD value subtracted from postprandial FMD value) occurred at 3 hours after both glucose or placebo load, respectively:4.80±1.41(P= .009) and2.34±1.47(P= .15). Glucose and insulin concentrations achieved maximum peaks at one hour post-glucose load.Conclusion. Oral glucose load does not induce endothelial dysfunction in healthy individuals with mean insulin and glucose values of 5.6 mmol/L and 27.2 mmol/L, respectively, 2 hours after glucose load.

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Elevated 1-h plasma glucose following 75-g oral glucose load is a predictor of arterial stiffness in subjects with normal glucose tolerance

Diabetic Medicine ◽

10.1111/dme.12026 ◽

2012 ◽

Vol 29 (12) ◽

pp. e457-e460 ◽

Cited By ~ 9

Author(s):

K. Niijima ◽

Y. Muranaka ◽

T. Ando ◽

S. Okada ◽

Y. Niijima ◽

...

Keyword(s):

Arterial Stiffness ◽

Glucose Tolerance ◽

Plasma Glucose ◽

Normal Glucose Tolerance ◽

Oral Glucose ◽

Oral Glucose Load ◽

Glucose Load ◽

Normal Glucose

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A new concept for the evaluation of the blood glucose and insulin responses of healthy subjects following an oral glucose load

Acta Diabetologica Latina ◽

10.1007/bf02581231 ◽

1974 ◽

Vol 11 (4) ◽

pp. 265-276 ◽

Cited By ~ 3

Author(s):

Olga Szabo ◽

Werner Oppermann ◽

Rafael A. Camerini-Dávalos ◽

Carl Victor

Keyword(s):

Blood Glucose ◽

Healthy Subjects ◽

Oral Glucose ◽

Oral Glucose Load ◽

Glucose Load ◽

Insulin Responses

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Oral Glucose Load and Human Cutaneous Microcirculation: An Insight into Flowmotion Assessed by Wavelet Transform

Biology ◽

10.3390/biology10100953 ◽

2021 ◽

Vol 10 (10) ◽

pp. 953

Author(s):

Henrique Silva ◽

Jernej Šorli ◽

Helena Lenasi

Keyword(s):

Wavelet Transform ◽

Reactive Hyperemia ◽

Oral Glucose ◽

Oral Glucose Load ◽

Glucose Load ◽

Short Term ◽

Doppler Flowmetry ◽

Chronic Hyperglycemia ◽

Cutaneous Microcirculation ◽

The Impact

Microcirculation in vivo has been assessed using non-invasive technologies such as laser Doppler flowmetry (LDF). In contrast to chronic hyperglycemia, known to induce microvascular dysfunction, the effects of short-term elevations in blood glucose on microcirculation are controversial. We aimed to assess the impact of an oral glucose load (OGL) on the cutaneous microcirculation of healthy subjects, quantified by LDF and coupled with wavelet transform (WT) as an interpretation tool. On two separate occasions, sixteen subjects drank either a glucose solution (75 g in 250 mL water) or water (equal volume). LDF signals were obtained in two anatomical sites (forearm and finger pulp) before and after each load (pre-load and post-load, respectively), in resting conditions and during post-occlusive reactive hyperemia (PORH). The WT allowed decomposition of the LDF signals into their spectral components (cardiac, respiratory, myogenic, sympathetic, endothelial NO-dependent). The OGL blunted the PORH response in the forearm, which was not observed with the water load. Significant differences were found for the cardiac and sympathetic components in the glucose and water groups between the pre-load and post-load periods. These results suggest that an OGL induces a short-term subtle microvascular impairment, probably involving a modulation of the sympathetic nervous system.

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