Effects Of Oral Glucose Load Research Articles

Metabolic and ventilatory effects of oral glucose load at rest and during incremental aerobic muscular work in young healthy adults.

We measured respiratory ratio (RR), pulmonary ventilation (VE) and end-tidal carbon dioxide partial pressure (ETPCO2) at rest and during cycling aerobic workloads (20%, 40%, 60% of estimated maximal oxygen uptake). Measurements were taken after overnight fasting and after an oral glucose load. RR, VE and ETPCO2 increased with workload. Glucose load caused RR and VE increments at rest (0.75 ± 0.01 vs. 0.86 ± 0.02, p < 0.01, and 10.8 ± 0.43 vs. 12.1 ± 0.49 l/min, p < 0.01, respectively) and for each workload (20% estimated maximal oxygen uptake: 0.77 ± 0.01 vs. 0.855 ± 0.02, p < 0.01, and 16.2 ± 0.73 vs. 17.7 ± 0.8 l/min, p < 0.01; 40% estimated maximal oxygen uptake: 0.76 ± 0.02 vs. 0.82 ± 0.01, p < 0.01, and 25.9 ± 1.1 vs. 28.3 ± 1.3 l/min, p < 0.05; 60% estimated maximal oxygen uptake: 0.85 ± 0.02 vs. 0.91 ± 0.02, p < 0.01, and 37.4 ± 1.7 vs. 40.9 ± 1.9 l/min, p < 0.05) but ETPCO2 did not change. The differences in RR before and after glucose load became smaller as the workload increased. Linear regression analysis of VE and carbon dioxide output yielded virtually identical results for both fasting and glucose load conditions. We have concluded that: a) for the metabolic carbon dioxide load increment due to glucose-induced RR increment, the physiological response is an increase of VE at all workloads. This response modulates constant ETPCO2 values; b) on workload increment, skeletal muscle increasingly utilises more and more glycogen stores, regardless of the blood glucose availability. This reduces the usefulness of dietary manipulations decreasing carbon dioxide metabolic load during muscular work in respiratory failure; c) the absolute value of metabolic carbon dioxide load exerts a role in ventilation regulation at rest and during aerobic exercise.

Ascorbic acid prevents vascular dysfunction induced by oral glucose load in healthy subjects

Objectives To examine the effects of oral glucose load on forearm circulatory regulation before and after ascorbic acid administration in healthy subjects. Design Microcirculation study with laser Doppler was performed at the hand in basal conditions, after ischemia and after acetylcholine and nitroprusside; strain gauge plethysmography was performed at basal and after ischemia. The tests were repeated in the same sequence 2 hour after oral administration of glucose (75 g). The subjects were randomised for administration of ascorbic acid (1 g bid) or placebo (sodium bicarbonate 1 g bid) for 10 days. After that, the tests were repeated before and after a new oral glucose load. Blood pressure and heart rate were monitored. Results Macrocirculatory flux, pressure values and heart rate were unvaried throughout the study. The glucose load caused a reduction in the hyperemic peak flow with laser Doppler and plethysmography; it reduced flux recovery time and hyperemic curve area after ischemia; acetylcholine elicited a minor increase in flux with laser Doppler. The response to nitroprusside was unvaried after glucose load as compared to basal conditions. Treatment with ascorbic acid prevented the decrease in hyperemia after glucose, detected with laser Doppler and plethysmography. Ascorbic acid prevented the decreased response to acetylcholine after glucose, the response to nitroprusside was unaffected by ascorbic acid. Results after placebo were unvaried. Conclusions Oral glucose load impairs endothelium dependent dilation and hyperaemia at microcirculation, probably via oxidative stress; ascorbic acid can prevent it.

Endothelium dependent vasodilation attenuated by acute glucose and fat loading in patients with essential hypertension

Objective To explore the influence of acute glucose and fat loading on endothelium dependent flow-mediated vasodilation (FMD) in patients with essential hypertension (EH). Methods 98 patients with EH were randomly divided into three groups. We evaluate the acute effect of oral glucose loading alone, oral standardized fat loading alone, combining glucose and fat loading on FMD of the brachial artery assessed by high resolution ultrasound technique respectively. Results (1) As compared to control group, EH had postrandial abnormal serum triglyceride metabolism and FMD, FMD was the lowest in 4h and returned to the basic level in 8h.

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

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) and 2.34 ± 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.

Effect of oral glucose loading on endothelial function in normal-weight and overweight children

The aim of the present study was to investigate the impact of acute hyperglycaemia on endothelial function in both normal-weight and overweight children. A total of 16 overweight [BMI (body mass index) > or =85th percentile] and 15 normal-weight (BMI <85th percentile) children were evaluated for FMD (flow-mediated dilation) at baseline and 30, 60 and 120 min after glucose ingestion. At 15 min following the measurement of the final FMD, 0.3 mg of sublingual nitroglycerine was administered and the brachial artery was imaged in order to assess endothelium-independent dilation. By design, the overweight children were significantly heavier (63.2+/-4.6 compared with 41.3+/-2.5 kg; P=0.0003) and had a greater percentage body fat (43.9+/-1.8 compared with 23.8+/-2.05%; P<0.0001) than the normal-weight children. The area under the curve in response to glucose administration was significantly (P<0.0001) greater in the overweight group for both glucose and insulin. The FMD area under the curve was not significantly different at baseline or between time points after glucose ingestion, nor was there a difference in response between the two groups. Endothelium-independent dilation in the normal-weight group was significantly greater compared with the overweight group (26.7+/-1.6 compared with 20.2+/-2.0% respectively; P=0.019). In conclusion, these results suggest that acute elevation of glucose and insulin in overweight and normal-weight children are not associated with impairment in endothelial function.

Oral glucose load inhibits circulating ghrelin levels to the same extent in normal and obese children

The presence of both the GH secretagogue (GHS) receptor and ghrelin in the pancreas indicates an involvement of this hormone in glucose metabolism. Ghrelin secretion is increased by fasting and energy restriction, decreased by food intake, glucose load, insulin and somatostatin in normal adults; however, food intake is not able to inhibit circulating ghrelin levels in children, suggesting that the profile of ghrelin secretion in children is different from that in adults. Moreover, how ghrelin secretion is regulated in childhood as a function of fat mass is still unclear. We studied the effect of oral glucose load (75 g solution orally) on circulating total ghrelin levels in 14 obese children (group A, four boys and 10 girls, aged 9.3 +/- 2.3 years) and 10 lean children (group B, five boys and five girls, aged 9.7 +/- 3.8 years). In all the sessions, blood samples were collected every 30 min from 0 up to +120 min. GH, insulin and glucose levels were assayed at each time point. Glucose peaks following an oral glucose tolerance test (OGTT) in groups A and B were similar; however, both basal and OGTT-stimulated insulin levels in group A were higher than in group B (P < 0.05). Basal total ghrelin levels in group A (281.3 +/- 29.5 pg/ml) were lower (P < 0.0005) than in group B (563.4 +/- 81.5 pg/ml). In both groups A and B, the OGTT inhibited total ghrelin levels (P < 0.005). In terms of absolute values, total ghrelin levels in group A were lower (P < 0.0005) than those in group B at each time point after glucose load. The percentage nadir in total ghrelin levels recorded in group A (-25% at 90 min) was similar to that recorded in group B (-31% at 120 min). Total ghrelin levels were negatively associated with BMI (r = 0.5, P < 0.005) but not with glucose or insulin levels. Ghrelin secretion is reduced in obese children. It is, however, equally sensitive in both obese and lean children to the inhibitory effect of oral glucose load.

Metabolic and haemodynamic effects of oral glucose loading in young healthy men carrying the 825T-allele of the G protein β3 subunit

BackgroundA C825T polymorphism was recently identified in the gene encoding the β3 subunit of heterotrimeric G-proteins (GNB3). The T-allele is significantly associated with essential hypertension and obesity. In order to further explore a possible pathogenetic link between the T-allele and impaired glucose tolerance we studied metabolic and haemodynamic responses to oral glucose loading in young, healthy subjects with and without the 825T-allele.MethodsTwelve subjects with and 10 without the 825T-allele were investigated at rest and following glucose ingestion (75 g). Blood glucose, serum insulin and haemodynamics were determined prior to and over 2 hours following glucose ingestion. We non-invasively measured stroke volume (SV, by impedance-cardiography), blood pressure (BP), heart rate (HR), and systolic-time-intervals. Cardiac output (CO) was calculated from HR and SV. Total peripheral resistance was calculated from CO and BP. Metabolic and haemodynamic changes were quantified by maximal responses and by calculation of areas under the concentration time profile (AUC). Significances of differences between subjects with and without the T-allele were determined by unpaired two-tailed t-tests. A p < 0.05 was considered statistically significant.ResultsMetabolic and haemodynamic parameters at baseline were very similar between both groups. The presence of the T-allele did not alter the response of any metabolic or haemodynamic parameter to glucose loading.ConclusionsIn conclusion, this study does not support the hypothesis that the C825T polymorphism may serve as a genetic marker of early impaired glucose tolerance.

Oral glucose loading acutely attenuates endothelium-dependent vasodilation in healthy adults without diabetes: an effect prevented by vitamins C and E

OBJECTIVESThe goal of this study was to determine whether postprandial hyperglycemia, induced by oral glucose loading, attenuates endothelial function in healthy subjects without diabetes and whether coadministration of vitamins C and E could prevent these postprandial changes.BACKGROUNDEpidemiologic evidence suggests that postprandial hyperglycemia, below diabetic levels, is a risk factor for cardiovascular disease. Postprandial hyperglycemia may promote atherosclerosis through endothelial dysfunction and oxidative stress.METHODSWe evaluated the acute effects of oral glucose loading (75 g), alone and with vitamins C (2 g) and E (800 IU), on endothelium-dependent flow-mediated dilation (FMD) of the brachial artery, in a randomized, double-blind, placebo-controlled, crossover study of 10 healthy volunteers. Changes in the levels of markers of oxidative stress (plasma malondialdehyde and erythrocyte glutathione, glutathione peroxidase and superoxide dismutase) were also assessed.RESULTSIncreases in plasma glucose and insulin after glucose loading were unaffected by vitamin coadministration. With glucose loading alone, FMD fell from 6.5 ± 2.2 at baseline to 5.4 ± 1.7, 3.7 ± 2.1∗, 4.1 ± 3.5∗ and 5.7 ± 1.9% at 1, 2, 3 and 4 h (∗p < 0.05 vs. 0 h). In contrast, FMD did not change significantly after glucose plus vitamins (6.4 ± 1.3, 7.6 ± 1.8, 7.9 ± 2.7, 6.9 ± 2.3, 6.9 ± 1.9% at 0, 1, 2, 3 and 4 h). By two-way repeated measures analysis of variance we found a significant interaction between vitamin treatment and time (p = 0.0003), indicating that vitamins prevented the glucose-induced attenuation of FMD. Oxidative stress markers did not significantly change with glucose loading alone or with vitamins.CONCLUSIONSOral glucose loading causes an acute, transient decrease of FMD in healthy subjects without diabetes, which is prevented by vitamins C and E.

Free plasma magnesium following glucose loading in healthy humans

The recognized existence of a circadian pattern in extracellular magnesium balance might mirror either an inherent rhythm in the homeostasis of this ion or dietary factors. Since in vitro insulin enhances cellular magnesium uptake, the circadian rhythm in extracellular magnesium metabolism might be modulated at least in part by carbohydrate intake. To assess this hypothesis, the effects of oral glucose loading on plasma total and ionized magnesium were investigated in lean healthy humans with a negative family history for essential hypertension and diabetes mellitus. Plasma total and ionized magnesium was similar before glucose loading and 30, 60, 90, 180, and 210 min thereafter. It is therefore concluded that in healthy humans the circadian pattern of extracellular magnesium is not modulated by the metabolic and hormonal mechanisms that adjust the concentration of glucose.

Endogenous Insulin Modulates Circulating Endothelin-1 Concentrations in Humans

To assess the effect of oral glucose loading on plasma endothelin-1 (ET-1) levels in humans. A total of 75 g D-glucose was given orally to 14 nonobese nondiabetic essential hypertensive subjects (eight men and six women, mean age 43.1 +/- 3.0 years) and eight normotensive subjects (four men and four women, mean age 45.2 +/- 4.1 years). Blood samples for plasma ET-1 measurement were drawn every 30 min for 2 h and then at 180 and 240 min. After glucose load, insulin increased more significantly in hypertensive subjects than in normotensive subjects at times 60 (P = 0.004) and 90 (P = 0.001) min. Glucose loading was followed by a mild but significant increase in circulating ET-1 levels in both groups (hypertensive subjects, from 0.87 +/- 0.25 pg/ml at time 0 to 1.64 +/- 0.33 pg/ml at 120 min and 1.74 +/- 0.38 pg/ml at 180 min, P < 0.05; normotensive subjects, from 0.82 +/- 0.38 pg/ml at time 0 to 1.42 +/- 0.18 pg/ml at 180 min, P < 0.05). Whereas baseline ET-1 levels were similar between the two groups, postload ET-1 levels were higher in hypertensive subjects than in normotensive subjects (P = 0.003 at 120 min; P = 0.04 at 180 min). This study indicates that significant changes in circulating ET-1 levels occur after oral glucose loading, probably due to a glucose-induced increment in endogenous insulin concentration.

Acute Effects of Oral Glucose Loading on the Renin-Angiotensin-Aldosterone System in Patients with Chronic Renal Disease

To determine the changes of the glucose-induced renin-angiotensin-aldosterone system in chronic renal disease, a standard oral glucose loading test (75g) was performed in patients with chronic glomerulonephritis (CGN) (n = 12) and compared with control subjects (10). Glucose loading resulted in a significant decrease of serum aldosterone as well as increases of blood glucose and insulin similarly in both CGN and C. However, the suppression of aldosterone was statistically milder in CGN than in C (p < 0.05). In contrast, significant elevations of plasma renin activity were observed in CGN at 60 and 120 min, but not in C after glucose loading. Urinary sodium excretion after glucose ingestion was lower in CGN than in C. These data demonstrated that the glucose-induced renin-angiotensin-aldosterone system in patients with chronic renal disease differed from that in healthy subjects.

The influence of oral glucose loading on baroreflex function in the elderly.

Blood pressure in the elderly may decrease after a meal or after oral glucose loading. It has been suggested that eating may affect blood pressure homeostasis through an insulin-induced blunting of baroreflex sensitivity. We investigated the effects of oral glucose loading on baroreflex sensitivity in young normotensives and in elderly normo-and hypertensive subjects. Blood pressure was measured by a new noninvasive device, Finapres, which measures blood pressure continuously in the finger. Baroreflex sensitivity was estimated with the phenylephrine and nitroglycerin method. In both elderly groups mean arterial pressure fell significantly after the glucose load (11 +/- 1 mm Hg, P less than .001 in the hypertensives, and 8 +/- 2 mm Hg, P less than .01 in the normotensive subjects), whereas no change in blood pressure was found in the young group. Baroreflex sensitivity was lower in both elderly groups than in young normotensives. Glucose loading had no influence on baroreflex sensitivity in the three groups. Therefore, we conclude that other factors are involved in the phenomenon of postprandial hypotension in the elderly.

P-6-17 Effect of oral glucose loading on erythrocyte sorbitol in diabetic and non-diabetic subjects

P-6-17 Effect of oral glucose loading on erythrocyte sorbitol in diabetic and non-diabetic subjects

Effect of oral glucose loading on erythrocyte sorbitol in diabetic and non-diabetic subjects

Effect of oral glucose loading on erythrocyte sorbitol in diabetic and non-diabetic subjects

Paradoxical elevations of plasma glucagon levels in patients after pancreatectomy or gastrectomy.

In twenty-five patients undergoing total pancreatectomy (TP), twenty distal gastrectomy (DG) and twenty healthy subjects, effects of oral glucose loading on the plasma glucagon (IRG) levels were determined. Plasma IRG levels were elevated after glucose loading in the TP and DG patients, but not in the healthy subjects. To clarify events related to the elevations in IRG, the plasma IRG components were analyzed by gel filtration in 6 of the TP patients, 5 of the DG patients and 4 of the controls. In the TP group, IRG3500 was not detectable either in the basal state or after glucose loading, while IRG9000 was markedly increased after glucose (p less than 0.002). In the DG group, IRG3500 was significantly suppressed after glucose (p less than 0.05), but IRG9000 was clearly increased (p less than 0.005). In the controls, IRG3500 was suppressed after glucose (p less than 0.05), however, IRG9000 was not detected throughout the examination. Thus, in patients with TP or DG, the essential cause of the high responses of plasma glucagon after oral glucose loading was the increase in IRG9000. Because the food passage route is much the same in TP and DG patients, the IRG9000 elevations are probably related to secretion in the digestive tract.

Effect of oral glucose loading on plasma insulin, potassium, renin and aldosterone in normal subjects and patients with primary hyperaldosteronism.

The effects of standard oral glucose loading (100 g) on plasma aldosterone and some regulatory factors were assessed in patients with primary hyperaldosteronism and normal subjects. Following overnight fast, mean plasma glucose was identical (10 patients and normal subjects approximately matched per age and sex); plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in the patients. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups; plasma renin activity was significantly increased only in normal subjects. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Relationships among glucose-induced changes in plasma aldosterone and other factors were assessed by multiple regression analysis in these patients and normal subjects as well as an additional group of 21 normal subjects; in the latter, plasma cortisol was also measured and found to decrease significantly after glucose loading. Changes in plasma aldosterone correlated (P less than 0.025) more closely with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that complex metabolic changes occur following glucose ingestion which are capable of modifying aldosterone secretion in normal subjects and primary hyperaldosteronism. The aldosterone-inhibitory effect of glucose tends to be blunted in the latter disorder. This could be related at least in part to an impaired insulin response in primary hyperaldosteronism.