Standard Oral Glucose Load Research Articles

The effect of glucose load on both cardiac and skeletal muscle FDG uptake

Background: The augmentation of the myocardial FDG uptake after a glucose load is very well established. However, the response of the skeletal muscle to the same glucose load has not been clearly demonstrated. The aim of this study is to demonstrate an increased skeletal muscle FDG uptake after a standard oral glucose load. To this end, we compared myocardial and skeletal muscle FDG uptake in a group of fasted patients to that of a second group of patients who underwent FDG PET scanning following oral glucose load. Methods: We included 41 patients (20 Male, 21 Female; age:26–72 years) without any cardiac pathology who had whole body FDG PET scan after several hours of fasting (4–24) in the first group. In the second group, we included 9 patients (8M; 1F; age 52–80 years) who had cardiac FDG PET imaging following a 50 g of oral glucose load. PET images were acquired with a Phillips Allegro scanner. We calculated the standard uptake values (SUV= Cts/injected dose/pt weight) of myocardium, arterial blood and skeletal muscle for both groups using regions of interest over the left ventricular myocardium, left ventricular cavity and skeletal muscle. Statistical analysis was performed using unpaired t test. Results: The results for both groups are given in table below. * Groups Heart SUV * Blood SUV Muscle SUV * Heart/Blood * Heart/Muscle Gp1 (n = 41) 4.8 ± 3.07 1.9 ± 0.64 0.88 ± 0.29 5.78 ± 3.70 2.54 ± 1.17 Gp2 (n = 9) 8.9 ± 5.25 2.39 ± 0.83 1.52 ± 0.50 6.62 ± 5.24 3.72 ± 1.70 * p < 0.05 There were statistically significant difference (p<0.05) between p values for heart and skeletal muscle uptake and for the heart to blood ratio. Conclusions: Both myocardial and skeletal muscle FDG uptake were higher in patients that received glucose load. However, the arterial concentration was similar. Skeletal muscle uptake could be used as an indicator of fasting status in patients undergoing FDG PET imaging.

Ghrelin secretion is modulated in a nutrient- and gender-specific manner.

Ghrelin is a potent GH secretagogue that also plays an important role in appetite and weight regulation. Ghrelin increases hunger and food intake, and its levels decrease after a standard meal or glucose. To examine the effects of standard oral glucose, lipid and protein loads on ghrelin levels, investigating the possibility that these responses may be modulated by several anthropometric and metabolic factors. There were 24 adult nondiabetic subjects (13 men/11 women; mean age 55.3 +/- 2.9 years, range 26-74 years). Each participant underwent one or more of the following nutrient loads: (i) a standard oral glucose (75 g) load (n = 18); (ii) an oral lipid load (40 g, with 24 g saturated fat; n = 13); (iii) an oral protein load (40 g; n = 11). Fasting ghrelin levels were negatively related to body mass index (BMI; r =-0.47; P = 0.02), waist circumference (r = -0.58; P = 0.0028), waist/hip ratio (r = -0.56; P = 0.0046), fasting insulin (r = -0.44, P = 0.03), and homeostasis model assessment insulin resistance index (HOMA-R; r = -0.43, P = 0.034). Glucose load induced a decrease in ghrelin levels (P < 0.0001), and this response was modulated by sex (P < 0.0001), in that levels were significantly higher in females. The presence of obesity affected ghrelin response to glucose (< 0.0217), in that log-transformed ghrelin levels started to increase back to baseline after its initial decline earlier in obese than in lean subjects. Ghrelin levels after a glucose load were lower over time in subjects with more pronounced insulin resistance (P < 0.0001). Similarly, ghrelin levels decreased significantly following the lipid meal (P = 0.035), and were modulated by HOMA-R (P = 0.027) and gender (P = 0.029). Protein did not affect ghrelin levels. This study demonstrates that ghrelin levels respond in a different manner to glucose, lipid and protein loads, and are subject to modulation according to gender, obesity and insulin sensitivity.

Fasting insulin sensitivity and post-oral glucose hyperinsulinaemia related to cardiovascular risk factors in adolescents with precocious pubarche.

Adolescents and young women with a history of precocious pubarche (PP, appearance of pubic hair before 8 years) exhibit hyperlipidaemia, and ovarian hyperandrogenism, indicating increased risk of coronary heart disease in the long term. The aim of this study was to determine the relative contribution of fasting insulin sensitivity, and post oral glucose tolerance test (OGTT) measures of insulin secretion to metabolic risk markers of adult disease. We have analysed data from 51 young women presenting with isolated PP (age range, 5.9-19.0 years) in early, mid and late puberty and 68 puberty-matched controls (age range, 6.2-16.8 years). Body composition data from a further 67 girls with PP are also presented. The homeostasis model of assessment insulin sensitivity index (HOMA Si) based on fasting glucose and insulin measurements and MSI120 based on insulin levels over the first 120 min following standard oral glucose load were selected as measures of fasting insulin sensitivity and 0-120-min insulinaemia, respectively. ISI30 was used as an index of insulin secretion 30 min following oral glucose load. The physiological decrease in fasting insulin sensitivity, 30-min insulin secretion and 0-120-min insulinaemia during puberty were exaggerated in PP girls. The relationship between fasting insulin sensitivity and 0-120-min insulinaemia was similar in PP girls and in controls but at each level of fasting insulin sensitivity the PP girls had a higher level of insulin secretion in response to an oral glucose load (P < 0.001). Fasting insulin sensitivity and 0-120 minute insulinaemia but not 30-min insulin secretion were strongly related to known cardiovascular risk factors. In a multivariate model incorporating fasting insulin sensitivity, 0-120-min insulinaemia, pubertal stage and body mass index (BMI) SDS as covariates, 0-120-min insulinaemia was strongly associated with elevated free androgen index, total cholesterol and truncal fat mass (P < 0.001) whereas fasting insulin sensitivity was associated only with reduced free androgen index (P < 0.02). Chronic exposure to insulin as reflected by 0-120 min hyperinsulinaemia, rather than 30 min insulin secretion, or fasting insulin senstivity, was most closely related cardiovascular disease risk in girls with PP.

A simple index for detection of gestational diabetes mellitus.

The conventional screening test for gestational diabetes mellitus is measurement of plasma glucose 1 hour after 50 g glucose by mouth. The sensitivity and specificity of this test are lower than desirable; we therefore developed an index including other plasma constituents. In a preliminary study, 138 pregnant women had the standard oral glucose load screening test, and plasma fructosamine and total proteins were measured, in addition to glucose, in the 1-hour samples. An index value (I) was calculated as [fructosamine (micro mol/L) divided by total proteins (g/L)]x[glucose (mmol/L) divided by 100]. Cut-off values for I were then assessed in a second prospective study, of 642 pregnant women. Definitive diagnosis of gestational diabetes was by oral glucose tolerance test (OGTT). The index was also assessed in terms of fetal macrosomia (birthweight>or=4000 g). With a cut-off value of I=27.2, sensitivity was 98%, specificity 89%, diagnostic efficiency 90%, positive likelihood ratio 8.76. Application of the index would have avoided 42% of the OGTTs demanded by the standard screening test, reducing false positives from about 24% to 10%. Predictive efficacy for macrosomia was 10.3% versus 7.9%. Our index offers an efficient screening test for gestational diabetes, and with more stringent cut-off points may be applicable as a single-step diagnostic procedure.

A Simple Index for Detection of Gestational Diabetes Mellitus

The conventional screening test for gestational diabetes mellitus is measurement of plasma glucose 1 hour after 50 g glucose by mouth. The sensitivity and specificity of this test are lower than desirable; we therefore developed an index including other plasma constituents. In a preliminary study, 138 pregnant women had the standard oral glucose load screening test, and plasma fructosamine and total proteins were measured, in addition to glucose, in the 1-hour samples. An index value (I) was calculated as [fructosamine (μmol/L)÷total proteins (g/L)]×[glucose (mmol/L)÷100]. Cut-off values for I were then assessed in a second prospective study, of 642 pregnant women. Definitive diagnosis of gestational diabetes was by oral glucose tolerance test (OGTT). The index was also assessed in terms of fetal macrosomia (birthweight ≥ 4000 g). With a cut-off value of I=27.2, sensitivity was 98%, specificity 89%, diagnostic efficiency 90%, positive likelihood ratio 8.76. Application of the index would have avoided 42% of the OGTTs demanded by the standard screening test, reducing false positives from about 24% to 10%. Predictive efficacy for macrosomia was 10.3% versus 7.9%. Our index offers an efficient screening test for gestational diabetes, and with more stringent cut-off points may be applicable as a single-step diagnostic procedure.

Insulin, sodium-lithium countertransport, and microalbuminuria in hypertensive patients.

Both microalbuminuria (>0.290 nmol/min [20 microg/min]) and high sodium-lithium countertransport (SLC) in diabetic or hypertensive humans are predictive of overt nephropathy and more aggressive cardiovascular complications, perhaps induced by insulin resistance. To analyze the relationships between microalbuminuria, SLC, microalbuminuria, and insulin in essential hypertension, we studied 90 hypertensive white patients, 25 of whom had microalbuminuria and 32 of whom were healthy. When urine sampling was completed for albuminuria determination, SLC was measured; all patients then underwent standard (75 g) oral glucose load to measure basal (0 minutes) and 2-hour glucose and insulin serum levels. Glucose-insulin ratio was used as insulin sensitivity index (ISI). In both hypertensive patients with normal microalbuminuria and those with pathological microalbuminuria, plasma insulin at 120 minutes was significantly higher than in control subjects. When the patients with pathological microalbuminuria were divided into thirds on the basis of their microalbuminuria, in the lower third, we found statistically significant less fasting insulin and higher basal ISI. SLC was higher in hypertensives than normotensives and, among hypertensives, higher in the subgroup with elevated microalbuminuria. In hypertensives, we found a weak but significant correlation between SLC and microalbuminuria, independent of insulin or ISI. The prevalence of high value of SLC (> or =0.383 mmol x L-1 x h-1) was significantly lower in hypertensives with normal rather than abnormal urinary albumin excretion. Our results indicate that in nondiabetic hypertensive whites, higher microalbuminuria is accompanied by signs of insulin resistance; moreover, a link exists between SLC and microalbuminuria, both predictive of aggressive complications of hypertension.

Glucose tolerance in adults after prenatal exposure to famine

Reduced growth in utero is associated with type 2 (non-insulin-dependent) diabetes and impaired glucose tolerance in adult life. There is no direct evidence in human beings that maternal nutrition during gestation affects insulin-glucose metabolism. We investigated glucose tolerance in people born around the time of famine in the Netherlands during 1944-45. We included 702 people born between Nov 1, 1943, and Feb 28, 1947, in Amsterdam, for whom we had detailed prenatal and birth records. We compared glucose and insulin responses to a standard oral glucose load in participants exposed to famine at any stage during gestation (exposed participants) with those who were born in the year before or conceived in the year after the famine (non-exposed participants). Glucose concentrations were increased 2 h after a standard glucose load among exposed participants (p = 0.006), and were highest in men and women exposed during mid and late gestation. Mean 2 h glucose concentration among non-exposed participants was 5.8 mmol/L; concentrations were 0.5 mmol/L (95% CI 0.1-0.9) higher among participants exposed during late gestation, 0.4 mmol/L (0-0.8) higher among those exposed during mid gestation, and 0.1 mmol/L (-0.4 to 0.6) among those exposed during early gestation. Participants born as thin babies to mothers with low bodyweights had the highest concentrations and concentrations were especially high among people exposed to famine who became obese as adults. Prenatal exposure to famine was related to increased fasting proinsulin (p = 0.05) and 2 h insulin concentrations (p = 0.04), which suggests an association with insulin resistance. Prenatal exposure to famine, especially during late gestation, is linked to decreased glucose tolerance in adults. Poor nutrition in utero may lead to permanent changes in insulin-glucose metabolism, even if the effect on fetal growth is small. This effect of famine on glucose tolerance is especially important in people who become obese.

Childhood size is more strongly related than size at birth to glucose and insulin levels in 10-11-year-old children.

In adults low birthweight and thinness at birth are associated with increased risk of glucose intolerance and non-insulin-dependent diabetes mellitus. We have examined the relations between size at birth (birthweight, thinness at birth) and levels of plasma glucose and serum insulin in children, and compared them with the effects of childhood size. We performed a school-based survey of 10-11-year-old British children (response rate 64%) with measurements made after an overnight fast. One group of children (n = 591) was studied fasting while the other (n = 547) was studied 30 min after a standard oral glucose load (1.75 g/kg). Serum insulin was measured by a highly specific ELISA method. Birthweight was assessed by maternal recall and thinness at birth using birth records. Neither fasting nor post-load glucose levels showed any consistent relationship with birthweight or ponderal index at birth. After adjustment for childhood height and ponderal index, both fasting and post-load insulin levels fell with increasing birthweight. For each kg increase in birthweight, fasting insulin fell by 16.9% (95% confidence limits 7.1-25.8%, p = 0.001) and post-load insulin by 11.6% (95% confidence limits 3.5-19.1%, p = 0.007). However, the proportional change in insulin level for a 1 SD increase in childhood ponderal index was much greater than that for birthweight (27.2% and -8.8%, respectively, for fasting insulin). We conclude that low birthweight is not related to glucose intolerance at 10-11 years, but may be related to the early development of insulin resistance. However, in contemporary children obesity is a stronger determinant of insulin level and insulin resistance than size at birth.

Blunted catecholamine responses after glucose ingestion in children with attention deficit disorder.

Eating simple sugars has been suggested as having adverse behavioral and cognitive effects in children with attention deficit disorder (ADD), but a physiologic mechanism has not been established. To address this issue, metabolic, hormonal, and cognitive responses to a standard oral glucose load (1.75 g/kg) were compared in 17 children with ADD and 11 control children. Baseline and oral glucose-stimulated plasma glucose and insulin levels were similar in both groups, including the nadir glucose level 3-5 h after oral glucose (3.5 +/- 0.2 mmol/L in ADD and 3.3 +/- 0.2 mmol/L in control children). The late glucose fall stimulated a rise in plasma epinephrine that was nearly 50% lower in ADD than in control children (1212 +/- 202 pmol/L versus 2228 +/- 436 pmol/L, p < 0.02). Plasma norepinephrine levels were also lower in ADD than in control children, whereas growth hormone and glucagon concentrations did not differ between the groups. Matching test scores were lower and reaction times faster in ADD than in control children before and after oral glucose, and both groups showed a deterioration on the continuous performance test in association with the late fall in glucose and rise in epinephrine. These data suggest that children with ADD have a general impairment of sympathetic activation involving adrenomedullary as well as well as central catecholamine regulation.

The Relationships Among Serum Uric Acid, Plasma Insulin, and Serum Lipoprotein Levels in Subjects with Spinal Cord Injury

Relationships were investigated among serum uric acid (UA), the insulin response to a standard oral glucose load (75 g), and serum lipoprotein levels in 197 individuals with chronic spinal cord injury (SCI). All subjects had normal liver and renal function. None had a prior history of diabetes mellitus or gout. The mean age of subjects was 50 +/- 1 years, duration of injury (DOI), 18 +/- 1 years, and body mass index (BMI), 25 +/- 0.4 kg/m2. No significant differences were found between those with paraplegia or quadriplegia for any of the parameters measured. The mean serum UA values were not significantly different among the subgroups of subjects with normal glucose tolerance, impaired glucose tolerance, or diabetes mellitus (5.6 +/- 0.2 mg/dl, 5.6 +/- 0.2 and 5.7 +/- 0.3, respectively). Approximately one-half of the subjects had an abnormality in oral glucose tolerance. The levels of serum UA (p < 0.001) and serum triglycerides (TG) (p < 0.01) in the subgroup with hyperinsulinemia were significantly higher than in the subgroup with normal insulin levels. By linear regression analyses, the serum UA concentration was positively correlated with peak plasma insulin level (r = 0.31, p < 0.001), and BMI (r = 0.20, p < 0.01), but not with age, DOI, or peak glucose. The data suggest that in subjects with chronic SCI, as in the healthy able-bodied population, hyperuricemia is associated with hyperinsulinemia, obesity and abnormal lipoprotein metabolism.

Mechanism of Sugar-Induced Behavioral Effects

The adrenomedullary response to a standard oral glucose load (1.75 gm/kg; maximum, 120 gm) and susceptibility to neuroglycopenia (assessed by the hypoglycemic clamp and measurements of P300 auditory evoked potentials [AEP]) were studied in 25 healthy children (8-16 years of age) compared to 23 young adults at the Children’s Clinical Research Center, Yale University School of Medicine, New Haven, CT.

Enhanced adrenomedullary response and increased susceptibility to neuroglycopenia: Mechanisms underlying the adverse effects of sugar ingestion in healthy children

Objective: Eating simple sugars has been suggested as having adverse behavioral and cognitive effects in children, but a physiologic mechanism has not been established. This study was performed to address this issue. Design: Metabolic, hormonal, and symptomatic responses to a standard oral glucose load (1.75 gm/kg; maximum, 120 gm) were compared in 25 healthy children and 23 young adults, and the hypoglycemic clamp, together with measurements of P300 auditory evoked potentials, was used to assess whether children are more vulnerable than adults to neuroglycopenia. Setting: Children's Clinical Research Center, Yale University School of Medicine. Results: Baseline and oral glucose-stimulated plasma glucose and insulin levels were similar in both groups, including the nadir glucose level 3 to 5 hours after oral administration of glucose (3.4 ± 0.1 mmol/L [61 ± 1.8 mg/dl] in children and 3.5 ± 0.1 mmol/L [63 ± 1.8 mg/dl] in adults). The late glucose decrease stimulated a rise in plasma epinephrine levels that was twofold higher in children than in adults (2260 ± 289 vs 1031 ± 147 pmol/L [407 ± 52 vs 186 ± 26 pg/ml], p < 0.01) and a significant increase in hypoglycemic symptom scores in children ( p < 0.01), but not in adults. During control experiments, in which six of the healthy children ingested a sugar-free drink, there were no significant changes in plasma glucose levels, hormone concentrations, or hypoglycemic symptom scores. During the hypoglycemic clamp, P300 potentials did not change in any of eight adult subjects until the plasma glucose concentration was lowered to 3.0 mmol/L (54 mg/dl), whereas similar changes in P300 potentials were ob-served in six of seven children at glucose levels 3.6 to 4.2 mmol/L (65 to 75 mg/dl). Conclusion: Enhanced adrenomedullary responses to modest reductions in plasma glucose concentration and increased susceptibility to neuroglycopenia may be important contributing factors to adverse behavioral and cognitive effects after sugar ingestion in healthy children. (J P EDIATR 1995;126:171-7)

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.

Intracellular free magnesium in hypertension

In order to study the importance of altered intracellular ion metabolism in hypertension, we used 31P nuclear magnetic resonance (NMR) spectroscopy to measure intracellular free magnesium levels in normotensive (n = 19), essential hypertensive (n = 17) and diet-controlled diabetic (n = 6) subjects given a standard 100-g oral glucose load. The intracellular Mg level was significantly lower in hypertensives compared with normotensives (183 +/- 7 versus 232 +/- 10 mumol/l, P less than 0.001), and for all subjects was closely linked to both systolic (r = -0.84, P less than 0.001) and diastolic (r = -0.76, P less than 0.001) pressure. Hypertensives also showed a significantly greater insulinaemic response to glucose loading (P less than 0.001), and intracellular Mg was also closely and inversely linked to the integrated insulin response (r = -0.78, P less than 0.001). Despite the absence of hyperinsulinaemia, diabetics had the lowest intracellular Mg levels (156 +/- 8 mumol/l). Thus, suppressed intracellular Mg is linked to hypertension and to decreased tissue insulin sensitivity, and is not consequent to the hyperinsulinaemia itself. We suggest that intracellular Mg may provide a common pathophysiological basis for understanding the clinical association of hypertension and diabetes mellitus.

The oral glucose tolerance test in men under 55 years of age with intermittent claudication.

Blood glucose at sixty, ninety, and one hundred twenty minutes after a standardized oral glucose load was compared in healthy middle-aged men and patients with intermittent claudication. No difference was found when the authors compared blood glucose at zero and sixty minutes. At both ninety and one hundred twenty minutes, however, they found a relative hypoglycemia in patients with peripheral arteriosclerotic disease in an early stage.

Effect of strength training on glucose tolerance and post-glucose insulin response

The effect of muscle strength training on glucose tolerance and the insulin response after glucose feeding was investigated in eight healthy male subjects. Glucose tolerance and the associated insulin response was assessed using a standard 100-g oral glucose load before and after a supervised 10-wk high-resistance, isotonic weight-lifting program. Blood samples were drawn before and at 30, 60, 90, 120, and 150 min after ingestion of glucose. Areas under the glucose and insulin curves were used to determine differences between treatments. Muscle strength training increased body weight 3.7% and lean body mass by 3.5%, but had no effect on fat mass as determined by hydrostatic weighing. Glucose tolerance was not changed by the training program. However, a significant reduction in the basal plasma insulin concentration (37.5%) and the area under the insulin response curve (18.0%) was found (P less than 0.05). This reduction in the insulin response was significantly correlated (r = 0.89; P less than 0.05) with the increase in lean body mass. These results suggest that the increased muscle mass resulting from strength training was responsible for the attenuated insulin response to a standard 100-g oral glucose challenge.

Studies on acute glucose-induced aldosterone suppression: role of renin-angiotensin system.

Glucose loading is known to cause acute suppression of plasma aldosterone and stimulation of plasma renin activity. The relative contribution of variations in circulating angiotensin II to the regulation of aldosterone secretion following glucose loading was assessed in ten normal subjects. The effects of a standard oral glucose loading test (100 g) on plasma concentrations of glucose, insulin, potassium, aldosterone, renin activity and cortisol were studied (a) under basal conditions, and (b) after inhibition of angiotensin II with the converting enzyme inhibitor captopril (50 mg t.i.d. during 3 days). Under basal conditions the acute increase in plasma glucose and insulin after glucose loading was accompanied by a significant decrease (P less than 0.01) in plasma cortisol and aldosterone and by a significant increase in plasma renin activity (P less than 0.01); plasma potassium was decreased slightly but not significantly. Following captopril treatment preloading plasma renin activity was increased significantly, most probably reflecting an effective reduction of angiotensin II. Glucose loading caused a similar suppression of plasma aldosterone, as observed under basal conditions. This observation suggests that renin activation does not substantially contribute to the acute regulation of plasma aldosterone after an oral glucose load.

Effect of standard oral glucose loading on aldosterone secretion in primary hyperaldosteronism.

The effects of mild acute decreases in plasma potassium induced by standard oral glucose loading (100 g) on plasma aldosterone and renin levels were assessed in 10 patients with primary hyperaldosteronism as compared with 10 normal subjects. Following overnight fast, mean plasma glucose was identical in both groups; plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in patients than in controls. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. glucose-induced changes in plasma aldosterone correlated significantly (P less than 0.025) with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that the metabolic changes induced by glucose ingestion are capable of modifying aldosterone secretion in primary hyperaldosteronism. However, the glucose-induced decreases in plasma aldosterone are blunted in this disorder; this could be related to the impaired insulin response to glucose loading.

Glucose tolerance in two unacculturated Indian tribes of Brazil.

Plasma levels of glucose, insulin, growth hormone, and pancreatic polypeptide in response to a standard oral glucose load were studied in the Yanomama and the Marubo, two relatively unacculturated Amerindian tribes of the Brazilian Amazon. The findings in the two tribes differed significantly from each other and in the degree of deviation from control subjects. The average responses in both tribes differed significantly from those of age- and sex-matched Caucasoid control subjects studied in Ann Arbor, Michigan; however, of the two tribes, the Marubo, the more acculturated group, resembled the controls more closely. Plasma concentrations of glucose and the hormones at three time points (fasting, 1 h, 2 h) were compared by means of a multivariate analysis. When the Marubo were compared with the control subjects, the only highly significant difference was in the plasma glucose concentrations (all three points were higher in the Marubo); however, the Yanomama differed significantly from the control subjects with respect to all four plasma indicators (p less than 0.05). Unlike the Marubo, the Yanomama showed no significant rise in plasma glucose at 1 h and no decrease at 2 h. Neither tribe exhibited the bimodality of the 2 h glucose value characteristic of acculturated Amerindians, such as the Pima, but the samples studied were small.

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.