Disease relevance of Glucose Tolerance Test

• Thus, prospective islet-cell antibody screening of high-risk first-degree relatives, in combination with intravenous glucose-tolerance testing, is capable of identifying immunologically abnormal persons with profoundly diminished beta-cell function, who are presumably at increased risk of insulin-dependent diabetes mellitus [1].
• Weight loss decreased fasting glucose concentrations by 2%, insulin by 18%, and glucose and insulin areas during the oral glucose tolerance test (OGTT) by 8% and 26%, respectively (P < .01) [2].
• 20 normoglycemic first degree relatives of non-insulin-dependent diabetes mellitus (NIDDM) patients were compared with 20 matched subjects without any family history of diabetes using the intravenous glucose tolerance test with minimal model analysis of glucose disappearance and insulin kinetics [3].
• Dogs were studied with glucose infusions (group I) or standard intravenous glucose tolerance tests (IVGTT) (group II) before and after the development of diet-induced hypophosphatemia [4].
• Ophthalmoscopically visible microvascular retinal disease was confined to men diagnosed as probably diabetic after the survey because their 2 h blood-sugar level (after a 50 g oral glucose load) in the survey examination or during a subsequent standard oral glucose-tolerance test was greater than or equal to 200 mg/dl (11.1 mmol/l) [5].

Psychiatry related information on Glucose Tolerance Test

• SETTING: Subjects were recruited from an urban community mental health clinic and were studied at a general clinical research center.Patients Fifty subjects signed informed consent and 41 underwent the frequently sampled intravenous glucose tolerance test [6].
• OBJECTIVE--To determine whether higher levels of physical activity are associated with lower fasting insulin levels and lower insulin areas under the oral glucose tolerance curve in individuals with impaired glucose tolerance (IGT) in a community setting [7].
• RESULTS: T groups showed normal oral glucose tolerance tests and metabolic parameters [8].
• Plasma levels of active form of ghrelin during oral glucose tolerance test in patients with anorexia nervosa [9].
• Individual differences in the ability to control blood glucose were measured by giving a glucose tolerance test (GTT) to 46 young adult females [10].

High impact information on Glucose Tolerance Test

• An oral glucose-tolerance test was performed annually; the diagnosis of diabetes was confirmed by a second test [11].
• METHODS: We measured steroids in serum and performed oral glucose-tolerance tests before and after the oral administration of 1200 mg of D-chiro-inositol or placebo once daily for six to eight weeks in 44 obese women with the polycystic ovary syndrome [12].
• We conclude that impaired glucose metabolism is common in the first-degree relatives of patients with NIDDM, despite their normal results on oral glucose-tolerance tests [13].
• MAIN OUTCOME MEASURE: Insulin sensitivity as measured by an intravenous glucose tolerance test [14].
• Nor was there a difference in glucose excursion between the groups of mice during oral glucose tolerance test, but insulin concentrations of the WT group were greater than those of the PPAR-gamma(+/-) group, and insulin-induced increase in glucose disposal rate was significantly increased in PPAR-gamma(+/-) mice [15].

Chemical compound and disease context of Glucose Tolerance Test

• These five groups were then compared on the basis of their insulin response during the oral glucose tolerance test and on the ability of exogenously infused insulin to limit hyperglycemia during a continuous infusion of glucose and insulin, while endogenous insulin was inhibited by the infusion of epinephrine and propranolol [16].
• The effects of subclinical vitamin D deficiency and vitamin D supplementation on oral glucose tolerance and secretion of pancreatic hormones were studied in 10 diphenylhydantoin-treated epileptic patients and 15 geriatric patients [17].
• CONCLUSIONS: The addition of orlistat to a conventional weight loss regimen significantly improved oral glucose tolerance and diminished the rate of progression to the development of impaired glucose tolerance and type 2 diabetes [18].
• METHODS: A sample of 2076 people aged 40 years or more participating in the population-based Cremona Study and classified in 1990 as having diabetes mellitus, impaired and normal glucose tolerance according to WHO criteria after an oral glucose tolerance test, were tested for antibodies to glutamic acid decarboxylase and IA-2 [19].
• Therefore, in addition to assessing beta-cell function by oral glucose tolerance testing (n = 318, normal glucose tolerance), we measured the secretory response to maximal stimulation by hyperglycemia (10 mM), glucagon-like peptide-1, and arginine administered in an additive fashion (n = 77, nondiabetic) [20].

Biological context of Glucose Tolerance Test

• To evaluate the effect of CCK on oral glucose tolerance, plasma CCK, insulin, and glucose levels and gastric emptying rates were measured in eight normal males before and after the ingestion of 60 g glucose with the simultaneous infusion of either saline or one of two doses of CCK-8 (12 or 24 pmol/kg per h) [21].
• The results of oral glucose tolerance testing in two patients were consistent with the development of insulin resistance, and daily insulin requirements increased 10-fold in a patient who had preexisting diabetes [22].
• MEASUREMENTS: An oral glucose tolerance test; assessment of insulin sensitivity and hormonal responses to insulin hypoglycemia; and assessment of lipid levels, blood pressure, left ventricular mass, and lipid peroxidation [23].
• METHODS: Modified oral glucose tolerance tests were performed in schizophrenic patients (n = 48) receiving clozapine, olanzapine, risperidone, or typical antipsychotics, and untreated healthy control subjects (n = 31), excluding subjects with diabetes and matching groups for adiposity and age [24].
• To determine hepatic futile cycling, we studied seven healthy controls (C) and eight mild, lean, type 2 diabetics with decreased oral glucose tolerance test and blood glucose of 123 +/- 4 mg/dl [25].

Anatomical context of Glucose Tolerance Test

• Marked improvements in oral glucose tolerance, suggesting enhanced insulin secretory capacity, were corroborated by pancreas perfusion and insulin content measurements that revealed two- to eightfold increases in both secretory function and insulin content after 7 weeks of treatment [26].
• Fasting muscle sympathetic nerve activity (MSNA) correlated positively with body fat (r = 0.73; P = 0.001) in Caucasians but not in Pima Indians, whereas the increase in MSNA during the OGTT correlated negatively with the percentage of body fat (r = -0.38, P = 0.03) independently of race [27].
• Insulin has important effects to increase skeletal muscle (leg) blood flow under euglycemic hyperinsulinemic clamp conditions and after oral glucose tolerance testing [28].
• We have demonstrated that acute infection has a unique metabolic profile with a high degree of local inflammation in adipose tissue, hypoadiponectinemia, hypoglycemia, and hypoinsulinemia but with relatively normal glucose disposal during an oral glucose tolerance test [29].
• He had a low insulin secretion rate during an OGTT, but a twofold increase in pancreatic beta-cell response after intravenous glucose and a 2.5- to 4-fold increase in beta-cell response after either intravenous tolbutamide or intravenous glucagon loads [30].

Associations of Glucose Tolerance Test with chemical compounds

• METHODS: We performed oral glucose-tolerance tests before and after the administration of 500 mg of metformin or placebo three times daily for 35 days in 61 obese women with the polycystic ovary syndrome [31].
• The insulin-sensitivity index, calculated from the results of intravenous glucose-tolerance tests, increased from 0.7 +/- 0.6 x 10(-4) to 1.6 +/- 0.9 x 10(-4) in subjects given troglitazone, and their glycemic response to oral glucose and to mixed meals decreased [32].
• On the third and fourth treatment days, respectively, an L-arginine stimulation test and an intravenous glucose tolerance test were performed [33].
• All members underwent oral and intravenous glucose tolerance tests (oGTT and ivGTT) and an insulin-sensitivity test (IST) using octreotide [34].
• OBJECTIVE: To study the 2 drugs most clearly implicated (clozapine and olanzapine) and risperidone using a frequently sampled intravenous glucose tolerance test [6].

Gene context of Glucose Tolerance Test

• Serum GIP levels in GLP-1R -/- mice were significantly elevated versus those in +/+ control mice after an oral glucose tolerance test (369 +/- 40 vs. 236 +/- 28 pmol/l; P < or = 0.02) [35].
• In this study, we addressed the question of whether the common -866G/A polymorphism in UCP2 gene contributes to the variation of insulin secretion in humans by genotyping 301 nondiabetic subjects who underwent an oral glucose tolerance test [36].
• The finding of an association between homozygosity for the codon 354 variant and reduced fasting and post oral glucose tolerance test (OGTT) serum C-peptide concentrations, however, calls for further investigations and could suggest that GIP even in the fasting state regulates the beta-cell secretory response [37].
• The subjects with IGFBP1 Bgl II AA (n = 8) showed greater increases in abdominal visceral fat (p < 0.01), OGTT insulin area (p = 0.05) and total cholesterol (p < 0.03) with overfeeding than the subjects with AG + GG (n = 16) [38].
• Insulin concentrations were higher in the glucokinase subjects throughout the OGTT [39].

Analytical, diagnostic and therapeutic context of Glucose Tolerance Test

• The development in the immediate postoperative period of blood glucose levels ranging from 300 to 500 mg/dl was totally unexpected, as the levels on the preoperative oral glucose tolerance test were normal [40].
• The Gly971Arg substitution was not associated with an impairment in insulin secretion capacity (estimated by insulin responses in an oral glucose tolerance test or by the hyperglycemic clamp) or insulin action (estimated by the euglycemic clamp) [41].
• Relatives and controls had a normal oral glucose tolerance, and were studied by means of the euglycemic hyperinsulinemic clamp technique, which included performance of indirect calorimetry and muscle biopsies [42].
• Eight lean and eight obese men with normal oral glucose tolerance tests were investigated with the subcutaneous microdialysis technique and 133Xe clearance [43].
• The offenders also received lumbar punctures for monoamine metabolites, an oral glucose tolerance test, and a measurement of fasting plasma cholesterol level [44].

References