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PubMed1983

Glucose intolerance in spinal cord injury.

Glucose intolerance occurs frequently in patients with spinal cord injuries (SCI). In a retrospective chart analysis 23% of 57 consecutive discharges from a large SCI service had fasting hyperglycemia, and in a screening study, 30% of a group of stable SCI patients had 2-hour glucose values exceeding 200mg/dl after a glucose load and another 40% had values exceeding 140mg/dl. The glucose intolerance in many SCI patients is characterized by hyperinsulinemia after glucose is administered orally or intravenously. More than 40% of a group of glucose intolerant SCI patients had elevated insulin levels, suggesting tissue resistance to endogenous insulin.

Adult↗

PubMed2007

Factors responsible for glucose intolerance in Japanese subjects with impaired fasting glucose.

Impaired fasting glucose (IFG) represents risk of development of diabetes (DM) and its complications. We investigated insulin secretion and insulin sensitivity in 403 IFG subjects divided into three levels of 2-hour postchallenge glucose (2-h PG) to clarify the factors responsible in the development of glucose intolerance in Japanese IFG. Nearly 60% of the subjects at annual medical check-up with FPG of 6.1-7.0 mmol/l at the first screening were diagnosed by 75 g oral glucose tolerance test (OGTT) to have impaired glucose tolerance (IGT; FPG <7.0 mmol/l and 7.8 mmol/l <2-h PG <11.1 mmol/l) or DM (isolated postchallenge hyperglycemia (IPH); FPG <7.0 mmol/l and 11.1 mmol/l <2-h PG level). The primary factor in the decreased glucose tolerance was a decrease in early-phase insulin, with some contribution of increasing insulin resistance. In addition, IFG/IGT and IFG/IPH subjects showed a compensatory increase in basal insulin secretion sufficient to keep FPG levels within the non-diabetic range. IFG is composed of three different categories in basal, early-phase insulin secretion, and insulin sensitivity.

Asian People↗

PubMed1980

Sepsis, glucose intolerance, and protein malnutrition: a metabolic paradox.

Glucose intolerance and its hormonal influence was examined in patients with sepsis. Eighteen patients were included in the protocol, which studied the response to a standard intravenous glucose tolerance test (GTT) in the postoperative stressed, septic, and septic protein malnourished (depressed albumin level) states. Four groups could be defined: stress (1), sepsis with depressed albumin level and normal glucose tolerance (2), sepsis with mild glucose intolerance and normal albumin levels (3), and sepsis with severe glucose intolerance and depressed albumin (4). Serial hormone levels were measured during the GTT, including insulin, glucagon, epinephrine, and human growth hormone values. Each group demonstrated a characteristic hormone profile. In a comparison with controls, group 2 was associated with mild suppression of insulin; group 3 exhibited mild glucose intolerance, hyperglucagonemia, and increased insulin; and group 4 demonstrated severe glucose intolerance, hyperglucagonemia, and marked suppression of growth hormone production.

Glucagon↗

PubMed1978

Pathogenesis of glucose intolerance in uremia.

The pathogenesis of glucose intolerance in uremia was examined with the glucose clamp technique. Hyperglycemic clamp (n = 8): The plasma glucose concentration is acutely raised and maintained at 125 mg/dl above basal levels. Under these steady state conditions the glucose infusion rate, M, equals the amount of glucose metabolized: Predialysis M averaged 4.23 +/- 0.36 mg/kg/min and increased to 7.71 +/- 0.43 postdialysis (p less than 0.001). The plasma insulin response predialysis was 90 +/- 20 microU/ml and decreased to 80 +/- 23 microU/ml following dialysis. Consequently the M/l ratio, a measure of tissue sensitivity to insulin, increased by 80% +/- 25% (p less than 0.001) but still remained less than controls (p less than 0.01). Euglycemic insulin clamp (n = 10): The plasma insulin concentration is acutely raised by 100 microU/ml and the plasma glucose concentration is held constant at the basal level. Predialysis both M (3.37 +/- 0.36 mg/kg/min) and M/l (3.56 +/- 0.33 mg/kg/min per microU/ml X 100) were significantly less than controls (p less than 0.01). Postdialysis both M and M/l increased significantly (p less than 0.01) to a mean that was not significantly different from controls. Basal hepatic glucose production (n = 6), 2.15 +/- 0.09 mg/kg/min, was similar to controls and fell (87% +/- 4%) normally during the insulin clamp. In five uremic subjects in wom insulin binding to monocytes was measured, there was no correlation with tissue sensitivity to insulin (M/l). Significant abnormalities in both growth hormone and glucagon physiology were present in uremic individuals, but no correlation with either the presence or degree of glucose intolerance was demonstrable. In conclusion, glucose intolerance is universally present in uremic subjects and results primarily from peripheral tissue insensitivity to insulin. Insulin secretion is usually enhanced in an attempt to compensate for this insulin resistance but in occasional subjects uremia also inhibits beta cell sensitivity to glucose. Hepatic glucose production is unaffected by uremia. The lack of correlation between insulin binding and tissue sensitivity to insulin suggests that the cellular mechanism accounting for the insulin resistance is probably the result of a defect in intracellular metabolism or in the glucose transport system.

Adult↗

PubMed1987

Chronic oral terbutaline tocolytic therapy is associated with maternal glucose intolerance.

Plasma glucose determinations were performed 1 hour after a 50 gm oral glucose load in 30 patients receiving long-term terbutaline therapy (20 to 40 mg/day for at least 1 week) and 247 normal control patients. A total of 63% of patients receiving terbutaline had an abnormal 1-hour value (greater than or equal to 140 mg/dl), an incidence much higher than that of control subjects (17.8%) (p less than 0.0001) for a relative risk of 3.54 (95% confidence intervals of 2.29 to 5.42). Mean 1-hour values were 112.1 mg/dl for control subjects and 149.8 mg/dl in the terbutaline group (p less than 0.0001). All abnormal values were followed by a 3-hour 100 gm oral glucose tolerance test. A total of 15.9% of the glucose tolerance tests performed in the control group (2.8% overall) were abnormal as opposed to 52.6% (33.1% overall) in patients receiving terbutaline (p less than 0.01). Nine patients were studied before and after terbutaline therapy. Results obtained during administration of terbutaline were significantly higher (102.2 mg/dl before therapy versus 145.2 mg/dl during therapy). We conclude that treatment with oral terbutaline appears to be associated with impairment of glucose tolerance in pregnancy.

Administration, Oral↗

PubMed1989

Effect of habitual physical activity on age-related glucose intolerance.

Plasma glucose and insulin responses to a standard oral glucose challenge and a mixed meal were determined for two groups of male volunteers (office workers and laborers) and a group of female housewives or office workers. Although glucose tolerance declined with age to a certain degree in all three groups, the age-related change varied as a function of both level of habitual physical activity and gender. Specifically, the decline in glucose tolerance was greatest in the male office workers and least in the females. The plasma insulin responses did not increase with age in any of the groups. These results suggest that glucose tolerance decreases with age because there is a decline in insulin action, which is not compensated for by an increase in insulin secretion. Insulin sensitivity appears to be enhanced in females as compared with males. Sensitivity is also enhanced in males habitually engaged in physical labor; thereby accounting for the age-related decline being greatest in the male office workers. Finally, the results showed that although the loss of glucose tolerance with age varied from group to group, the quantitative nature of the change was modest in all three groups. These data further emphasize that very little change in glucose tolerance is associated with aging in generally healthy, nonobese individuals.

Adult↗

PubMed1996

[Screening of glucose intolerance with fasting blood samples].

Oral glucose tolerance test (OGTT) has been accepted as the standard test for screening of glucose intolerance in spite of its poor reproducibility, especially, in the impaired glucose intolerance (IGT). There have been widely assessed the diagnosis of diabetes mellitus with using glycemic control markers such as HbA1c, 1,5-AG, and FRA as an alternative method, which are not so much affected by sampling conditions. However, it has been found a wide overlap of the glycemic control marker's values between the normal and the IGT. In OGTT, subjects with lower blood glucose values 2 hours after glucose load turned out to be the normal glucose tolerance at the second examination as well. Therefore, it might be reasonable to identify people with a higher blood glucose value 2 hours after glucose load as a high risk group by the screening with fasting blood samples. We have evaluated the combination test of FBG, HbA1c and 1,5-AG for screening of the diabetes and the high risk IGT, and this combination revealed to be durable for screening. But it would be important to elucidate the natural history and the extent of the risk of the IGT, and select a proper test with a clear cut-off value for screening of impaired glucose intolerance at risk.

Biomarkers↗

PubMed1999

High incidence of glucose intolerance in Vogt-Koyanagi-Harada disease.

AIMS: To evaluate glucose tolerance of patients with Vogt-Koyanagi-Harada (VKH) disease before systemic corticosteroid therapy, and to assess changes brought on by treatment. METHODS: 20 VKH patients with acute bilateral panuveitis were studied. 20 healthy adults and 11 Behçet's disease patients with active uveoretinitis served as controls. A 75 g oral glucose tolerance test (OGTT) was given in the acute stage of ocular inflammation before systemic corticosteroid therapy. The OGTT was repeated in the convalescent stage of VKH disease in the patients with glucose intolerance before treatment. Insulin response was examined at the same time as the OGTT when possible. RESULTS: 55% of VKH patients (11/20) showed glucose intolerance but no apparent insulin secretion deficiency was detected. Four of seven patients in the convalescent stage showed improvement of glucose tolerance. None of the normal controls or disease controls showed glucose intolerance. CONCLUSION: A high incidence of glucose intolerance was found in the acute stage of VKH disease. However, glucose intolerance improved in most cases after systemic corticosteroid therapy. It is possible that glucose intolerance seen in VKH patients may be related to the autoimmune inflammatory process of this disease.

Adrenal Cortex Hormones↗

PubMed1991

Contribution to postprandial hyperglycemia and effect on initial splanchnic glucose clearance of hepatic glucose cycling in glucose-intolerant or NIDDM patients.

Excessive amounts of glucose enter the systemic circulation when patients with non-insulin-dependent diabetes mellitus (NIDDM) eat a carbohydrate-containing meal. To determine the contribution of hepatic glucose cycling (defined as the net effect of glucose/glucose-6-phosphate cycling and uptake and release of glucose from hepatic glycogen) to postprandial hyperglycemia, diabetic, glucose-intolerant, and nondiabetic subjects were fed mixed meals. The meal contained both [2-3H]glucose (an isotope that is extensively detritiated during hepatic glucose cycling) and [6-3H]glucose (an isotope that is not detritiated during hepatic glucose cycling). Of the 50 g of carbohydrate contained in the meal, approximately 4-8 g underwent hepatic glucose cycling. Although total cycling of ingested glucose did not differ between diabetic, glucose-intolerant, and nondiabetic subjects (361 +/- 67 vs. 494 +/- 106 vs. 322 +/- 44 mumol.kg-1.5 h-1, respectively), the data suggested that hepatic cycling was increased in the diabetic and glucose-intolerant individuals but not in the nondiabetic subjects during the first 2 h after eating. Hepatic cycling during the first 2 h after eating was correlated with the prevailing glucagon concentration (r = 0.6, P less than 0.01) and increased (P less than 0.05) as hepatic glucose release increased. Hepatic glucose cycling had a marked effect on the measurement of so-called initial splanchnic glucose uptake. Nevertheless, however measured, initial splanchnic glucose uptake was not decreased and, if anything, was increased in diabetic and glucose-intolerant patients. Integrated postprandial hepatic glucose release increased (r less than 0.01) with the severity of fasting hyperglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗

PubMed1994

Glucose intolerance exaggerates left ventricular hypertrophy and dysfunction in essential hypertension.

The influence of glucose intolerance, the preclinical stage of diabetes mellitus, on the progression of left ventricular hypertrophy and left ventricular dysfunction in essential hypertension, was assessed with two-dimensional M-mode echocardiography in age- and sex-matched essential hypertensive patients with (n = 28) or without (n = 44) glucose intolerance, and normotensive control subjects (n = 29). Left ventricular mass index in hypertensive patients with glucose intolerance was significantly higher than that in hypertensive patients without glucose intolerance (mean +/- SD, 115.6 +/- 28.2 v 102.1 +/- 22.1 g/m2; P < .05). Left ventricular diastolic function as reflected by peak lengthening rate was reduced in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.68 +/- 0.71 v 3.16 +/- 0.82/sec; P < .05). End-systolic wall stress/left ventricular end-systolic volume index, an index of left ventricular contractility, was reduced more in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.75 +/- 0.55 v 3.13 +/- 0.55 10(3) dyn.m2/cm2.mL-1; P < .01). These findings suggest that glucose intolerance accelerates progression of left ventricular hypertrophy and deteriorates left ventricular diastolic function and contractility in essential hypertension.

Blood Glucose↗

PubMed1993

Development of glucose intolerance in obese (fa/fa) Zucker rats.

Development of glucose intolerance in genetically obese (fa/fa) rats was investigated. Comparisons were made with lean (FA/?) control rats. Oral glucose tolerance tests were performed in 7-8 weeks, 9-10 weeks, 12-13 weeks and 16-17 weeks old rats. Irrespectively of age, the obese rats showed impaired glucose tolerance and insulin sensitivity compared with age-matched lean rats. While in FA/? rats only minor changes of glucose-stimulated insulin secretion and glucose tolerance were observed with progression of age, glucose intolerance in obese animals became more pronounced with aging. Obese rats older than 12-13 weeks showed no further progression of glucose intolerance. Glucose-stimulated insulin secretion increased with aging, but basal insulinemia was unaffected. Hence, we conclude that glucose intolerance and insulin resistance in genetically obese (fa/fa) rats is almost completely developed with approximately 12 weeks.

Animals↗

PubMed1995

Glucose intolerance in pulmonary tuberculosis.

The frequency of glucose intolerance was studied in 106 patients with pulmonary tuberculosis attending Nazimabad Chest Clinic. Diagnosis was based on X-ray and a positive sputum smear. An oral glucose tolerance test (OGTT) was performed and evaluated according to the WHO criteria. Glucose intolerance was detected in 52 (49%) patients, 31 Impaired Glucose Tolerance (IGT), 21 Diabetes Mellitus (DM). After adequate antitubercular therapy and sputum conversion, the OGTT was repeated in 23 cases. Of these 13 (56.5%) patients had a normal glucose tolerance indicating that glucose intolerance observed during active pulmonary tuberculosis improves or normalizes after adequate therapy.

Adolescent↗

PubMed2005

Discrepancies in the regulation of plasma adiponectin and TNF-alpha levels and adipose tissue gene expression in obese African Americans with glucose intolerance: a pilot study using rosiglitazone.

OBJECTIVES: We examined the effects of rosiglitazone: 1) on glucose homeostasis, insulin action, beta-cell function, and plasma adiponectin and TNF-alpha (TNF-alpha) levels; and 2) the expression of adipose tissue TNF-alpha and adiponectin mRNA in African Americans with parental history of type 2 diabetes and with varying degrees of glucose intolerance. SUBJECTS AND METHODS: The study groups comprised 11 African Americans with normal glucose tolerance and six with diabetes and impaired glucose tolerance. The glucose-intolerant subjects received rosiglitazone (4-8 mg/day) every morning for 12 weeks. They underwent oral glucose tolerance test (OGTT) and subcutaneous adipose tissue biopsy (under local anesthesia) before and after 12 weeks of rosiglitazone therapy. Beta cell function and insulin resistance were calculated by using homeostasis model assessment (HOMA). Adipose tissue gene expression (mRNA) was measured by real-time polymerase chain reaction in both groups. RESULTS: Rosiglitazone monotherapy improved both fasting and two-hour serum glucose levels during OGTT in the glucose-intolerant group. However, mean serum insulin and C-peptide levels did not change when compared with baseline. Rosiglitazone monotherapy improved insulin resistance but not overall beta-cell secretion. Mean adiponectin levels at fasting and two hours after oral glucose ingestion were significantly (50%) lower in the glucose-intolerant group than in the control group. Rosiglitazone monotherapy significantly increased plasma adiponectin levels at fasting and two hours after oral challenge by two-fold in the glucose-intolerant group. Mean plasma TNF-alpha levels were not significantly different at fasting and after two hours during OGTT. Rosiglitazone had no significant effect on plasma TNF-alpha levels during OGTT. No significant differences were seen in the expression of adipose tissue TNF-alpha and adiponectin mRNA in the groups at baseline. Rosiglitazone did not significantly change the adipose tissue adiponectin and TNF-alpha mRNA. Rosiglitazone was well tolerated, without experiencing weight gain, edema, and liver function test abnormality in the glucose intolerant subjects. SUMMARY: Rosiglitazone improved glucose homeostasis and insulin resistance in high-risk African Americans. We found that adiponectin was lower in the glucose-intolerant group, while TNF-alpha was similar. While rosiglitazone increased plasma adiponectin, it had no effect on adipose tissue adiponectin mRNA. In addition, rosiglitazone had no effect on plasma TNF-alpha and adipose tissue TNF-alpha mRNA. We conclude that the metabolic effects of rosiglitazone could be mediated by adiponectin but not TNF-alpha in African Americans with glucose intolerance. Our study demonstrates that: 1) the role of adipocytokines in the etiology of type 2 diabetes in African Americans is complex; and 2) that adiponectin, but not TNF-alpha, could mediate the metabolic benefits of thiazolidinediones in African Americans with glucose intolerance.

Adiponectin↗

PubMed1983

Secondary hyperparathyroidism and glucose intolerance in children with uremia.

Glucose metabolism was studied using the glucose clamp technique in 8 children with CRF (4 pubertal and 4 prepubertal) before and after correction of secondary hyperparathyroidism (HPD) by a regime of phosphate binders and dietary phosphate restriction. Glucose metabolic rate (M) increased by 34%, insulin response (I) increased by 32%, and insulin sensitivity (M/I) did not change. Compared to corresponding normal values, these patients were glucose-intolerant (low M) before treatment and became glucose-tolerant after treatment (normal M). They were insulin-resistant (low M/I) before treatment and remained so after treatment. The 5 uremic children without secondary HPD were treated with the same regime to prevent the secondary HPD. Their M, I, and M/I did not change after treatment. The change in I correlated closely with the change in M in all 13 patients. One pubertal patient with uremia was studied on three occasions. Initially, without secondary HPD, he had a normal M and a low M/I. When he developed secondary HPD, M decreased by 39%, I decreased by 37%, and M/I did not change. Treatment of his secondary HPD restored M and I values back to initial levels, and M/I again did not change. Treatment of secondary HPD by correction of phosphate retention led to an improvement of glucose intolerance with an increase in insulin secretion.

Adolescent↗

PubMed1983

Glucose intolerance in an employed population.

Differences in glucose intolerance within various occupational groups, i.e. laborers, clerks, and managers, and the related environmental factors were studied in ca. 9000 male workers of a certain factory. Age-and weight-adjusted prevalence rates of glucose intolerance were 3.2% in the laborers, 5.8% in the clerks, and 9.3% in the managers. In the managers, the total intake of calories was excessive for the amount of exercise expended; food intake was relatively low in complex carbohydrates and high in animal fats. The clerks were characterized by a high sugar intake. The low prevalence of glucose intolerance in the laborers was ascribed to the greater amount of exercise. Assigned work hours, however, probably affected the prevalence of diabetes in the laborers, which was 2.1% in subjects who worked all three shifts, but 0.9% in subjects working only day shifts. Thirty laborers from all 3 shifts consented to give urine specimens during their working time (8 hr), after the same amount of food and exercise in all of them. Urinary excretion of HGH and VMA during the midnight shift was significantly higher (p less than 0.05) than that during the day shift although urinary 170HCS was significantly low (p less than 0.01) at midnight. There were no significant changes in urinary CPR excretion between day and night shifts. These data indicate the importance of environmental factors, such as exercise, nutrition and stress, in glucose intolerance.

Adult↗

PubMed2004

Hypoxia causes glucose intolerance in humans.

Hypoxic respiratory diseases are frequently accompanied by glucose intolerance. We examined whether hypoxia is a cause of glucose intolerance in healthy subjects. In a double-blind within-subject crossover design, hypoxic versus normoxic conditions were induced in 14 healthy men for 30 minutes by decreasing oxygen saturation to 75% (versus 96% in control subjects) under the conditions of a euglycemic clamp. The rate of dextrose infusion needed to maintain stable blood glucose levels was monitored. Neurohormonal stress response was evaluated by measuring catecholamine and cortisol concentrations as well as cardiovascular parameters, and symptoms of anxiety. To differentiate between the effects of stress hormonal response, and hypoxia itself, on glucose intolerance, we performed hypoglycemic clamps as a nonspecific control. We found a significant decrease in dextrose infusion rate over a period of 150 minutes after the start of hypoxia (p < 0.01). Hypoxia also increased plasma epinephrine concentration (p < 0.01), heart rate (p < 0.01), and symptoms of anxiety (p < 0.05), whereas the other parameters remained unaffected. Glucose intolerance was closely comparable between hypoxic and hypoglycemic conditions (p < 0.9) despite clear differences in stress hormonal responses. Hypoxia acutely causes glucose intolerance. One of the factors mediating this effect could be an elevated release of epinephrine.

Adult↗

PubMed1985

Peripheral and autonomic nerve function in glucose intolerance.

In 19 middle aged subjects, glucose intolerant according to WHO criteria, obtained from a health survey, peripheral and autonomic nerve function were studied in comparison with 25 control subjects with normal glucose tolerance. Clinically detectable signs of peripheral nerve dysfunction were not more common in glucose intolerant subjects than in the control group. In measurements of sensory thresholds for vibration, nerve conduction velocities and autonomic nerve function, small differences, mainly non-significant, were found in favour of the controls. It is concluded that minor reduction of some peripheral nerve function may be associated with glucose intolerance, but it is not readily demonstrated. Clinically apparent polyneuropathy is not likely to develop.

Autonomic Nervous System↗

PubMed2003

Glucose intolerance in Chinese patients with chronic hepatitis C.

AIM: To investigate the prevalence and the risk factors of glucose intolerance in Chinese patients with chronic hepatitis C and to evaluate the relationship between interferon (IFN) treatment and glucose intolerance in these patients. METHODS: Prospective cross-sectional study was done to evaluate the prevalence of glucose intolerance in Chinese patients with chronic hepatitis C virus (HCV) infection from the outpatient clinic of Department of Family Medicine, Taipei Veterans General Hospital. Chronic hepatitis C was defined as persistent presence of anti-HCV and persistent elevation of liver transaminase for at least 1.5 folds for at least 6 months. Moreover, patients were further categorized into normal fasting glucose and glucose intolerance (diabetes mellitus (DM) and impaired fasting glucose) according to the diagnostic criteria of American Diabetic Association. RESULTS: Totally, 359 Chinese patients with chronic hepatitis C were enrolled (212 males and 147 females, mean age=58.1+/-13.0 years). One hundred and twenty-three patients (34.3 %) had received various forms of IFN treatment. One hundred and twenty-five patients (34.6 %) had glucose intolerance, including 99 patients (27.6 %) with DM and 26 patients (7.0 %) with impaired fasting glucose. In comparison with those with normal fasting glucose levels, patients with chronic hepatitis C with glucose intolerance were significantly older, had a significantly higher body mass index, and they were more likely to suffer from obesity, to have family history of diabetes and to have had previous IFN treatment. Stepwise multivariate logistic regression revealed significantly that age >=57 years, obesity, previous history of IFN treatment and the presence of family history of diabetes were independent risk factors associated with the presence of glucose intolerance in chronic hepatitis C patients. CONCLUSION: In conclusion, 34.6 % of Chinese patients with chronic hepatitis C had glucose intolerance. Chronic hepatitis C patients who were older in age, obese, had previous IFN treatment history and had family history of diabetes were prone to develop glucose intolerance. To our knowledge, this is the first population-based report to confirm that interferon treatment to be an independent risk factor to develop glucose intolerance.

Aged↗