SEARCH · PubMed Health

Results for “Glucose Intolerance”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1990

Effect of physical activity on age-related glucose intolerance.

Glucose tolerance tends to deteriorate with age, but a major portion of this deterioration can be explained by changes in other age-related variables--obesity, physical inactivity, use of medications, and chronic illness. This review has focused on the role that physical activity can play in preventing the age-associated decline in glucose tolerance. Pathophysiologically, most of the decline in glucose tolerance appears to be caused by a decrease in insulin action with aging. Given that it has been shown that exercise increases insulin action, there is a plausible biologic mechanism explaining the observed association between physical activity and the preservation of insulin sensitivity and glucose tolerance with aging. Finally, it appears from the published data that it is life-long maintenance of physical activity, beginning long before individuals reach the geriatric age group, that will be most beneficial to the health of aging Americans.

Aging↗

PubMed1976

Relationships between maternal glucose intolerance and neonatal blood glucose.

Blood glucose changes in 63 infants during the first three hours of life were related to indices of glucose tolerance of their mothers. Of the mothers, 34 had insulin-dependent diabetes, 16 had gestational diabetes, and 11 had minor abnormalities of glucose tolerance. The fasting blood glucose level of the mother and the umbilical cord blood glucose level were both proportional to the rate of glucose decline in the infant after birth which, in turn, was inversely related to the lowest glucose level attained within three hours. Hypoglycemia occurred in 77% of the infants of diabetic mothers, 25% of the infants of mothers with gestational diabetes, and one of 12 (8%) of infants of mothers with minor degrees of glucose intolerance. The blood glucose level at two hours during an oral glucose tolerance test in the mother can be used to predict the probability of her infant having neonatal hypoglycemia.

Blood Glucose↗

PubMed1989

Should all pregnant women be screened for gestational glucose intolerance?

Although gestational glucose intolerance is associated with the remote development of diabetes mellitus, the risk to the mother during the index pregnancy and the risk to her fetus remain uncertain. Nevertheless, universal screening for gestational glucose intolerance has many strong advocates. The scientific data supporting a universal screening programme--showing that treatment of gestational glucose intolerance does more good than harm--are limited. Until the evidence can be extended beyond that on infant birthweight, a more restrained approach than universal screening may be appropriate.

Birth Weight↗

PubMed1992

[Research of factors for glucose intolerance in mucoviscidosis].

Glucose tolerance has been assessed in cystic fibrosis (CF) children using HbA1C and plasma glucose and insulin determinations during an oral glucose tolerance test (OGTT), along with the determination of HLA-DR and islet-cell (ICA) and anti-insulin (IAA) antibodies. Of 49 patients (25 males, 24 females), aged 2 to 21 years (mean = 10.9 years), 29 had normal glucose tolerance (WHO criteria) during OGTT, 14 had impaired glucose tolerance (IGT) and 6 had an isolated hyperglycemia at 120 min. Fasting plasma glucose and HbA1C were significantly higher in IGT than in normoglycemic patients. However, these two parameters showed poor individual predictive value of disturbance in glucose tolerance. Of 14 patients with abnormal OGTT, 7 were aged below 10 years, with 2 as young as 5 years; 8 patients were females. HLA antigens characteristic of type I diabetes tended to be found less frequently in CF patients than in the general population: 9% were DR3, 7% were DR4 and none was DR3/DR4. There were no HLA differences according to glucose tolerance. ICA and IAA were respectively detected in only one patient. Stimulated plasma insulin was low but did not correlate with glucose tolerance. In conclusion, impaired glucose tolerance is common in cystic fibrosis and can be found early in life. Although insulin secretion is decreased in this population, it does not seem to be the only factor responsible for impaired glucose intolerance. The absence of the genetical and immunological characteristics of type I diabetes confirms that glucose intolerance in cystic fibrosis is due to other pathogenetic mechanisms.

Adolescent↗

PubMed1992

Insulin resistance and endogenous digoxin-like factor in obese hypertensive patients with glucose intolerance.

Hypertensive obese subjects with glucose intolerance have hyperinsulinaemia, insulin resistance and intracellular cation imbalance resulting in increased sodium content. The aim of our study was to assess in these patients plasma levels of endogenous digoxin-like factor (EDLF), an inhibitor of the sodium-pump mechanism. We studied 14 hypertensive and 12 normotensive subjects with obesity and glucose intolerance for fasting blood glucose, and plasma insulin, C-peptide and EDLF levels: the two groups were matched for age and BMI and were studied after a 2-week wash-out period from hypotensive drugs. Compared with normotensives, hypertensive subjects had higher plasma insulin levels, a greater immunoreactive insulin/C-peptide ratio, a lower glucose/insulin ratio and higher plasma EDLF levels. Our results confirm that among obese people with glucose intolerance, hypertensives are more hyperinsulinaemic and insulin-resistant than normotensives and indicate that the intracellular cation imbalance in these patients may be attributable, at least in part, to EDLF.

Blood Glucose↗

PubMed1979

The sepsis-glucose intolerance riddle: a hormonal explanation.

Glucose intolerance has been commonly observed in sepsis and has been attributed to a multitude of endocrine and metabolic disorders. From 1977 to 1978, 19 patients were studied using intravenous glucose tolerance tests to evaluate this phenomenon; 15 patients presented with ongoing sepsis and four patients served as stress controls. Glucose intolerance was found to be a significant finding in less than 40% of the septic group. This state of intolerance was noted to be associated with a high mortality rate (60%), whereas glucose tolerance in sepsis was associated with a much improved mortality rate (10%). Hormone levels were correlated with glucose tolerance curves using the parameters of insulin, glucagon, growth hormone, cortisol, and epinephrine levels. Glucose intolerance and a high mortality rate were linked to sustained hyperglucagonemia, which was unresponsive to glucose challenge, and to marked suppression of growth hormone. This apparently represents a decompensated peripheral metabolic energy deficit, which results in the increased mortality rate.

Bacterial Infections↗

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↗

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↗

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↗

PubMedDate not supplied

Use of antihypertensive agents in patients with glucose intolerance.

The selection, use, and potential adverse effects of antihypertensive agents in patients with glucose intolerance are reviewed. Thiazide diuretics frequently impair glucose tolerance, but this deterioration is usually modest and should not preclude use of these agents in most patients with glucose intolerance. The loop diuretics furosemide and ethacrynic acid have also been associated with decreased glucose tolerance. The beta-adrenergic blocking agents may inhibit insulin secretion, but few patients will experience clinically important elevations in blood glucose. Rather than producing glucose intolerance, these agents may delay recovery from hypoglycemic episodes and may mask catecholamine-induced symptoms of hypoglycemia. In certain cases, use of cardioselective beta blockers or avoidance of beta-blocker therapy may be indicated, especially in insulin-dependent diabetics. The calcium-channel blocking agents nifedipine and verapamil have been reported to produce diabetogenic effects in a few studies, but further investigations are needed to define the extent of these effects. Available evidence indicates that sympatholytic agents such as guanethidine and reserpine, alpha 2-adrenergic agonists such as methyldopa and clonidine, the alpha 1-blocking agent prazosin, and the vasodilators captopril and hydralazine produce few, if any, clinically important changes in glucose tolerance. While no antihypertensive agents are absolutely contraindicated in patients with glucose intolerance, patients with glucose intolerance who are receiving thiazide diuretics, beta blockers, and calcium-channel blocking agents should be monitored with extra care for hyperglycemia or deterioration in glucose tolerance.

Adrenergic alpha-Agonists↗

PubMed1990

The impact of universal screening for gestational glucose intolerance on outcome of pregnancy.

Universal screening for gestational glucose intolerance has strong support, despite the lack of scientific evidence documenting its benefit. In the early 1980s, practicing obstetricians were split concerning the clinical importance of gestational glucose intolerance, so that some practitioners tested virtually all the patients they treated while others tested none. This historical reality provided concurrent screened and unscreened populations in whom to assess the impact of screening. We studied all 1,307 singleton pregnancies cared for and delivered at the New York Hospital-Cornell University Medical Center during a five month period. Large infants (birth weight greater than or equal to 4,000 grams) were born to 10.5 per cent of the women who were not screened (533) and to 11.2 per cent of the women who were screened (774). The process of screening not only failed to decrease the rate of large infants, but also failed to improve otherwise pregnancy outcomes and was associated with more intensive surveillance during pregnancy and a significantly higher rate of primary cesarean delivery. Given the unexpected concomitants of the screening process, we conclude that recommendations for universal screening for gestational glucose intolerance should be reconsidered.

Adult↗

PubMed1992

Relationship of glucose intolerance and hyperinsulinaemia to body fat pattern in south Asians and Europeans.

Type 2 (non-insulin-dependent) diabetes mellitus and insulin resistance are associated with centrally-distributed obesity. These disturbances are especially prevalent in people of South Asian (Indian, Pakistani and Bangladeshi) descent. We examined the relationship of glucose intolerance to body fat pattern in a population survey of 2936 men and 537 women of South Asian and European origin living in London, UK. In both groups glucose intolerance (defined as diabetes or impaired glucose tolerance) was more strongly associated with waist-hip girth ratio than with skinfolds or body mass index. The associations between body mass index and glucose intolerance were fully accounted for by waist-hip ratio. In European men with normal glucose tolerance fasting insulin levels were more strongly correlated with body mass index than with waist-hip ratio. Physical activity scores were lower in South Asians than in Europeans but no statistically significant associations between glucose intolerance and low physical activity were detectable. Leisure-time physical activity scores were inversely correlated with 2 h insulin levels in both groups. In contrast with other studies these results suggest that a specific effect of intra-abdominal fat deposition underlies the association between glucose intolerance and obesity. The association between hyperinsulinaemia and obesity is less specific for centrally-distributed fat. When measured appropriately waist-hip ratio is the most valid anthropometric index for identifying individuals whose obesity predisposes them to glucose intolerance.

Adipose Tissue↗

PubMed1976

Fetal lung lecithin metabolism in the glucose-intolerant Rhesus monkey pregnancy.

Fetal lung lecithin metabolism was examined in rhesus monkey gestations complicated by glucose intolerance secondary to maternal streptozotocin (STZ) administration. Fetuses of STZ-treated mothers were delivered at 85% to 89% of term and were compared to two control groups of fetuses from normal pregnancies--one group age-matched to the STZ pregnancies, and the other composed of fetuses delivered in the final 10% of gestation. In the glucose-intolerant pregnancies, two measures of fetal lung lecithin biosynthesis--the amniotic fluid lecithin-to-sphingomyelin (L/S) ratio and the rate of 14C-choline incorporation into lecithin in fetal lung slices--were significantly greater than in age-matched normal gestations and were similar to results in late-gestation controls. However, lung lecithin concentrations in the glucose-intolerant group were comparable to the age-matched controls, and both were significantly less than in the late-gestation controls. Since the gestational age, mode of delivery, and fetal acid-base status were the same in the age-matched groups, we conclude that these changes in fetal lung lecithin metabolism are due to the effects of maternal glucose intolerance.

Amniotic Fluid↗

PubMed1992

Pathogenic factors responsible for glucose intolerance in patients with NIDDM.

To define the pathogenic factors responsible for glucose intolerance in NIDDM, we estimated insulin secretory capacity, SI, and SG in 11 healthy, nondiabetic subjects and 9 NIDDM patients who had no SI impairment. All subjects studied were nonobese and normotensive. Each underwent a 75-g OGTT and a modified FSIGT: glucose was administered (300 mg/kg body weight), and insulin was infused (20 mU/kg over 5 min) from 20 to 25 min after the administration of glucose. SI and SG were estimated by Bergman's minimal-model method. The insulin response to oral glucose was significantly lower in NIDDM patients than in normal control subjects. First-phase insulin secretion expressed as the integrated area of plasma insulin above the basal level during the first 20 min was much smaller in NIDDM subjects (214 +/- 112 pM.min) than in control subjects (4643 +/- 885 pM.min, P < 0.01). SI was not statistically different in normal control subjects (1.27 +/- 0.18 x 10(-4) min-1.pM-1) versus diabetic patients (1.62 +/- 0.33 x 10(-4) min-1.pM-1). However, SG was significantly lower in diabetic subjects (1.11 +/- 0.17 x 10(-2) min-1) than in control subjects (2.35 +/- 0.26 x 10(-2) min-1, P < 0.01). These results suggest that impaired insulin secretion and decreased SG are the factors responsible for glucose intolerance of Japanese NIDDM patients with normal insulin sensitivity. Because SI and SG are the factors responsible for glucose intolerance of NIDDM patients with insulin resistance, it is conceivable that decreased SG is common in NIDDM patients regardless of their SI index.

Adult↗

PubMed1991

A controlled trial of insulin infusion and parenteral nutrition in extremely low birth weight infants with glucose intolerance.

To determine whether a continuous insulin infusion improves glucose tolerance in extremely low birth weight infants, we conducted a prospective, randomized trial in 24 neonates 4 to 14 days old (mean birth weight 772.9 +/- 128 gm; mean gestational age 26.3 +/- 1.6 weeks). Infants who had glucose intolerance were randomly assigned to receive either intravenous glucose and total parenteral nutrition with insulin through a microliter-sensitive pump or standard intravenous therapy alone. One infant assigned to receive insulin never required it. The groups were similar in birth weight, gestational age, race, gender, medical condition, and energy intake before the study. The mean duration of therapy was 14.6 days (range 7 to 21 days). During the study, the 11 insulin-treated infants tolerated higher glucose infusion rates (20.1 +/- 2.5 vs 13.2 +/- 3.2 mg/kg/min (1.1 +/- 0.1 vs 0.7 +/- 0.2 mmol/L); p less than 0.01), had greater nonprotein energy intake (124.7 +/- 18 vs 86.0 +/- 6 kcal/kg/day; p less than 0.01), and had better weight gain (20.1 +/- 12.1 vs 7.8 +/- 5.1 gm/kg/day; p less than 0.01) than the 12 control infants. The incidence of hypoglycemia, electrolyte imbalance, chronic lung disease, and death did not differ between groups. We conclude that a controlled insulin infusion improves and sustains glucose tolerance, facilitates provision of calories, and enhances weight gain in glucose-intolerant premature infants.

Blood Glucose↗

PubMed1991

Carbohydrate intake and body mass index in relation to the risk of glucose intolerance in an elderly population.

The association between the intake of carbohydrates, body mass index (BMI), and the 4-y incidence of impaired glucose tolerance and diabetes mellitus (glucose intolerance) was investigated in elderly men and women aged 64-87 y. In 1971 the baseline population consisted of 175 normoglycemic subjects. During the follow-up period (1972-1975) an oral glucose-tolerance test (OGTT) was carried out annually. In univariate analyses, baseline BMI and the habitual intake of carbohydrates and pastries, as determined from a cross-check dietary history, were positively associated with the incidence of glucose intolerance. The habitual intake of legumes was inversely related to the incidence of glucose intolerance. These results could not be explained by potential confounding factors such as age, gender, alcohol use, energy intake, prescribed diet, medication use, and comorbidity. These results suggest that energy balance and the use of carbohydrate-rich foods are related to the development of glucose intolerance in an elderly population.

Aged↗

PubMed1992

Effect of prolonged in vivo glucose infusion on insulin secretion in rats with previous glucose intolerance.

This work was designed to investigate the effect of an additional hyperglycemia on the subsequent in vivo insulin secretion in rats with various degrees of glucose intolerance. Four groups of rats received a unique injection of a low concentration of streptozotocin (STZ): 20, 27, 30, or 35 mg/kg corresponding, respectively, to STZ 20, STZ 27, STZ 30, or STZ 35 rats. Control rats were injected with citrate buffer. In all STZ groups, impaired glucose tolerance and insulin secretion were observed. These defects were roughly proportional to STZ concentration. Three weeks after STZ administration, hyperglycemia (17 mM) was produced by a 48-h glucose infusion via an indwelling catheter. Insulin secretion in response to glucose was investigated 3 h after stopping glucose infusion, by performing iv glucose tolerance tests. Insulin secretion in response to glucose doubled in control rats previously submitted to glucose infusion, and still more in rats with mild glucose intolerance (three and four times higher in STZ 20 and STZ 27 rats, respectively). By contrast, glucose infusion increased insulin secretion only slightly in STZ 30 rats and it was unchanged in STZ 35 rats. These data show that prolonged hyperglycemia has an improving effect on insulin secretion in rats with mild glucose intolerance, whereas the potentiating effect of previous hyperglycemia is lost in rats with more severe glucose intolerance.

Animals↗

PubMed1978

Age-related glucose intolerance in hyperthyroid patients.

In an attempt to study age-related metabolic abnormalities, glucose intolerance and serum insulin were examined in normal subjects and hyperthyroid patients. For comparison, serum concentrations of thyroxine (T4), triiodothyronine (T3), and total cholesterol were also measured in normal subjects and hyperthyroid patients. Although serum T4 concentration remained unchanged, serum T3 concentration decreased significantly in an elderly group of normal subjects. Similarly, serum T4 did not change with age and serum T3 decreased slightly but progressively with age in hyperthyroid patients. In addition, serum total cholesterol concentration increased progressively with age in normal subjects. Oral glucose tolerance decreased with age in normal subjects despite the same timing, peak level attained, and total magnitude of insulin response for old and young subjects. Although the severity of hyperthyroidism decreases with age, age-related glucose intolerance was much more apparent in hyperthyroid patients because of the age-related decrease of basal concentration, the peak level attained, and the total magnitude of insulin response. It is suggested that age-related glucose intolerance is magnified by the hyperthyroid state.

Adolescent↗