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PubMed2002

Glucose intolerance with atypical antipsychotics.

BACKGROUND: Previous studies have suggested that the atypical antipsychotics clozapine and olanzapine may be associated with an increased risk of glucose intolerance and diabetes mellitus. Early studies have also suggested an association between use of conventional antipsychotics and the development of glucose intolerance. OBJECTIVE: To examine quantitatively the association between glucose intolerance including diabetes mellitus and the use of the atypical antipsychotics clozapine, olanzapine or risperidone, and to identify possible risk factors for the development of glucose intolerance during treatment with these drugs. METHODS: All reports suggestive of glucose intolerance for clozapine, olanzapine and risperidone were identified in the WHO database for adverse drug reactions. In the analyses of possible risk factors for glucose intolerance all other reports of adverse drug reactions for clozapine, olanzapine and risperidone were used as reference. Using the Bayesian Confidence Propagation Neural Network method, the strengths of the associations over time between glucose intolerance and the use of these drugs were analysed. For comparison, the strengths of the associations between glucose intolerance and the use of the conventional antipsychotics haloperidol and chlorpromazine were also analysed. RESULTS: Clozapine, olanzapine and risperidone were significantly associated with glucose intolerance. In contrast, chlorpromazine and haloperidol were not associated with glucose intolerance. For clozapine, olanzapine and risperidone grouped together, the following potential risk factors for glucose intolerance were identified: an underlying diabetic condition (odds ratio [OR] 10.22, 95% CI 8.20-12.73), an increase in weight (OR 2.36, 95% CI 1.76-3.17), male gender (OR 1.27, 95% CI 1.11-1.47), and concomitant use of valproic acid (OR 1.97, 95% CI 1.61-2.40), selective serotonin reuptake inhibitors (OR 1.63, 95% CI 1.33-1.99) or buspirone (OR 2.24, 95% CI 1.33-3.77). CONCLUSION: Treatment with clozapine, olanzapine or risperidone appears to be associated with an increased risk of glucose intolerance.

Adverse Drug Reaction Reporting Systems↗

PubMed1997

Monosodium glutamate (MSG)-obese rats develop glucose intolerance and insulin resistance to peripheral glucose uptake.

Different levels of insulin sensitivity have been described in several animal models of obesity as well as in humans. Monosodium glutamate (MSG)-obese mice were considered not to be insulin resistant from data obtained in oral glucose tolerance tests. To reevaluate insulin resistance by the intravenous glucose tolerance test (IVGTT) and by the clamp technique, newborn male Wistar rats (N = 20) were injected 5 times, every other day, with 4 g/kg MSG (N = 10) or saline (control; N = 10) during the first 10 days of age. At 3 months, the IVGTT was performed by injecting glucose (0.75 g/kg) through the jugular vein into freely moving rats. During euglycemic clamping plasma insulin levels were increased by infusing 3 mU.kg-1.min-1 of regular insulin until a steady-state plateau was achieved. The basal blood glucose concentration did not differ between the two experimental groups. After the glucose load, increased values of glycemia (P < 0.001) in MSG-obese rats occurred at minute 4 and from minute 16 to minute 32. These results indicate impaired glucose tolerance. Basal plasma insulin levels were 39.9 +/- 4 microU/ml in control and 66.4 +/- 5.3 microU/ml in MSG-obese rats. The mean post-glucose area increase of insulin was 111% higher in MSG-obese than in control rats. When insulinemia was clamped at 102 or 133 microU/ml in control and MSG rats, respectively, the corresponding glucose infusion rate necessary to maintain euglycemia was 17.3 +/- 0.8 mg.kg-1.min-1 for control rats while 2.1 +/- 0.3 mg.kg-1.min-1 was sufficient for MSG-obese rats. The 2-h integrated area for total glucose metabolized, in mg.min.dl-1, was 13.7 +/- 2.3 vs 3.3 +/- 0.5 for control and MSG rats, respectively. These data demonstrate that MSG-obese rats develop insulin resistance to peripheral glucose uptake.

Animals↗

PubMed1996

[Mild glucose intolerance in the elderly].

Glucose tolerance has been shown to decline with age. Mechanisms of this phenomenon are not yet completely defined. The insulin response to glucose shows little change with age. The primary cause results from resistance to the ability of insulin to stimulate glucose uptake. Many factors, including composition of diet with regard to both caloric adequacy and carbohydrate content, decreased physical activity and decreased lean body mass, probably contribute to the insulin resistance. Mild glucose intolerance in the elderly, as in young adults, increases the risk for the development of overt diabetes mellitus and is a risk factor for the development of atherosclerotic diseases.

Aged↗

PubMed2006

Active and passive smoking and development of glucose intolerance among young adults in a prospective cohort: CARDIA study.

OBJECTIVE: To assess whether active and passive smokers are more likely than non-smokers to develop clinically relevant glucose intolerance or diabetes. DESIGN: Coronary artery risk development in young adults (CARDIA) is a prospective cohort study begun in 1985-6 with 15 years of follow-up. SETTING: Participants recruited from Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California, USA. PARTICIPANTS: Black and white men and women aged 18-30 years with no glucose intolerance at baseline, including 1386 current smokers, 621 previous smokers, 1452 never smokers with reported exposure to secondhand smoke (validated by serum cotinine concentrations 1-15 ng/ml), and 1113 never smokers with no exposure to secondhand smoke. MAIN OUTCOME MEASURE: Time to development of glucose intolerance (glucose > or = 100 mg/dl or taking antidiabetic drugs) during 15 years of follow-up. RESULTS: Median age at baseline was 25, 55% of participants were women, and 50% were African-American. During follow-up, 16.7% of participants developed glucose intolerance. A graded association existed between smoking exposure and the development of glucose intolerance. The 15 year incidence of glucose intolerance was highest among smokers (21.8%), followed by never smokers with passive smoke exposure (17.2%), and then previous smokers (14.4%); it was lowest for never smokers with no passive smoke exposure (11.5%). Current smokers (hazard ratio 1.65, 95% confidence interval 1.27 to 2.13) and never smokers with passive smoke exposure (1.35, 1.06 to 1.71) remained at higher risk than never smokers without passive smoke exposure after adjustment for multiple baseline sociodemographic, biological, and behavioural factors, but risk in previous smokers was similar to that in never smokers without passive smoke exposure. CONCLUSION: These findings support a role of both active and passive smoking in the development of glucose intolerance in young adulthood.

Adult↗

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↗

PubMed1998

[Prevalence of glucose intolerance in Japan--from the National Circulatory Disorders Basic Survey, 1990].

The prevalence of glucose intolerance was surveyed in 8,063 people over 30 years old from the general population of Japan. The data used in the analysis were from the Fourth National Circulatory Disorders Basic Survey, which was conducted in 1990. Survey items included history of diabetes mellitus, body mass index (BMI) and daily life activity. Blood and urine were also examined, and the blood glucose levels, presence or absence of sugar in urine, and levels of glycohemoglobin (HbA1c) were determined. Glucose intolerance was identified from the blood glucose level, HbA1c level and history of diabetes mellitus. The frequency of glucose intolerance was 8.6% in all subjects (11.9% in men and 6.3% in women). The frequency was higher in older people: 1.7 times higher in men over 65 years old and 2.5 times higher in women over 65 years old. Among people over 40 years old, glucose intolerance was significantly more prevalent in men than in women. It was also significantly more prevalent in men living in big cities than in men living in rural areas. Among obese male subjects and men with a low level of activity in daily life, the frequency of glucose intolerance was higher than in normal male subjects. The level of activity in daily life tended to be lower for people living in big cities than for those in rural areas. The results suggest that the prevalence of glucose intolerance depends on the environment in which people live. The results also indicate that raising the level of activities in daily life might help prevent diabetes mellitus.

Activities of Daily Living↗

PubMed1983

Further support for heterogeneity of insulin response and insulin sensitivity in non-obese subjects with glucose intolerance.

The relationship of insulin secretion and insulin sensitivity was studied in 67 age- and body weight-matched non-obese subjects, classified as having a normal glucose tolerance or glucose intolerance (50 g oral glucose load). Insulin response was studied by means of a 2 h glucose infusion. For the determination of insulin sensitivity a 1 h priming dose-constant insulin infusion technique was used. The per cent decrease of plasma glucose level at comparable steady-state insulin levels served as a measure of body sensitivity to exogenous insulin. In patients with glucose intolerance the early (delta IRI area 0-5 min) and late (delta IRI area 30-120 min) insulin responses to iv glucose were significantly reduced in comparison to controls. Controls and subjects with glucose intolerance showed considerable heterogeneity of insulin responses. Patients with glucose intolerance and relative insulin deficiency were not less responsive to insulin than subjects with normal glucose tolerance. There was, however, a wide variation of insulin sensitivity within the two groups. There was a weak significant inverse correlation between insulin response to glucose and insulin sensitivity for the two groups combined and for controls and subjects with glucose intolerance separately. The results demonstrate that the majority of non-obese patients with glucose intolerance and relative insulin deficiency does not exhibit a reduced responsiveness to insulin and therefore hypoinsulinaemia but not insulin resistance is the primary defect for an abnormal glucose tolerance in these group of subjects.

Adult↗

PubMed2004

Effect of macronutrient intake on the development of glucose intolerance during pregnancy.

BACKGROUND: Dietary intake influences glucose tolerance status, yet the relation between macronutrient intake and the development of glucose intolerance during pregnancy has not been adequately examined. OBJECTIVE: We examined the relation between macronutrient intake early in pregnancy and the development of glucose intolerance. DESIGN: Data are from 1698 women in the Pregnancy, Infection, and Nutrition Study. Dietary intake during the second trimester was assessed with a food-frequency questionnaire. Women were classified into 1 of 3 glucose categories: gestational diabetes mellitus (GDM), impaired glucose tolerance (IGT), and normal glucose tolerance. Multivariate logistic regression was used to calculate the relative risk of IGT and GDM, with adjustment for potential confounders. A series of models were specified to test alternate hypotheses about the relation of diet to risk of IGT or GDM. RESULTS: The overall prevalences of IGT and GDM in the cohort were 2.6% and 5.2%, respectively. The addition model showed that adding 100 kcal from carbohydrates to the diet was associated with a 12% decrease in risk of IGT and a 9% decrease in risk of GDM. The substitution model showed that substituting fat for carbohydrates (per each 1% of total calories) resulted in a significant increase in risk of both IGT and GDM [relative risk = 1.1 (95% CI: 1.02, 1.12) and 1.1 (1.02, 1.10), respectively]. Predicted probabilities of IGT and GDM were reduced by one-half with a 10% decrease in dietary fat and a 10% increase in carbohydrate. CONCLUSIONS: This study found an association between increased fat intake and the development of glucose abnormalities in pregnancy.

Adult↗

PubMed1993

Association between fish intake and coronary heart disease mortality. Differences in normoglycemic and glucose intolerant elderly subjects.

OBJECTIVE: To compare the association of habitual fish intake with 17-yr mortality of coronary heart disease between normoglycemic and glucose intolerant elderly subjects. RESEARCH DESIGN AND METHODS: In 1971, 272 men and women, 64-87 yr of age, were examined in a general practice in the town of Rotterdam, The Netherlands. Glucose intolerance (impaired glucose tolerance or diabetes mellitus) was observed in 83 subjects, and 189 subjects were found to be normoglycemic and free of clinically diagnosed diabetes mellitus. Information on usual dietary intake was obtained using the cross-check dietary history method. RESULTS: Fish consumption was found in 58.7% of the normoglycemic population and in 62.4% of the glucose intolerant population. Among normoglycemic subjects, the age- and sex-adjusted 17-yr mortality for coronary heart disease was 10.9/1000 person-yr for those who ate fish and 25.1/1000 person-yr for those who did not. For the glucose intolerant population, the rates were 20.6/1000 and 31.2/1000 person-yr, respectively. Adjusted for age, sex, body mass index, smoking, alcohol use, intake of energy, polyunsaturated fat, and carbohydrates, the risk ratio for normoglycemic population was 0.34 (95% confidence interval: 0.16-0.72). For glucose intolerant subjects, an adjusted risk ratio of 0.80 (95% confidence interval: 0.31-2.05) was observed. CONCLUSIONS: These results suggest that in a glucose intolerant population the possible protective effect of fish intake on coronary heart disease may be smaller than in normoglycemic subjects.

Age Factors↗

PubMed2003

Gestational diabetes mellitus in Korea: prevalence and prediction of glucose intolerance at early postpartum.

To determine the prevalence of glucose intolerance in Korean women with gestational diabetes mellitus (GDM) between 6 and 8 weeks postpartum and identify which antepartum variables were predictive of postpartum diabetes and impaired glucose tolerance (IGT), we prospectively performed 75 g oral glucose tolerance test (OGTT) between 6 and 8 weeks postpartum in women with GDM. WHO criteria were used for classification of glucose tolerance postpartum. Of 392 women with GDM were detected during the study period, 311 women participated in this study. Of the 311 participants, 119 (38.3%) women were found to have persistent glucose intolerance; 47 (15.1%) had diabetes and 72 (23.2%) had IGT. The prevalence of postpartum IGT and diabetes increased in parallel with the metabolic severity during pregnancy. Multiple logistic regression analysis revealed that pre-pregnancy weight, gestational age at diagnosis of GDM, 2-h glucose and 3-h insulin concentrations of diagnostic OGTT were independently associated with postpartum diabetes. Pre-pregnancy weight, 2-h glucose and 1-h insulin concentrations were independently associated with postpartum IGT. Our results support the importance of postpartum testing in Korean women with GDM, and demonstrated that impaired beta-cell function and pre-pregnancy obesity were associated with glucose intolerance at early postpartum.

Adult↗

PubMed1986

[Clinical investigation on the mechanism of glucose intolerance in Cushing's syndrome].

We investigated the mechanism of glucose intolerance in 51 patients with Cushing's syndrome. In an oral 100g glucose tolerance test, although prevalence of decreased glucose tolerance was very high as revealed in 36 of 47 patients (77%) studied, impairment was rather mild in the majority of patients and only 10 patients (21%) were judged as diabetic. Plasma insulin was measured in 12 patients and the mean values of these patients reached above normal levels after oral glucose load. When insulin secreting capacity was assessed by measuring the ratio of the incremental area of insulin above fasting level to the corresponding area of glucose during the test, Cushing's syndrome as a whole exhibited a normal ratio compared to 9 control subjects (113 +/- 115 vs. 144 +/- 78 microU/mg, M +/- SD, ns), but in 3 patients with severe impairment of glucose tolerance reaching the diabetic range, the ratio was lower than normal (27 +/- 20 vs. 144 +/- 78 microU/mg, M +/- SD, p less than 0.05). The hypoglycemic effect of iv insulin was studied in 23 patients and was demonstrated to have decreased. Thus, we confirmed the presence of decreased insulin sensitivity, i.e. insulin resistance in Cushing's syndrome. The age of patients showed positive correlation with the degree of impairment in glucose tolerance and insulin secreting capacity, but not with that of insulin sensitivity, that is, in patients with advanced age, glucose intolerance appeared to be severe with decreased insulin secreting capacity. 125I-insulin binding to red blood cells in 8 patients was examined to elucidate the mechanism of insulin resistance in Cushing's syndrome. Percent specific binding at tracer concentration of insulin in Cushing's syndrome was not different from the value obtained in 19 normal subjects (8.2 +/- 3.0 vs. 7.7 +/- 1.0%, M +/- SD, ns). Receptor concentration and affinity were also normal. From these observations, it is likely that glucose intolerance in Cushing's syndrome is primarily due to the effects of chronic glucocorticoid excess on tissue metabolism of glucose as characterized by the presence of insulin resistance, which is not due to a defect in insulin-receptor binding but rather caused by the alteration in post-receptor mechanism, and increased secretion of insulin can be considered as a compensatory mechanism. In some patients, however, a decrease in insulin secreting capacity, the cause of which is not clear but at least related to the patient's age, is found and seems to lead to severe glucose intolerance.

Adenoma↗

PubMed2002

Impaired saline-stimulated diuresis and natriuresis in the conscious hypertensive glucose-intolerant rat.

BACKGROUND: A major complication of type 2 diabetes is renal dysfunction, a condition that worsens with coexistence of systemic hypertension. However, less is known regarding the renal impact of the prediabetic condition characterized by glucose intolerance. Therefore, we tested the hypothesis that chronic glucose intolerance leads to abnormal renal function, a condition also exacerbated by concurrent systemic hypertension. METHODS: A rat model of concomitant NaCl-sensitive hypertension and glucose intolerance was used to study renal function. Glucose intolerance was produced by administering streptozotocin to neonatal Wistar-Kyoto rats, and systemic hypertension was induced by combining dietary NaCl excess with unilateral nephrectomy. Hemodynamic and renal excretory responses were determined in conscious animals before and after administration of a 30-min isotonic saline challenge (5% of body weight, intravenously). RESULTS: Nine-month-old glucose-intolerant rats fed a normal NaCl diet did not manifest impairment in saline-stimulated diuresis and natriuresis. By contrast, 3-month-old glucose-intolerant rats fed a high NaCl diet displayed an exaggerated diuretic and natriuretic response to a saline challenge. Although saline-stimulated diuresis and natriuresis were enhanced in the hypertensive rats, they were reduced in the hypertensive glucose-intolerant animals. The reduction in renal excretory function of the latter group was caused by alterations in both glomerular function and tubular reabsorption of fluid and sodium. CONCLUSIONS: The coexistence of systemic hypertension and glucose intolerance result in impaired renal excretory function. This defect could be important, as hypertension can develop before the onset of overt type 2 diabetes.

Animals↗

PubMed1980

Increased insulin resistance in obese, glucose-intolerant Southwestern American Indians: evidence for a defect not explained by obesity.

Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. To determine whether the insulin resistance of glucose-intolerant obese subjects can be accounted for by obesity alone, insulin-mediated glucose disposal was measured in 14 glucose-intolerant and 21 nondiabetic. Southwestern American Indians with similar degrees of obesity. A mixture of insulin, glucose, and somatostatin was infused which delivered the same quantity of glucose and achieved similar plasma insulin concentrations in all subjects. Despite similar steady state plasma insulin levels, the mean steady state plasma glucose concentration was higher in the glucose-intolerant subjects than in weight-matched subjects with normal glucose tolerance (226 +/- 10 vs. 136 +/- 13 mg/dl; P < 0.0001). This increased resistance to insulin action was found in the presence of similar insulin binding to mononuclear cells (measured in 8 glucose-intolerant subjects and 9 subjects with normal glucose tolerance). In obese Southwestern American Indians with glucose intolerance, abnormalities beyond the site of insulin binding to its receptor may explain the observed increase in in vivo insulin resistance.

Adult↗

PubMed2003

Influences of increased oxidative stress on endothelial function, platelets function, and fibrinolysis in hypertension associated with glucose intolerance.

The effect of oxidative stress on endothelial function, platelet function, and fibrinolysis in hypertension with or without glucose intolerance was examined. The endothelium, platelets and fibrinolysis play important roles in the progression of atherosclerosis and interact with each other. We have previously demonstrated that glucose intolerance impairs endothelial function in hypertension, but its precise mechanisms have not been clarified. Hypertensive patients were divided by the results of 75-g oral glucose tolerance test into a normal glucose metabolism group (n = 65) and a glucose intolerance group (n = 47). The plasma level of thiobarbituric acid-reactive substances (TBARS) was assessed as a marker of oxidative stress. Endothelial function was assessed by flow-mediated dilatation (FMD), platelet function by the concentration of ADP dose inducing half-maximal aggregation (EC50), and fibrinolytic parameters by radioimmunoassay. These functions were assessed before and after acute administration of vitamin C. FMD was reduced while TBARS and fibrinolytic parameters were higher in patients with glucose intolerance than in those with a normal glucose metabolism. Vitamin C increased FMD and reduced fibrinolytic parameters significantly in the glucose intolerance group, but not in the group with normal glucose metabolism. On the other hand, the EC50 was similar in both groups. In conclusion, glucose intolerance aggravates oxidative stress, thereby contributing to the impairment of endothelial function in patients with hypertension. These abnormalities affect fibrinolysis but not platelet function.

Adult↗

PubMed1994

Relationship of glucose intolerance to coronary risk in Afro-Caribbeans compared with Europeans.

Afro-Caribbeans have low mortality rates from coronary heart disease, despite a high prevalence of diabetes mellitus. We examined 1166 Afro-Caribbean and European men and women aged 40-64 years in a community survey in London, UK. Prevalence of glucose intolerance (combining impaired glucose tolerance, new and known diabetes) was 31% in Afro-Caribbeans and 14% in Europeans (p < 0.001). In men, the prevalence of probable coronary heart disease was 6% in Afro-Caribbeans and 13% in Europeans (p < 0.01). Triglyceride was lower in Afro-Caribbeans than Europeans; in men, HDL cholesterol was higher. Afro-Caribbean men were less centrally obese, while Afro-Caribbean women were more centrally obese than their European counterparts. Fasting and 2-h insulin levels were higher in Afro-Caribbeans than Europeans. Glucose intolerance was associated with high triglyceride, low HDL cholesterol and central obesity in European but not in Afro-Caribbean men. In Europeans, fasting triglyceride was 1.49 mmol/l in normoglycaemic and 1.89 mmol/l in glucose intolerant men (p < 0.05), in Afro-Caribbean men triglyceride was 1.08 and 1.22 mmol/l, respectively. Waist hip ratio was 0.94 in normoglycaemic, and 0.98 in glucose intolerant European men (p < 0.001). In Afro-Caribbean men, waist hip ratio was 0.93 in both groups. At each level of insulin, glucose or central obesity, triglyceride was lower in Afro-Caribbean men and women than in Europeans. We speculate that despite high insulin levels, Afro-Caribbeans have a favourable lipoprotein pattern which persists in the presence of glucose intolerance, and may be related to body fat distribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Outcome of diabetic pregnancy and glucose intolerance in pregnancy: an audit of fetal loss in Newcastle General Hospital 1977-1990.

The outcome of pregnancy complicated by established diabetes or gestational glucose intolerance (diabetes mellitus or impaired glucose tolerance) is compared with the outcome of non-diabetic pregnancy. Between 1977 and 1990, 169 pregnancies in women with established diabetes and 61 pregnancies in women with gestational glucose intolerance were referred to the Newcastle General Hospital. The perinatal mortality (PNM) in women with established diabetes was 8.2/1000 and the viable fetal loss (sum of PNM, neonatal and infant loss) was 41/1000. The PNM in women with gestational glucose intolerance was 49.2/1000 and the viable fetal loss was 82/1000. The PNM in the background population was 11.6/1000. The fetal malformation rate was 17.3% for established diabetes, 9.8% in gestational glucose intolerance and 2.2% in the background population. Fetal abnormality remains the major cause of viable fetal loss in both established diabetes and gestational glucose intolerance.

Adult↗

PubMed1986

Insulin response in obese and nonobese offspring of conjugal Indian diabetic parents with increasing glucose intolerance.

Pancreatic beta cell function in response to glucose was assessed in three different groups of offspring of conjugal diabetic parents (OCDP): those with normal glucose tolerance, those with impaired glucose tolerance (IGT), and those with diabetes. Serum immunoreactive insulin (IRI), C-peptide (CP), insulin/glucose (I/G) ratio, and IRI/CP ratios were estimated at fasting and 90 min after glucose load. Insulin secretion, measured as CP, was found to be low even in normal nonobese OCDP, but the change was not reflected in IRI value as the IRI/CP ratio was found to be elevated. The values decreased with increasing glucose intolerance. In obese OCDP, all the parameters were abnormal even among those with normal glucose tolerance, and further deterioration occurred with increasing glucose intolerance. The study shows that insulin secretory defects are detectable even in normal OCDP, and these changes deteriorate with increasing glucose intolerance. Differences are noted in the peripheral concentrations of IRI and CP between obese and nonobese OCDP before development of diabetes. After development of diabetes mellitus, these differences disappear, and the CP and IRI values in both groups are similar and low.

Adult↗

PubMed1981

[Glucose intolerance in injured patients (author's transl)].

Glucose intolerance occurring in injured patients is known to be a part of the general response to injury described by Cuthbbertson: early "ebb phase" with a decrease of energy production, then "flow phase" with hypermetabolism. Several processes can be responsible for the abnormalities observed: 1) Alterations in peripheral glucose uptake. 2) Absolute or relative insulin lack in connection with increased catecholamine release which is know to inhibit insulin secretion. 3) Decreased sensitivity and responsiveness to insulin in connection with increased levels of counter regulatory hormones (catecholamines, glucagon, growth hormone). 4) Non-suppressibility of hepatic gluconeogenesis by glucose. Glucose intolerance decreases glucose utilisation and leads to increased proteolysis always unfavorable for patients.

Glucose↗