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PubMed2002

Epidemiology of glucose intolerance and associated factors in Uzbekistan: a survey in Sirdaria province.

Prevalence of glucose intolerance and other noncommunicable diseases has been examined in subjects aged 35 years and over in a rural community in Sirdaria, which lies in the central part of Uzbekistan. Diabetes and impaired glucose tolerance (IGT) were diagnosed according to the recommendations of the latest WHO Study Group on diabetes. The overall response to the survey was 82%. Crude prevalence of diabetes was 4% in women and 11% in men. However, young men were under-represented and the age-standardised prevalence was 7.5% in women and 10.0% in men. Subjects with abnormal glucose tolerance had higher mean body mass index (BMI), waist-hip ratio (WHR), systolic and diastolic blood pressures and prevalence of hypertension, and were less physically active than those with normal glucose tolerance. Women were younger, had higher mean BMI, similar WHR, lower mean systolic and diastolic blood pressures and were less physically active than men. Approximately one-third of all subjects were centrally obese (WHR 0.85 or above for women and 0.95 or above for men). Of these, one-third had coexisting glucose intolerance. It is concluded that glucose intolerance and central obesity are common in this rural Central Asian community.

Adult↗

PubMed1983

Decreased hepatic insulin extraction in subjects with mild glucose intolerance.

The fact that hyperinsulinemia occurs in simple obesity and mild glucose intolerance has been well established. Altered hepatic insulin extraction may influence the levels of circulating hormone. The simultaneous measurement of insulin and C-peptide concentrations in peripheral blood enables an in vivo estimation of hepatic insulin removal. To evaluate hepatic insulin extraction, insulin and C-peptide responses to oral glucose were studied in 176 obese and nonobese subjects with normal, impaired, or diabetic glucose tolerance. Insulin levels as well as insulin incremental areas in glucose intolerant subjects were significantly higher than in weight-matched controls. The levels of C-peptide as well as C-peptide incremental areas were only slightly enhanced in subjects with impaired glucose tolerance, whereas they were reduced in subjects with diabetic tolerance. The molar ratios of C-peptide to insulin, both in the fasting state and after ingestion of glucose, as well as the relationship between the incremental areas of the two peptides were used as measures of hepatic insulin extraction. They were significantly reduced in glucose intolerant subjects and, to a lesser extent, in nondiabetic obese subjects. These results indicate that peripheral hyperinsulinemia in subjects with simple obesity or impaired glucose tolerance is a result of both pancreatic hypersecretion and diminished hepatic insulin extraction. In subjects with a more severe degree of glucose intolerance, decreased hepatic insulin removal is the primary cause of hyperinsulinemia.

Adolescent↗

PubMed1997

Glucose intolerance in spontaneously hypertensive and Wistar-Kyoto rats: enhanced gene expression and synthesis of skeletal muscle glucose transporter 4.

To clarify the relationship between blood pressure and insulin resistance, we studied the role of glucose transporter 4 (GLUT4) in skeletal muscle and the effect of angiotensin-converting enzyme inhibitor on insulin resistance. Blood pressure and plasma glucose and plasma insulin responses to glucose loading (2 g/kg, i.p.) were measured in spontaneously hypertensive rats (SHRs), Wistar-Kyoto rats (WKYs), and Wistar rats at 8, 12, and 20 wk of age. GLUT4 gene expression and plasma membrane protein content were also determined in the gastrocnemius muscle. SHRs and WKYs at the age of 8 wk had significantly higher plasma glucose levels than did age-matched control Wistar rats. Insulin response also tended to be higher. Glucose intolerance was also present in 12-wk-old SHRs, but normalized at the age of 20 wk. In contrast, WKYs were glucose intolerant at 12 and 20 wk. Gene expression and plasma membrane content of GLUT4 were augmented in both 8-wk-old SHRs and WKYs, indicating a compensatory increase in these variables. Effects of captopril (20-30 mg/kg/d from 8 to 20 wk) on GLUT4 were also investigated in these three strains. Captopril improved steady state plasma glucose levels in association with 1.2- to 2.5-fold higher GLUT4 gene expression and a 1.4-fold increase in skeletal muscle GLUT4 protein in SHRs and WKYs. Our results suggest that (1) not only SHRs but also WKYs may have glucose intolerance and hence insulin resistance; (2) gene expression and protein synthesis of skeletal muscle GLUT4 are probably increased compensatorily, indicating that abnormalities in GLUT4 do not have a pivotal role in the development of insulin resistance in SHRs and WKYs; and (3) captopril stimulates skeletal muscle gene expression and synthesis of GLUT4, providing further evidence of its beneficial effect on glucose metabolism.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

Glucose intolerance, physical signs of peripheral artery disease, and risk of cardiovascular events: the Framingham Study.

BACKGROUND: Diabetes and peripheral artery disease (PAD) are acknowledged hallmarks of development of atherosclerotic cardiovascular disease (CVD). The prognostic implications of physical indicators of PAD, compared with and in conjunction with glucose intolerance based on population based data, are not well documented. METHODS AND RESULTS: The influence of carotid and femoral bruits and nonpalpable pedal pulses, with and without glucose intolerance, on development of coronary disease (CHD), congestive heart failure (CHF), and stroke (CVA) was investigated in a cohort of 1672 men and 2264 women ages 47 to 99 years participating in the Framingham Study. Cross-sectional pooling yielded 29,063 2-year person-examination units based on the sample of whom 440 men and 484 women had glucose intolerance develop. Over the 26 years of follow-up, 210 men and 199 women had 1 or more of the specified CVD events. Logistic regression analysis was used to estimate age-adjusted odds ratios comparing incidence of CVD events in subjects with glucose intolerance, signs of PAD, or both conditions with those with neither condition. Glucose intolerance was associated with a 2-fold excess occurrence of physical signs of PAD (P< .01 ). Femoral and carotid bruits were generally associated with greater increased risk of CHD, CHF, and CVA than was glucose intolerance alone. Particularly in women, the concomitant presence of bruits augmented the CVD risk of glucose intolerance. Nonpalpable pedal pulses were a stronger risk factor for CVD end points than glucose intolerance; particularly in men and in both sexes, those with both conditions were at substantially greater risk of CVD events than those with either alone. CONCLUSIONS: Physical findings of PAD appear to signify a compromised arterial circulation to the heart and brain as well as the limbs in persons with glucose intolerance. Persons with the combination are candidates at high risk for CHD, CHF, and CVA.

Aged↗

PubMed1985

Neonatal morbidities in infants of mothers with glucose intolerance in pregnancy.

Of 1839 pregnant women screened prospectively, 52 were identified to have glucose intolerance. Ten additional pregnant women identified as having glucose intolerance before the universal screening were also included in the study cohort. These 62 patients were followed in a perinatal high-risk clinic with weekly plasma glucose determinations. The patients were treated with diet and, in addition, 21 of 62 were treated with insulin therapeutically. By observational cohort design, the infants and a comparable number of matched controls were evaluated for evidence of neonatal morbidities and classified into percentile for birth weight. Compared with the control group, the operative mode of delivery, the mean birth weight, the birth-weight percentile, the male/female ratio, the frequency of low Apgar score (less than or equal to 6 at 1 min), and the number of infants with congenital anomalies were significantly higher in the infants born to the glucose-intolerant mothers. Although the mean maternal blood sugar was maintained within a reasonably euglycemic range, the usual neonatal morbidities were not eliminated entirely. Further understanding and management of glucose intolerance in pregnancy is necessary to further diminish or eliminate neonatal morbidities.

Apgar Score↗

PubMed1996

Glucose intolerance in thalassemia major is related to insulin resistance and hepatic dysfunction.

Glucose intolerance is a common consequence of transfusion therapy in patients with thalassemia major (TM), but the relative contribution of pancreatic damage and insulin resistance to glucose intolerance is unclear. We have investigated oral (OGTT) and intravenous (IVGTT) glucose tolerance, insulin sensitivity, and fasting concentrations of insulin, proinsulin, and des 31,32 proinsulin in 12 patients with TM (seven hepatitis C virus [HCV] antibody-negative and five-positive), eight patients with hepatic cirrhosis, and nine healthy controls. Two-hour plasma glucose concentrations were marginally higher in anti-HCV-negative (median, 7.4 mmol/ L; range, 4.0 to 8.2) and significantly so in anti-HCV-positive thalassemics (median, 8.5 mmol/L; range, 6.4 to to 23.0) and cirrhotics (median, 8.0 mmol/L; range, 4.7 to 17.6) than in controls (median, 5.5 mmol/L; range, 3.0 to 6.3). Insulin sensitivity was also reduced in the three patient groups (P < .05). Insulin resistance was the main determinant of oral glucose intolerance in all patient groups (partial r2 = .49, P < .0001, n = 28). In turn, the main determinants of insulin insensitivity in TM patients were liver damage (albumin, r = .67, P = .02) and serum ferritin concentration (r = -.62, P = .03). There was no relationship of either 2-hour or incremental insulin concentrations with ferritin levels or with HCV status in TM subjects. Moreover, these patients showed no elevation of concentrations of proinsulin and des 31,32 proinsulin, markers of pancreatic beta-cell damage, in excess of those observed in cirrhotic patients. In conclusion, the glucose intolerance of TM, like that of cirrhosis, is associated with insulin resistance, not insulin deficiency, and may be a direct or indirect consequence of hepatic damage.

Adolescent↗

PubMed2005

Variation in the eNOS gene modifies the association between total energy expenditure and glucose intolerance.

Endothelium-derived nitric oxide (NO) facilitates skeletal muscle glucose uptake. Energy expenditure induces the endothelial NO synthase (eNOS) gene, providing a mechanism for insulin-independent glucose disposal. The object was to test 1) the association of genetic variation in eNOS, as assessed by haplotype-tagging single nucleotide polymorphisms (htSNPs) with type 2 diabetes, and 2) the interaction between eNOS haplotypes and total energy expenditure on glucose intolerance. Using multivariate models, we tested associations between eNOS htSNPs and diabetes (n = 461 and 474 case and control subjects, respectively) and glucose intolerance (two cohorts of n = 706 and 738 U.K. and Spanish Caucasians, respectively), and we tested eNOS x total energy expenditure interactions on glucose intolerance. An overall association between eNOS haplotype and diabetes was observed (P = 0.004). Relative to the most common haplotype (111), two haplotypes (121 and 212) tended to increase diabetes risk (OR 1.22, 95% CI 0.96-1.55), and one (122) was associated with decreased risk (0.58, 0.39-0.86). In the cohort studies, no association was observed between haplotypes and 2-h glucose (P > 0.10). However, we observed a significant total energy expenditure-haplotype interaction (P = 0.007). Genetic variation at the eNOS locus is associated with diabetes, which may be attributable to an enhanced effect of total energy expenditure on glucose disposal in individuals with specific eNOS haplotypes. Gene-environment interactions such as this may help explain why replication of genetic association frequently fails.

Aged↗

PubMed1995

Factors influencing the development of glucose intolerance in Cushing syndrome.

BACKGROUND: Although the frequency of glucose intolerance in endogenous Cushing syndrome has been repeatedly evaluated, no attempt has been made so far at analyzing simple clinical factors in order to quantify their influence on the development of glucose intolerance. METHODS: The influence of 6 factors on the development of glucose intolerance (family history of diabetes, age and body mass index of patients, duration of hypercortisolism, its pathogenetic form, and the extent of its clinical manifestation) was evaluated by means of multiple regression in 74 patients with Cushing syndrome. RESULTS: The disappearance of a normal glucose tolerance in Cushing syndrome was a function of the time of duration of hypercortisolism. The emergence of diabetes mellitus, but not of impaired glucose tolerance, was supported by ageing. Surprisingly, the family history failed to have any predictive value. CONCLUSIONS: The results suggest that diabetes mellitus in endogenous Cushing syndrome is a disorder genetically different from primary diabetes mellitus.

Adult↗

PubMed2005

Glucose intolerance: the hidden danger in hypertensives!

Both systemic hypertension and abnormalities of glucose metabolism are independent recognised risk factors for the development of cardiovascular morbidity and mortality, but their effects become additive when they coexist. Hypertension and glucose intolerance increase arterial stiffness and lead to cardiac structural and functional changes such as left ventricular hypertrophy and diastolic dysfunction of the left ventricle. Oral glucose tolerance tests have shown that 58% of patients with systemic hypertension who have no cardiac history and who are not known to have diabetes, suffer from unrecognised abnormalities of glucose metabolism i.e. either diabetes or impaired glucose tolerance. Using the fasting plasma glucose level and/or glycated haemoglobin concentration to diagnose glucose intolerance in patients with systemic hypertension is insufficient because of their low sensitivity for the diagnosis of diabetes and their inability to identify impaired glucose tolerance. It is important to recognise abnormalities of glucose metabolism early in patients with systemic hypertension in order to implement appropriate management and avoid further complications. Failure to identify glucose intolerance results in serious underestimation of the cardiovascular risk of these patients and denies patients primary preventative measures, which are based on risk assessment. All patients referred to Hypertension Clinics for the management of raised blood pressure should therefore be investigated by glucose tolerance test.

Arteries↗

PubMed1994

Role of glucose intolerance in cardiac diastolic function in essential hypertension.

Insulin resistance and glucose intolerance have been suggested to be involved in the pathogenesis of various cardiovascular diseases. We examined the role of glucose intolerance in cardiac performance and cardiac hypertrophy in 33 patients with essential hypertension (28 to 71 years of age, mean +/- SD: 53 +/- 13 years) who had never been treated. Patients with obesity (body mass index > 30 kg/m2) or overt diabetes were excluded. Plasma glucose and insulin were measured after oral administration of 75 g glucose. The incremental areas of glucose and insulin were used as indices of glucose intolerance and insulin resistance, respectively. Patients with impaired glucose tolerance according to World Health Organization criteria (n = 12) showed a significantly higher ratio of peak velocity during atrial contraction to early left ventricular filling phase (A/E ratio) than those with normal glucose tolerance (n = 21) despite similar age, blood pressure, and left ventricular mass index. By regression analysis, left ventricular mass index positively correlated with systolic blood pressure (r = .392, P < .05) but not with any parameters of glucose and insulin metabolism. A/E ratio determined by a Doppler system significantly correlated with age ( r = .776) and fasting and peak levels and incremental area of plasma glucose (r = .529, r = .468, and r = .634) but not with those parameters of insulin. In contrast, ejection fraction was not related to blood pressure, glucose tolerance, or insulin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Dietary change and obesity associated with glucose intolerance in Alaska Natives.

OBJECTIVE: To investigate frequency of food intake, body weight, and glucose intolerance in Alaska Natives. DESIGN: Height, weight, and random blood glucose levels were measured and a frequency-of-food-intake questionnaire was obtained. This questionnaire classified persons as consumers of indigenous foods or nonindigenous foods within three food groups. Those with a random blood glucose measurement > or = 6.72 mmol/L received an oral glucose tolerance test. SETTING: Community screening in 15 villages in Alaska. SUBJECTS: Nutrition screenings were done for 1,124 Alaska Native residents aged 20 years or older. An oral glucose tolerance test was done for 202 subjects. OUTCOMES MEASURED: Subjects were classified as consumers of indigenous or nonindigenous foods within three food groups. A diagnosis of non-insulin-dependent diabetes mellitus (NIDDM) was made on the basis of World Health Organization criteria. A determination of overweight was made on the basis of National Center for Health Statistics criteria. STATISTICAL ANALYSIS: A chi 2 test with Yates correction, t test, and linear regression, with two-sided P values. RESULTS: Athabascan Indians had twice the rate of NIDDM as Yup'ik Eskimos with significantly higher frequency of nonindigenous food intake, plus lower frequency of indigenous carbohydrate and fat intake. Subjects < or = 30 years old consumed significantly more nonindigenous protein and fat and low-nutrient-density carbohydrates than those > or = 60 years old. Persons who had glucose intolerance reported significantly greater consumption of nonindigenous protein and less seal oil. Incidence of overweight was significantly higher than was found 25 years ago. Participants with glucose intolerance were significantly more overweight than others. CONCLUSION: A pattern of increased frequency of nonindigenous protein, low-nutrient-density carbohydrate, and fat intake with less indigenous carbohydrate and fat consumption was found in subjects < or = 30 years old and in association with the higher rate of NIDDM found in the Athabascan Indians. Persons with glucose intolerance were significantly more overweight than others. APPLICATIONS: Although the nutritional value of indigenous foods for reducing disease risk should be promoted, nutrition education, especially among young adults, should also include building skills to select and prepare nonindigenous foods to attain a healthful diet. Although snacking is a concern, dietary fat was the most significant factor in obesity and NIDDM.

Adult↗

PubMed2003

Maternal ante-natal parameters as predictors of persistent postnatal glucose intolerance: a comparative study between Afro-Caribbeans, Asians and Caucasians.

AIMS: To measure the prevalence of persistent glucose intolerance at 6-12 weeks postpartum in various ethnic groups to assess the value of targeted postpartum screening. METHODS: A retrospective study was performed using computerized databases from two large maternity units within one UK region. Both units used the same screening strategy for gestational diabetes mellitus (GDM) and the same postpartum follow-up at 6-12 weeks using a 75-g oral glucose tolerance test (OGTT). A total of 221 women with a diagnosis of GDM/impaired glucose tolerance (IGT) in the index pregnancy in addition to a completed postpartum 75-g OGTT were studied. Of these, 91 were Caucasian, 89 were of Indo-Asian (Asian) origin and 41 were of Afro-Caribbean origin. RESULTS: The study showed that 35% Indo-Asians had persistent postpartum glucose intolerance compared with 7% Caucasians and 5% Afro-Caribbeans (P < 0.003). Insulin requirement during pregnancy and a diagnosis of gestational diabetes prior to 20 weeks of pregnancy were predictive for persistent postpartum glucose intolerance amongst Indo-Asians. CONCLUSIONS: The frequency of postpartum glucose intolerance among Indo-Asian women is significantly greater than among age-matched Caucasian and Afro-Caribbean women. We suggest that all Indo-Asian women with gestational diabetes should undergo postpartum screening for persistent glucose intolerance. However, in non-Asian women selective screening may be more cost effective.

Adult↗

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↗

PubMed1981

Obesity, very low density lipoproteins, and glucose intolerance over fourteen years: The Framingham Study.

A total of 5082 men and women in the Framingham Heart Study population who were free of any glucose abnormality and aged 33 to 67 years were followed prospectively over 14 years for the occurrence of glucose intolerance. The diagnosis of glucose intolerance was defined as developing documented hyperglycemia or being placed on justified treatment by a physician. The 14-year incidence was 6.7% in men and 5.5% in women. Multivariate analysis was used and future glucose intolerance in men and women was highly associated with casual blood glucose, Metropolitan Relative Weight and very low density lipoproteins at the baseline exam. Other factors showed only sex-specific or univariate associations. Obesity and lipoprotein abnormalities were shown to be independent markers in the prediction of future glucose intolerance.

Adult↗

PubMed2004

Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study.

Clinic-based studies suggest that sleep-disordered breathing (SDB) is associated with glucose intolerance and insulin resistance. However, in the available studies, researchers have not rigorously controlled for confounding variables to assess the independent relation between SDB and impaired glucose metabolism. The objective of this study was to determine whether SDB was associated with glucose intolerance and insulin resistance among community-dwelling subjects (n=2,656) participating in the Sleep Heart Health Study (1994-1999). SDB was characterized with the respiratory disturbance index and measurements of oxygen saturation during sleep. Fasting and 2-hour glucose levels measured during an oral glucose tolerance test were used to assess glycemic status. Relative to subjects with a respiratory disturbance index of less than 5.0 events/hour (the reference category), subjects with mild SDB (5.0-14.9 events/hour) and moderate to severe SDB (> or =15 events/hour) had adjusted odds ratios of 1.27 (95% confidence interval: 0.98, 1.64) and 1.46 (95% confidence interval: 1.09, 1.97), respectively, for fasting glucose intolerance (p for trend < 0.01). Sleep-related hypoxemia was also associated with glucose intolerance independently of age, gender, body mass index, and waist circumference. The results of this study suggest that SDB is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus.

Aged↗

PubMed2004

Reversal of glucose intolerance by by pioglitazone in high fat diet-fed rats.

The present study was undertaken to determine the effect of pioglitazone (3, 10 and 30 mg/kg p.o.), an insulin sensitizer, on glucose intolerance in high fat diet- (HFD) fed rats (a nongenetic model of insulin resistance). In addition, the effect of pioglitazone (3, 10 and 30 mg/kg p.o.) on diet-induced changes in body weight, plasma glucose, insulin, triglyceride and total cholesterol levels were also determined. The feeding of HFD for 4 weeks produced a significant increase in body weight, total fat pad weight, basal/fasting plasma glucose, insulin, basal triglyceride (TG) and total cholesterol (TC) levels in male rats. Furthermore, the rats fed HFD exhibited fasting hyperglycemia and hyperinsulinemia as well as enhanced glycemic response to exogenously administered glucose (2 g/kg p.o.) during an oral glucose tolerance test (OGTT) at the end of 4 weeks of dietary manipulation, indicating that the rats had developed insulin resistance and glucose intolerance. Treatment with pioglitazone (10 and 30 mg/kg p.o.) once daily for 2 weeks significantly diminished the elevated basal plasma insulin and TG levels in HFD-fed rats. In addition, a statistically significant reduction in TC level was observed only with the high dose of pioglitazone (30 mg/kg p.o.). However, pioglitazone had no significant effect on body weight, total fat pad weight and basal plasma glucose level. Pioglitazone (10 and 30 mg/kg p.o.) significantly reduced fasting hyperglycemia and reversed oral glucose intolerance to normal in HFD-fed rats compared with control normal rats. The above findings suggest that pioglitazone has potent insulin-sensitizing and lipid-lowering properties in a HFD-fed rat model. In conclusion, the present study demonstrates that the adult male rats on a HFD for 4 weeks exhibited the characteristic features of obesity, insulin resistance and glucose intolerance, namely increased body weight, increased total fat pad weight, mild basal/fasting hyperglycemia, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia and impaired oral glucose tolerance, that closely resemble the human prediabetic obese insulin-resistant and glucose-intolerant state. Further treatment with pioglitazone once daily for 2 weeks significantly ameliorated changes in basal plasma insulin, TG and TC, and reversed oral glucose intolerance to normal in HFD-fed rats, suggesting its potential in the treatment of insulin resistance and glucose intolerance associated with abnormal lipid metabolism.

Animals↗

PubMed1994

[Glucose intolerance during interferon therapy in patients with chronic hepatitis type C].

A new side effect of interferon (IFN) therapy, glucose intolerance was investigated using insulin-clamp study. In 75 g oral glucose tolerance tests before and after the IFN therapy showed no significant difference, whereas clamp study showed a significant decrease of glucose disposal. Our data suggested that insulin resistance was the main reason for glucose intolerance observed during INF therapy in the patients with chronic active hepatitis C. Early detection and strict control of glucose intolerance could avoid the progress of glucose intolerance.

Chronic Disease↗

PubMed2006

[Fasting glucose versus oral glucose tolerance test for detection of glucose intolerance in obese children].

BACKGROUND: Recently, the cut-off point for normal fasting glucose (FG) level, was decreased to 100 mg/dl. AIM: To determine the frequency of abnormal carbohydrate abnormalities in children with obesity and evaluate if the fasting glucose level is a useful tool for the screening of glucose intolerance (GI). PATIENTS AND METHODS: Children and adolescents, referred for evaluation of obesity were evaluated with an oral glucose tolerance test (OGTT) and FG. The sensitivity of FG for detection of GI, using the 100 and 110 mg/dl cut-off point, was evaluated. RESULTS: We studied 186 patients (125 females) aged 12.1 (range: 5.4-19.3) years with a body mass index (BMI) of 29.9 (18.3-44.6) kg/mt2 and a BMI Z score of 2.1 (1.7-3.2). Seven patients (3.8%) had abnormalities in the carbohydrate metabolism. The sensitivity of FG for the detection of GI using the 100 and 110 mg/dl cut-off values was 42.9 and 14.3%, respectively. Receiver operating characteristic (ROC) curves showed that the optimal diagnostic level for FG corresponds to 80 mg/dl (sensitivity: 85.7% and specificity of 74.9%). CONCLUSIONS: An abnormal carbohydrate metabolism was detected in 3.8% of the obese children and adolescents in this sample. FG of 100 mg/dl does not detect 57.1% of the patients with glucose intolerance. These data suggest that FG is not a useful screening tool for glucose intolerance in young patients.

Adolescent↗