Cases Of Impaired Glucose Tolerance Research Articles

Insulin sensitivity in growth hormone-deficient children: influence of replacement treatment.

In adults, excessive GH secretion may lead to secondary diabetes mellitus, while prolonged GH treatment may accelerate the onset of type 2 diabetes mellitus in predisposed children. The aim of the study was to evaluate insulin sensitivity (IS) and glucose tolerance (GT) in a group of GH-deficient children treated with GH for a period of 6 years. One hundred and twenty-eight children (40 females, 88 males) were included in the study. At the beginning of treatment chronological age was 8.9 +/- 3.2 years, height standard deviation score (SDS) -2.43 +/- 0.90 and body mass index (BMI) SDS 0.18 +/- 1.60. At the end of the study chronological age was 13.0 +/- 2.9 years, height SDS -1.24 +/- 1.27 and BMI SDS 0.23 +/- 1.54. GH was administered at a mean weekly dosage of 0.3 mg/kg, injected subcutaneously over 6-7 days. GT was assessed according to the criteria of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. IS was evaluated with the quantitative insulin sensitivity check index (QUICKI). No cases of impaired GT or diabetes were recorded during the follow-up period. IS, already lower than in controls before starting treatment with GH, decreased significantly during the first year of therapy (QUICKI: 0.346 +/- 0.033 vs. 0.355 +/- 0.044, P < 0.05), with no further decrease in the following years. No correlation was found between QUICKI, BMI, years of treatment and onset of puberty. GH treatment in GH-deficient children does not lead to an impaired GT or type 2 diabetes mellitus, although it does significantly decrease IS.

Lack of agreement between the revised criteria of impaired fasting glucose and impaired glucose tolerance in children with excess body weight.

The aim of this study was to describe the agreement between impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) in children with excess body weight using the original and the revised definitions of IFG. Obese and overweight children aged 4-17 years were included (n = 533). Anthropometric parameters and biochemical tests (fasting and 2-h glucose tests after an oral glucose load [1.75 g/kg]) were performed. Case subjects with a fasting plasma glucose >/=126 mg/dl were excluded. The diagnostic parameters of the original and the revised definitions of IFG for detecting IGT were estimated. The analysis of agreement between these categories was made using the kappa test. The prevalence of IFG increased from 6.2 to 13.3% using the new criteria. The prevalence of IFG became closer to the prevalence of IGT (14.8%). The revised criteria increased the sensitivity from 26.6 to 36.7%. However, the new IFG definition was not useful for identifying IGT cases. Of the 71 case subjects with IFG, only 29 (40.8%) had IGT. In addition, 50 case subjects with IGT (9.4%) and 13 with diabetes (2.4%) had a fasting glycemia <100 mg/dl. A poor agreement was found between the 2003 IFG definition and abnormal 2-h postchallenge plasma glucose (kappa = 0.359). The proportion of false-positive cases increased (36.3-59.1%) under the new definition. The new definition modestly increases the sensitivity of IFG for detecting IGT in children with excess body weight. Despite this, more than one-half of these cases are not detected. In addition, the false-positive rate was increased by 61%.

Visceral adiposity and the risk of impaired glucose tolerance: a prospective study among Japanese Americans.

Greater visceral adiposity, higher insulin resistance, and impaired insulin secretion increase the risk of type 2 diabetes. Whether visceral adiposity increases risk of impaired glucose tolerance (IGT) independent of other adipose depots, insulin resistance, and insulin secretion is not known. Study subjects included 128 Japanese Americans with normal glucose tolerance at entry. Baseline variables included plasma glucose and insulin measured after an overnight fast and during a 75-g oral glucose tolerance test, fat areas by computed tomography, insulin secretion (incremental insulin response [IIR] [30 min insulin - fasting insulin]/30 min glucose), and insulin resistance index (homeostasis model assessment for insulin resistance [HOMA-IR]). During the 10- to 11-year follow-up period, we confirmed 57 cases of IGT. Significant predictors of IGT included intra-abdominal fat area (IAFA) (odds ratio [OR] for a 1 SD increase 3.82, 95% CI 1.63-8.94 at a fasting plasma glucose [FPG] level of 4.5 mmol/l), HOMA-IR (2.41, 1.15-5.04), IIR (0.30, 0.13-0.69 at an FPG level of 4.5 mmol/l), the interactions of IAFA by FPG (P = 0.003), and IIR by FPG (P = 0.030) after adjusting for age, sex, FPG, and BMI. The multiple-adjusted OR of IAFA increased and that of IIR decreased as FPG level decreased because of these interactions. Even after adjustment for total fat area, total subcutaneous fat area, or abdominal subcutaneous fat area, all of these associations remained a significant predictor of IGT incidence. Greater visceral adiposity increases the risk of IGT independent of insulin resistance, insulin secretion, and other adipose depots in Japanese Americans.

Estimating the consequences of anti-psychotic induced weight gain on health and mortality rate

Many anti-psychotic medications produce marked weight gain. In this study, we estimate the expected impact of degrees of antipsychotic-induced weight gain on selected mortality rate and incidence rates of impaired glucose tolerance (IGT) and hypertension (HTN) among US adults. Using raw data from 5209 respondents from the Framingham Heart Study's public use data set and national statistics on population demographics, we estimated the expected effect of weight gain on number of deaths and incident cases of IGT and HTN for a 10-year period commencing in 1999. Results indicated that the estimated deleterious effects of weight gain were greater for people with higher BMIs at baseline, for greater degrees of weight gain, for men than women, and for older than younger persons. Because there is a ‘U-shaped’ relation between BMI and mortality rate, small to moderate weight gains among people with baseline BMIs less than 23 were predicted to decrease mortality rates, whereas weight gains among people with baseline BMIs above that level were expected to increase mortality rates. However, the relations of IGT and HTN with BMI are monotonically increasing. Thus, the anticipated effect of weight gain on IGT and HTN is deleterious regardless of baseline BMI. Because it is unclear whether the beneficial effects of the atypical agents on, for example, reducing suicide mortality, outweigh the putative increase in mortality due to weight gain, we estimate the beneficial effects due to decreased death from suicide with the potential deleterious effects due to a 10-kg weight gain. We found that 492 suicide deaths per 100 000 schizophrenic patients would be prevented over 10 years with the use of clozapine compared to 416 additional deaths due to antipsychotic induced weight gain. Although this estimate is rather crude and should be seen only as offering a sense of the likely situation, results suggest that the lives saved via clozapine may essentially be offset by the deaths due to weight gain. As we discuss, it is not possible to provide definitive estimates of the effect of antipsychotic-induced weight gain on health and mortality, but our findings suggest that the magnitude of weight gains induced by many antipsychotic agents is likely to have important deleterious effects on mortality and health.

Alcohol consumption, Type 2 diabetes mellitus and impaired glucose tolerance in middle-aged Swedish men.

To investigate the association between alcohol consumption and impaired glucose tolerance and Type 2 diabetes mellitus. A population-based cross-sectional study consisting of 3,128 Swedish men, aged 35-56 years. Oral glucose tolerance testing identified 55 cases of Type 2 diabetes and 172 cases of impaired glucose tolerance. Information on alcohol consumption, family history of diabetes, smoking and physical activity was obtained by questionnaire. After adjustment for family history, smoking, physical activity and body mass index, the odds ratio of diabetes was 2.1 (95% confidence interval (CI) 1.0-4.5) in men with high consumption of alcohol (corresponding to over 12 drinks per week) and 0.7 (0.3-1.8) in moderate consumers (7-12 drinks), compared to occasional drinkers. For impaired glucose tolerance, the corresponding odds ratios were 0.7 (0.5-1.1) and 0.6 (0.4-1.0), respectively. Separate analyses for type of beverage indicated that high consumers of beer, spirits and wine had an odds ratio for diabetes of 2.9 (1.2-6.9), 3.3 (1.4-7.8) and 1.2 (0.5-2.7), respectively. The results indicated that high consumption of alcohol increases the occurrence of Type 2 diabetes and that this may primarily concern consumption of beer and spirits. For impaired glucose tolerance, regular alcohol consumption was associated with a reduced prevalence, particularly at moderate levels.

Low birth weight, family history of diabetes, and glucose intolerance in Swedish middle-aged men.

To investigate the association between low birth weight and glucose intolerance in relation to family history of diabetes. We conducted a population-based cross-sectional study of 2,237 men born in 1938-1957 in four municipalities in the outskirts of Stockholm, 50% of whom had a family history of diabetes (at least one first-degree or two second-degree relatives with diabetes). Oral glucose tolerance testing detected 35 cases of type 2 diabetes, 102 cases of impaired glucose tolerance, and 57 cases of impaired fasting glucose. In subjects without a family history of diabetes, low (< or = 3,000 g) birth weight was associated with an odds ratio of 2.3 (95% confidence intervals = 0.4-14.4) for diabetes, 1.8 (0.7-4.3) for impaired glucose tolerance, and 3.3 (1.0-10.4) for impaired fasting glucose. In subjects with a family history of diabetes, the corresponding figures were approximately similar, except for diabetes, for which the odds ratio was 5.4 (2.0-14.9). For men with low birth weight in combination with a family history of diabetes, the odds ratio was 10.9 (2.9-41.2) for diabetes, 2.4 (1.1-5.6) for impaired glucose tolerance, and 5.9 (2.1-16.3) for impaired fasting glucose. This study indicated that low birth weight is associated with type 2 diabetes, impaired glucose tolerance, and impaired fasting glucose in men. This finding was most pronounced in subjects with diabetes in the family, but it was also indicated in those without a family history of diabetes. Men with the combination of low birth weight and family history of diabetes seem to be at particularly high risk of developing type 2 diabetes.

The Protective Effect of Good Physical Fitness When Young on the Risk of Impaired Glucose Tolerance When Old

Background. The role of physical activity or fitness on preventing impaired glucose tolerance (IGT) has not been widely investigated. The present case-control study examined the relationship between the occurrence of IGT in men in their 50s and the level of their physical fitness while in their 30s.Methods. The subjects consisted of 38 male Japan Self-Defense Forces officials in their 50s who had IGT, as diagnosed by the 75-g oral glucose tolerance test, and 60 control individuals. Nine diabetics were included in the IGT cases. As an indicator of physical fitness between the ages of 30 and 39 years, we selected the best time recorded for each individual during that decade of life for the 1,500-m physical fitness test run. We calculated the odds ratio for IGT in relation to selected risk factors (including physical fitness), and a logistic regression analysis was used to adjust for possible confounding variables.Results. The odds ratio (95% confidence interval,Pvalue) for IGT with physical fitness in their 30s was 0.25 (0.11–0.58,P< 0.05). With adjustment for a parental history of diabetes and body mass index in both their 30s and their 50s, the odds ratio was 0.31 (0.11–0.86,P< 0.05).Conclusions. We concluded that the occurrence of IGT, including diabetes, in men in their 50s can be reduced by maintaining a high level of physical fitness while in their 30s.

Weight history, glucose intolerance, and insulin levels in middle-aged Swedish men.

The association between weight history and glucose intolerance was examined in a cross-sectional study consisting of 3,128 Swedish men aged 35-56 years, 52 percent of whom had a family background of diabetes mellitus. Oral glucose tolerance testing detected 55 cases of type 2 (non-insulin-dependent) diabetes and 172 cases of impaired glucose tolerance. Among men with no family history of diabetes, the estimated odds ratios for impaired glucose tolerance associated with short (<5 years) and long (> or =10 years) durations of obesity (body mass index (weight (kg)/height2 (m2) > or =25.0) were 1.3 (95% confidence interval (CI) 0.2-7.7) and 11.8 (95% CI 3.3-41.9), respectively. Among men with a family history of diabetes, the odds ratios were 2.0 (95% CI 0.8-4.7) and 4.0 (95% CI 1.8-9.1), respectively. Corresponding estimates of the odds of type 2 diabetes, adjusted for family history of diabetes, were 1.9 (95% CI 0.5-7.1) and 7.3 (95% CI 2.2-23.7), respectively. The odds of high (> or =30.0 mU/liter) fasting insulin levels in subjects with impaired glucose tolerance were 6.9 (95% CI 0.6-74.2) and 21.0 (95% CI 2.1-206.4) for short and long durations of obesity, respectively. Corresponding estimated odds of low 2-hour insulin response (< or =71.9 mU/liter) were 0.7 (95% CI 0.2-2.9) and 3.3 (95% CI 1.2-8.9). Homeostasis model assessment of insulin resistance yielded an odds ratio of 6.7 (95% CI 0.6-73.4) for a short duration of obesity and 20.0 (95% CI 2.0-200.6) for a long duration. Examination of beta-cell function with homeostasis model assessment resulted in odds ratios of 0.2 (95% CI 0.0-1.6) and 2.0 (95% CI 0.7-5.4) for short and long durations of obesity, respectively. These data indicate that obesity decreases glucose tolerance by way of progressively increased insulin resistance and, in the case of prolonged duration, by decreased insulin secretion as well.

A natural history of impaired glucose tolerance in North Jordan

AbstractThe objective of the study was to determine the conversion rate of subjects with impaired glucose tolerance (IGT) to Type 2 diabetes mellitus (NIDDM) and to identify factors which predict such conversion.Sixty eight subjects previously diagnosed with IGT in a survey conducted in 1995 in Sikhra, a Jordanian town of 10,000 people located in North Jordan, were reassessed for conversion to Type 2 diabetes two years later. A control group of 144 participants in the 1995 survey with normal glucose tolerance was also similarly reassessed for conversion to Type 2 diabetes. Diagnosis of IGT and NIDDM was based on WHO criteria1.Of the 68 IGT cases, 10 (14.7%) progressed to Type 2 diabetes, 27 (29.7%) reverted to normal, and the remainder persisted with IGT. A positive family history was a significant predictor of progression to diabetes irrespective of the IGT status. During the two year follow‐up period a significantly larger increase in systolic blood pressure (SBP) was observed among those who progressed to Type 2 diabetes compared with those who did not. Age ±40 and hypertension were consistent with a higher rate of progression to Type 2 diabetes but the association failed to attain statistical significance at the 0.05 level (p = 0.055 and 0.07 respectively).

Erratum: Early metabolic defects in the first-degree relatives of patients with non-insulin-dependent diabetes mellitus

glucose. venous blood sampres were taken before and 120 minutes termination. several characteristics of metabolic abnormalities control subjects. They needed higher insulin to maintain the normar had 7 (l2Vo) impaired glucose tolerance cases and only I in atives of NIDDM with normnl glucose tolerance (NGT). This patients with NIDDM in Indonesia. ortant early metabolic defects among thefirst-degree relatives of

Chromium in Human Nutrition: A Review

This review summarizes the results of 15 controlled studies supplementing defined Cr(III) compounds to subjects with impaired glucose tolerance. Three of these (3-4 mumol Cr/d for > 2 mo) produced no beneficial effects: serum glucose, insulin and lipid concentrations remained unchanged. The remaining 12 interventions improved the efficiency of insulin or the blood lipid profile of subjects (ranging from malnourished children and healthy middle-aged individuals to insulin-requiring diabetics). In addition, three cases of impaired glucose tolerance after long-term total parenteral alimentation responding to Cr supplementation have been reported. Chromium potentiates the action of insulin in vitro and in vivo; maximal in vitro activity requires a special chemical form, termed Glucose Tolerance Factor and tentatively identified as a Cr-nicotinic acid complex. Its complete structural identification is a major challenge to chromium research. The development and validation of a procedure to diagnose chromium status is the second challenge. Such a test would allow the assessment of incidence and severity of deficiency in the population and the selection of deficiency in the population and the selection of chromium-responsive individuals. The third challenge is the definition of chromium's mode of action on parameters of lipid metabolism that have been reported from some studies but not others. Future research along these lines might establish whether chromium deficiency is a factor in the much discussed "Syndrome X" of insulin resistance.

Epidemiological study of diabetes mellitus in the Hiroshima area-prevalence of diabetes mellitus and follow-up studies using the glucose tolerance test 5-19 years after initial testing.

Tests for diabetes mellitus have been performed annually since 1963 on about 100,000 A-bomb survivors living in Hiroshima. We report here on the trends over the 19 years leading up to 1981 for the glycosuria positive rate, the 75 g GTT results of positive cases and the findings of the 5-19 year follow-up. The glycosuria positive rate was 3-4 times higher in males. During the period of 1963-1979, the positive rate increased annually in both sexes, reaching 2.6 and 3.0 times the male-female values for 1963, but subsequently levelling off. When Body Mass Index (BMI) less than 25, 24.9% of the sample was diabetic (including those under treatment), 26.0% had Impaired Glucose Tolerance (IGT) and 49.1% were normal, whereas when BMI greater than or equal to 25, the rates were significantly higher being 45.0%, 27.4% and 27.6% respectively (p less than 0.001). Frequency increased with BMI, reaching 75.0% at BMI 33.3). Results of the 5-19 year follow-up showed the annual diabetes onset rate by the person year method in those with BMI less than 25 at initial GTT to be 1.72% among 848 normals, while it was a significantly higher 4.82% in those suffering from IGT. For those with BMI greater than or equal to 25, the rates were 3.77% among 161 normals and 7.93% among 132 IGT cases.