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At least 19 recordsLinked to original sources
PubMed2002

Healthy diet and lifestyle clustering and glucose intolerance.

Glucose intolerance represents a spectrum of abnormalities, including impaired fasting glucose, impaired glucose tolerance and type 2 diabetes. It is a major public health challenge worldwide, with rapidly increasing prevalence rates in both developed and developing countries. This global epidemic of diabetes is largely driven by the globalisation of Western culture and lifestyles. Specifically, there is now evidence from large-scale observational studies, and from intervention studies, of powerful synergistic interactions between diet, obesity, exercise, smoking and alcohol in the development of glucose intolerance. It is estimated that >90% of cases of type 2 diabetes in the population could be prevented with the adoption of a prudent diet (high in cereal fibre and polyunsaturated fatty acids and low in trans-fatty acids and glycaemic load), avoidance of overweight and obesity (BMI<25 kg/m2), engagement in moderate to vigorous physical activity for at least 0.5 h/d, non-smoking and moderate alcohol consumption. These findings are biologically plausible and have major public health implications. They form the basis for a clear, simple and coherent message for health promotion and public policy. However, to make progress on these issues health will need to be placed at the centre of public policy and relevant vested interests tackled, notably in the food, entertainment, tobacco and automobile industries.

Adolescent↗
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↗
PubMedDate not supplied

Senile cataract and glucose intolerance: the Israel Study of glucose Intolerance Obesity and Hypertension (The Israel GOH Study).

Association of "senile" cataract (SC) with glucose intolerance (impaired tolerance and diabetes) was assessed by sex and age in a random population sample comprising 930 individuals aged 40-70 yr, who underwent concurrent oral glucose tolerance test and ophthalmoscopy. The eye examination was performed without knowledge of the glucose tolerance status. SC was defined as lens opacification preventing visualization of the eyeground or as surgical aphakia due to SC. To assess the independent effect of hyperglycemia, glycosylated hemoglobin (HbA1) was determined in 769 participants. In men, no association was found between SC, glucose intolerance, and HbA1. In women of all ages, glucose intolerance was associated with an SC risk ratio of 6.1 (95% confidence limits 3.3-11.1; P less than 0.001). Furthermore, SC was associated in women with increased HbA1 independently of the effect of glucose intolerance (P less than 0.01). These findings confirm the reported association of SC with diabetes (although unlike the Framingham and HANES population studies, the association was confined in women), indicate its presence at all degrees of glucose intolerance, and suggest a possible independent role of nonenzymatic glycosylation in its pathogenesis.

Adult↗
PubMed1988

Beta 2-sympathomimetic activation as a cause of posthypoglycemic glucose intolerance.

Posthypoglycemic glucose intolerance is related to counter-regulatory hormones. We have tested the role of the beta 2-sympathomimetic activity of the catecholamines in healthy volunteers. beta 2-stimulation with fenoterol for 25 minutes caused glucose intolerance and insulin resistance for 4 hours. This suggests that the beta 2-sympathomimetic activity induces glucose intolerance after an episode of hypoglycemia.

Blood Glucose↗
PubMed2000

Glucagon-like peptide-1 induces cell proliferation and pancreatic-duodenum homeobox-1 expression and increases endocrine cell mass in the pancreas of old, glucose-intolerant rats.

Glucose homeostasis in mammals is maintained by insulin secretion from the beta-cells of the islets of Langerhans. Type 2 diabetes results either from primary beta-cell failure alone and/or a failure to secrete enough insulin to overcome insulin resistance. Here, we show that continuous infusion of glucagon-like peptide-1 (7-36) (GLP-1; an insulinotropic agent), to young and old animals, had effects on the beta-cell of the pancreas other than simply on the insulin secretory apparatus. Our previous studies on a rodent model of glucose intolerance, the aging Wistar rat, show that a plateau in islet size, insulin content, and beta-cell mass is reached at 13 months, despite a continuing increase in body weight. Continuous sc infusion of GLP-1 (1.5 pM/kg x min), over 5 days, resulted in normal glucose tolerance. Our current results in both young and old rats demonstrate that treatment caused an up-regulation of pancreatic-duodenum homeobox-1 (PDX-1) expression in islets and total pancreas, induced pancreatic cell proliferation, and beta-cell neogenesis. The effects on levels of PDX-1 messenger RNA were abrogated by simultaneous infusion of Exendin (9-39), a specific antagonist of GLP-1. PDX-1 protein levels increased 4-fold in whole pancreata and 6-fold in islets in response to treatment. Beta-cell mass increased to 7.2 +/- 0.58 from 4.88 +/- 0.38 mg, treated vs. control, respectively, P < 0.02. Total pancreatic insulin content also increased from 0.55 +/- 0.02 to 1.32 +/- 0.11 microg/mg total pancreatic protein. Therefore, GLP-1 would seem to be a unique therapy that can stimulate pancreatic cell proliferation and beta-cell differentiation in the pancreas of rodents.

Aging↗
PubMed1986

Effect of past and concurrent body mass index on prevalence of glucose intolerance and type 2 (non-insulin-dependent) diabetes and on insulin response. The Israel study of glucose intolerance, obesity and hypertension.

A representative sample (n = 2140) of the Israeli Jewish population aged 40-70 (excluding known diabetic patients), whose body mass index had been measured 10 years earlier, underwent an oral glucose tolerance test and redetermination of body mass index. Irrespective of weight changes, high concurrent and high past body mass index values (greater than or equal to 27) were associated with similarly increased rates of glucose intolerance as compared with body mass index values less than 27 at both time-points (rate ratio 1.76, 90% confidence limits 1.56-1.99). Glucose intolerance here includes borderline and impaired tolerance as well as Type 2 diabetes. The rate of Type 2 diabetes increased only with increasing past body mass index, while concurrent body mass index had no effect [rate ratios: 2.36 (1.48-3.75) and 1.99 (1.48-2.68) respectively for the medium-(23-26.9) versus-low (less than 23) and high- (greater than or equal to 27) versus-medium past body-mass-index categories]. Weight reduction was associated with only slightly reduced rate of glucose intolerance and had no effect on the rate of diabetes. Mean sum insulin (summed 1 and 2 h levels, mU/l) increased significantly with increasing concurrent body mass index (123, 150 and 190 in the low, medium and high categories) with no effect of past body mass index. It also increased significantly (p less than 0.001) in all concurrent body mass index categories from normal tolerance through borderline to impaired tolerance, and decreased significantly (p less than 0.001) in diabetes relative to impaired tolerance, although it remained above normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

The effect of defective early phase insulin secretion on postload glucose intolerance in impaired fasting glucose.

Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are two risk groups for type 2 diabetes. Type 2 diabetes is characterized by both impaired insulin secretion and insulin resistance but their relative contribution to the development of hyperglycemia may differ due to heterogeneity of the disease. Combined glucose intolerance (CGI), on the other hand, seems to represent a more advanced stage of prediabetes that bears a distinctly higher risk of progression to diabetes and its comorbidities. This study has the aim to compare isolated IFG and CGI categories with respect to the degree of early phase insulin secretion abnormalities and insulin resistance. Subjects who had IFG (fasting glucose: 110-126 mg/dl) were included in the study. A 75-g oral glucose tolerance test (OGTT) with insulin response was done and subjects were classified according to the WHO criteria. Six subjects were excluded because they had diabetic glucose tolerance. A total of 66 patients (53.4 +/- 11.1 years, female/male: 48/18) were divided into two groups according to their glucose tolerance in OGGT (Group 1: isolated IFG and group 2: CGI). Early phase insulin secretion was measured by intravenous glucose tolerance test (IVGTT) and OGTT. Insulin resistance was assessed by the R value of the homeostasis model assessment (HOMA). We did not find any statistically significant difference between groups according to age, gender, body mass index (BMI), fasting glucose, fasting insulin, insulin-AUC (0-180 min) and HOMA-R values. In OGGT there was no statistically significant difference between 0', 30', 60' and 90' insulin levels of the groups; only 120' and 180' insulin levels were higher in CGI than in IFG group (p<0.05). In IVGTT, there was no statistically significant difference between glucose levels of the groups. Furthermore, insulin response to intravenous glucose was higher in IFG than in CGI (p<0.05). Our data demonstrate that isolated IFG and CGI are similar with respect to the degree of insulin resistance, and that subjects with CGI had a more prominent deficit in early phases of insulin secretion.

Adult↗
PubMed2001

Elevated plasma cortisol in glucose-intolerant men: differences in responses to glucose and habituation to venepuncture.

Recent evidence suggests that variations in cortisol activity within the physiological range contribute to associations between multiple cardiovascular risk factors. Plasma cortisol measurements during a glucose tolerance test differ in men with hypertension, insulin resistance, and glucose intolerance, but it is unclear whether this reflects altered responses of cortisol to glucose, altered circadian rhythm, or altered habituation to multiple sampling. We performed a single-blind randomized cross-over study comparing 75 g oral glucose with placebo in 39 fasted men (22 glucose intolerant and 17 controls) aged 68-77 yr. In all subjects, plasma cortisol fell during the glucose tolerance test. Subjects with glucose intolerance had significantly higher plasma cortisol following placebo (P = 0.001), suggesting an altered circadian rhythm. Treatment with an oral glucose load blunted the circadian fall in plasma cortisol (P = 0.002), but this response was no different in controls or glucose intolerant subjects. In addition, 0900 h plasma cortisol was higher in the first study phase in controls (P = 0.01) but not in glucose-intolerant subjects (P = 0.18), who showed a lack of habituation to repeated plasma measurements. These data support the hypothesis that alterations in central regulation of the hypothalamic-pituitary-adrenal axis may be important in glucose intolerance.

Aged↗
PubMed1998

[The selective detection of glucose intolerance and diabetes in primary care. The ITG-Reus (Tarragona) Study. The Glucose Intolerance Research Group].

OBJECTIVE: To investigate the number of people with intolerance to glucose (ITG) and undiagnosed diabetes (DM) among primary care users at risk. DESIGN: Prospective, selective urban polling of a representative sample of those attended in the city of Reus (88,000 inhabitants). SETTING: Two base health areas (10 Primary Care teams) with an approximate overall reference population of 45,000 inhabitants. PATIENTS AND OTHER PARTICIPANTS: Clinical and examination data were recorded with a pre-designed questionnaire. Diagnoses were established by means of base glycaemia (mmol.l-1 or a 75 g glucose oral overload (0 and 120 minutes) for users over 40 with some Diabetes risk factor. Further tests were HbA1C (%), base peptide-C (nmol.l-1, total cholesterol, HDL cholesterol, triglycerides (mmol.l-1 and 24-hour microalbuminuria (mg). MEASUREMENTS AND MAIN RESULTS: After a year included in the survey, the data of 345 people were evaluated: 151 men, 58 years old (95% CI, 57-60) and BMI of 30.8 (30.3-31.4), with 197 diagnoses (57.1%) of normal tolerance to glucose (52-62%). 82 (23.8%) of ITG (20-28%) and 66 (19.1%) of undiagnosed DM (15-23%). Significant differences between the three were detected in age (56/61.5/61.7 years, p < 0.001), proportion of men (38/50/53%, p < 0.05), diagnosis of hypertension (40.6/59.8/53%, p < 0.01), previous anomaly in tolerance 28.4/45.1/51.5%; p < 0.001), HbA1C (4.6/4.9/5.4; p < 0.001), systolic pressure (140.5/143.6/151 mmHg, p < 0.007). Triglycerides (1.4/1.6/2.1, p < 0.001) and microalbuminuria (16/29/51, p < 0.001). Base peptide-C (3.5/3.8/3.8) showed no statistical differences. CONCLUSIONS: Selective detection in primary care amply exceeds opportunist detection in identifying patients with ITG who might be susceptible to preventive measures. In function of the intolerance level, from normality through to DM, statistical differences were found in HbA1C, systolic pressure, Triglyceridaemia and urinary excretion of albumin. These were not extendable to the rest of the lipid profile or to endogenous insulinaemia.

Adult↗
PubMed1989

Increased skeletal muscle Na/K-ratio in obese men, but not in women, with glucose intolerance.

Obesity is associated with glucose intolerance. Glucose is to a large extent disposed in the skeletal muscle. Peripheral insulin resistance, as well as decreased enzymatic activity in the skeletal muscle, has been suggested in type II diabetes. Potassium is essential for such enzymatic reactions. In this study, obese men, but not women, with glucose intolerance tended to have a lower total body potassium per kg body weight, indicating a smaller muscle mass, than weight-matched normoglycaemic men. They also had a lower skeletal muscle potassium content per 100 g dry weight (P less than 0.05) and a higher muscle Na/K-ratio (P less than 0.05) compared with obese men with normal glucose tolerance. Muscle fat and muscle sodium content were higher in obese men than in women with the same body mass index (P less than 0.01). The muscle electrolyte changes can be explained by a decrease in the insulin mediated Na/k-pump activity across the cell membrane or a smaller number of insulin receptors on the skeletal muscle cell in patients with glucose intolerance.

Anthropometry↗
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↗
PubMed2000

Reduced GLP-1 and insulin responses and glucose intolerance after gastric glucose in GRP receptor-deleted mice.

By applying a newly developed ELISA technique for determining biologically active intact glucagon-like peptide [GLP-1, GLP-1-(7-36)amide] in mouse, plasma baseline GLP-1 in normal NMRI mice was found to be normally distributed (4.5 +/- 0.3 pmol/l; n = 72). In anesthetized mice, gastric glucose (50 or 150 mg) increased plasma GLP-1 levels two- to threefold (P < 0.01). The simultaneous increase in plasma insulin correlated to the 10-min GLP-1 levels (r = 0.36, P < 0.001; n = 12). C57BL/6J mice deleted of the gastrin-releasing peptide (GRP) receptor by genetic targeting had impaired glucose tolerance (P = 0.030) and reduced early (10 min) insulin response (P = 0.044) to gastric glucose compared with wild-type controls. Also, the GLP-1 response to gastric glucose was significantly lower in the GRP receptor-deleted mice than in the controls (P = 0.045). In conclusion, this study has shown that 1) plasma levels of intact GLP-1 increase dose dependently on gastric glucose challenge in correlation with increased insulin levels in mice, and 2) intact GRP receptors are required for normal GLP-1 and insulin responses and glucose tolerance after gastric glucose in mice.

Animals↗
PubMed2006

[Glucose intolerance: postprandial hyper glucose, risk factor for diabetic macroangiopathy].

Major prospective studies about diabetes showed simply improving glucose control is not sufficient to prevent diabetes macroangiopathy. Hence, postprandial hyperglycemia is focused as new risk factor of diabetes macroangiopathy. It is getting common that IGT (impaired glucose tolerance) is a major risk of cardiovascular disease. Our previous data suggest that the risk of macroangiopathy is not postprandial hyperglycemia itself but pathophysiology of causing postprandial hyperglycemia; reducing insulin sensitivity and/or delayed and hyper insulin level. To prevent postprandial hyperglycemia, there are three strategies according to pathophysiology. Improving insulin sensitivity of liver, delaying glucose flux to portal vein and reviving fast insulin secretion. Recent study shows each strategy can reduce risk of diabetes macroangiopathy.

Animals↗
PubMed1985

Hyperinsulinemia. A link between hypertension obesity and glucose intolerance.

Hypertension and glucose intolerance, determined in a random population sample (n = 2,475), showed a highly significant (P less than 0.001) association from the mildest levels of both conditions, independent of the confounding effects of age, sex, obesity, and antihypertensive medications. Summary rate ratios for hypertension were 1.48 (1.18-1.87) in abnormal tolerance and 2.26 (1.69-2.84) in diabetes compared with normal tolerance. Altogether, 83.4% of the hypertensives were either glucose-intolerant or obese--both established insulin-resistant conditions. Fasting and post-load insulin levels in a representative subgroup (n = 1,241) were significantly elevated in hypertension independent of obesity, glucose intolerance, age, and antihypertensive medications. The mean increment in summed 1- and 2-h insulin levels (milliunits per liter) compared with nonobese normotensives with normal tolerance was 12 for hypertension alone, 47 for obesity alone, 52 for abnormal tolerance alone, and 124 when all three conditions were present. The prevalence of concentrations (milliequivalents per liter) of erythrocyte Na+ greater than or equal to 7.0, K+ less than 92.5, and plasma K+ greater than or equal to 4.5 in a subsample of 59 individuals with all combinations of abnormal tolerance obesity and hypertension was compared with those in 30 individuals free of these conditions. Altogether, 88.1% of the former vs. 40.0% of the latter group presented at least one of these three markers of internal cation imbalance (P less than 0.001). We conclude that insulin resistance and/or hyperinsulinemia (a) are present in the majority of hypertensives, (b) constitute a common pathophysiologic feature of obesity, glucose intolerance, and hypertension, possibly explaining their ubiquitous association, and (c) may be linked to the increased peripheral vascular resistance of hypertension, which is putatively related to elevated intracellular sodium concentration.

Adult↗
PubMed1986

Further evidence that insulin metabolism is a major determinant of peripheral insulin response to oral glucose in subjects with mild glucose intolerance.

In mild glucose intolerance plasma concentration of C-peptide seems to give an estimate of pancreatic B cell secretion more reliable than plasma insulin itself. In the present study we measured the plasma levels of insulin and C-peptide after oral glucose load in 100 mildly glucose intolerant subjects, focusing our attention on high and low insulin responders. According to an insulin incremental area after oral glucose higher or lower than the mean +/- SD of the mean, 16 subjects were classified as "high insulin responders", and 17 as "low insulin responders". The two groups were similar for sex, age and bw. Mean insulin incremental area was almost 9-fold greater in high insulin responders than in low insulin responders (0.88 +/- 0.03 vs 0.10 +/- 0.01 pmol/ml min, p less than 0.001). Also mean C-peptide incremental area was significantly greater in high insulin responders than in low insulin responders, but the differences between the two groups were smaller. Indeed, mean C-peptide area was approximately 2.5-fold greater in high insulin responders than in low insulin responders (1.58 +/- 0.12 vs 0.66 +/- 0.07 pmol/ml min, p less than 0.001). These results give further support to the concept that in mild glucose intolerance insulin metabolism is a major determinant of peripheral insulin response to oral glucose load.

Adult↗
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↗
PubMed2005

Left ventricular diastolic function in normotensive subjects 2 months after acute myocardial infarction is related to glucose intolerance.

BACKGROUND: Both glucose intolerance and myocardial infarction are independently associated with impaired left ventricular (LV) function. This study was carried out to relate LV diastolic function in normotensive subjects 2 months after acute myocardial infarction (AMI) to glucose tolerance status. METHODS: Left ventricular ejection fraction (LVEF), LV mass index, peak velocity of the early phase/atrial contraction wave, deceleration time of E wave, and isovolumic relaxation time were measured during echocardiograph/Doppler cardiography in 200 normotensive patients 2 months after AMI. Twenty-nine patients were known to be diabetic on admission with AMI. Glucose tolerance test was carried out in the 171 patients who are not known to be diabetic. RESULTS: Independent of LVEF, restrictive LV filling (peak velocity of the early phase/atrial contraction wave > 1 but < 2 associated with deceleration time of E wave < or = 140 milliseconds) was found in 72% of the known-diabetic patients, 70% of the 20 preclinical diabetic patients, 23% of the 35 patients with impaired glucose tolerance, 13% of the 15 patients with stress hyperglycemia, and 7% of the euglycemic patients (P < .01). In the rest of these patients, LV filling was nonrestrictive. No significant difference was observed in LVEF and LV mass index between patient groups. CONCLUSION: Independent of LVEF, the pattern of abnormal LV filling in normotensive subjects 2 months after AMI is a function of the severity of glucose intolerance, restrictive in the majority of the diabetic patients and nonrestrictive in the majority of the euglycemic patients, impaired glucose tolerance, and stress hyperglycemia. After AMI, abnormal LV filling occurs even in the absence of detectable systolic dysfunction or left ventricular hypertrophy.

Adult↗