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Results for “Glucose Intolerance”

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PubMed2005

Are plasma total homocysteine and other amino acids associated with glucose intolerance in uncomplicated pregnancies and preeclampsia?

OBJECTIVE: To evaluate the possible association between plasma total homocysteine or other amino acid concentrations and gestational diabetes or glucose intolerance (GI), in normotensive and preeclamptic pregnant women. STUDY DESIGN: Prospective study including 243 pregnant women without previous risk factors. O'Sullivan test (plus oral glucose tolerance test when necessary) was performed, and homocysteine, B vitamins and plasma amino acids (AA) were measured at 24-25 weeks. Homocysteine and other amino acids were also measured in the third trimester. RESULTS: Significant differences were observed in the incidence of preeclampsia in relation to abnormal glucose tolerance (P < 0.012). In normotensive patients, the glucose intolerance group showed significantly lower tHcy (P = 0.021) and increased plasma alanine concentrations in comparison with controls (P = 0.046), although no correlation was observed between both amino acid concentrations. CONCLUSIONS: (a) A higher incidence of preeclampsia was observed in abnormal glucose tolerance patients, (b) total homocysteine and alanine were the only individual amino acids whose plasma concentrations varied according to the glucose tolerance classes, and (c) an association between hyperhomocysteinemia and glucose intolerance in our preeclamptic patients could not be demonstrated.

Adult↗

PubMed2002

Circulating concentrations of insulin-like growth factor-I and development of glucose intolerance: a prospective observational study.

BACKGROUND: Results of experimental and clinical studies suggest that insulin-like growth factor-I (IGF-I) and IGF binding protein-1 (IGFBP-1) could be important determinants of glucose homoeostasis. However, experimental models might also reflect compensatory and adaptive metabolic processes. We therefore prospectively examined the associations between circulating concentrations of IGF-I and IGFBP-1 and development of glucose tolerance. METHODS: Participants in this cohort study were a random sample of 615 normoglycaemic men and women aged 45-65 years. Participants underwent oral glucose tolerance testing based on WHO definitions and criteria in 1990-92 and 1994-96. At the baseline visit, we measured serum concentrations of IGF-I and IGFBP-1, and assessed the relation between these peptides and subsequent glucose intolerance. FINDINGS: At 4.5 years of follow-up, 51 (8%) of 615 participants developed impaired glucose tolerance or type-2 diabetes. After adjustment for correlates of IGF-I and risk factors for glucose intolerance, the odds ratio for risk of impaired glucose tolerance or type-2 diabetes for participants with IGF-I concentrations above the median (> or = 152 microg/L) compared with those with concentrations below the median (<152 microg/L) was 0.50 (0.26-0.95). Consistent with this finding, IGF-I also showed a significant inverse association with subsequent 2-h glucose concentrations, which was independent of correlates of IGF-I and risk factors for glucose tolerance (p for linear trend=0.026). We also found that this inverse association was independently modified by IGFBP-1 (p for interaction=0.011). INTERPRETATION: These data show that circulating IGF-I and its interaction with IGFBP-1 could be important determinants of glucose homoeostasis and provide further evidence for the possible protective role of IGF-I against development of glucose intolerance.

Aged↗

PubMed2004

Exercise protects against glucose intolerance in individuals with a small body size at birth.

BACKGROUND: Small body size at birth is a risk factor for Type 2 diabetes. We investigated whether regular exercise is related to lower rates of glucose intolerance in individuals with a small body size at birth and whether birth size affects exercise habits in adulthood. METHODS: Five hundred subjects aged 65-75 years with data on birth measurements underwent an oral glucose tolerance test. They reported their weekly exercise frequency and intensity and yearly physical leisure time activity. RESULTS: Frequent (> or = 3/week) or moderate weekly exercise and yearly physical activity were all related to lower rates of glucose intolerance. This effect was, however, dependent on birth size, being strongest among subjects with a small body size at birth (birth weight < or = 3000 g and/or ponderal index < or = 26 kg/m3). Among men, frequency (P = 0.033) and intensity (P = 0.030) of exercise as well as yearly physical activity (P = 0.005) correlated inversely with birth size. CONCLUSIONS: Subjects predisposed to Type 2 diabetes due to a small birth size are strongly protected from glucose intolerance by regular exercise. Although a small body size at birth is related to a smaller muscle mass in adulthood, men born thin exercised more in adulthood than those not born thin. In these elderly subjects this might indicate the survival of the fittest.

Aged↗

PubMedDate not supplied

Glucose intolerance in the elderly: an open debate.

The presence of glucose intolerance in aged people is a well known physio-pathological condition. Nevertheless, the mechanisms by which it takes place are still unclear. In the present report we have reviewed the possible mechanisms (impaired insulin secretion and action, role of the environmental factors) which may contribute to the impaired glucose handling of aging. Moreover, we have also pointed out that not all aged subjects are glucose intolerant; in fact it seems clear that only aged subjects who present more than one of the pathological findings reported above may develop impaired glucose handling.

Journal Article↗

PubMed1995

The relationship between blood pressure and serum insulin response in glucose intolerant subjects.

One hundred newly diagnosed IGT and type 2 diabetic subjects both normotensive and hypertensive and of age between 40-55 years were studied by oral glucose stimulation. Serum insulin concentrations were measured in the fasting and at 30, 60 and 120 minutes after glucose administration. Postglucose serum insulin responses were found to be significantly higher in the hypertensive subjects with FPG < 7.8 mmol/l (p < 0.05 at 30, 60 and 120 minutes) as compared with the corresponding values of the normotensive subjects with comparable fasting hyperglycemia. No significant difference in insulin responses between hypertensive and normotensive subjects was found in those with FPG > 7.8 mmol/l. A positive correlation was observed between diastolic blood pressure and 2 hour postglucose serum insulin concentration in those with FPG < 7.8 mmol/l (P < .05). The results suggested that hyperinsulinemia is a feature of hypertensive subjects with mild glucose intolerance and not of those with severe glucose intolerance. The absence of elevated insulin response in hypertensive subjects with advanced type 2 diabetes might be due to severe B cell decompensation. It appears that insulin resistance is somehow associated with essential hypertension and hyperinsulinemia is not necessary for the maintenance of raised blood pressure.

Adult↗

PubMed1995

[Glucose intolerance in elderly persons in The Netherlands; the Twello Study].

OBJECTIVE: To determine the prevalence of grades of glucose intolerance in subjects over 64 years of age. DESIGN: Point prevalence study. SETTING: Twello, a rural village in the Netherlands. METHODS: Of a total of 696 persons aged over 64 years recruited from a general practice, 460 subjects had an oral glucose tolerance test (OGTT) in 1985, 56 were known with non-insulin-dependent diabetes mellitus. Glucose estimations were done in capillary whole blood with a Glucometer. OGTT results were classified according to WHO 1985 recommended cut-off points and combination rules. RESULTS: The prevalence of normal glucose tolerance was 42%, of impaired glucose tolerance 27% and of diabetes mellitus 31%. The estimated prevalence in the source population were 45% (44.4-44.6), 28% (28.3-28.5) and 27% (95% CI: 27.1-27.2) respectively, adjusted for age and gender by standardization to the Dutch population of 1985. Re-evaluation of the earlier diagnoses of 'diabetes mellitus' according to the new WHO guidelines revealed that 55% of earlier diabetic with diet as the only therapy were no longer classified as diabetics. The prevalence of diabetes mellitus in persons over 64 was 10% before the investigation took place, and 30% afterwards. CONCLUSIONS: Te prevalence of diabetes mellitus as well as of impaired glucose tolerance from the Twello study rank among the higher rates reported in Caucasian populations. Case finding of glucose intolerance in those at risk over 64 years of age is recommended.

Aged↗

PubMedDate not supplied

Hypoinsulinaemia, glucose intolerance and diminished beta-cell size in S6K1-deficient mice.

Insulin controls glucose homeostasis by regulating glucose use in peripheral tissues, and its own production and secretion in pancreatic beta cells. These responses are largely mediated downstream of the insulin receptor substrates, IRS-1 and IRS-2 (refs 4-8), through distinct signalling pathways. Although a number of effectors of these pathways have been identified, their roles in mediating glucose homeostasis are poorly defined. Here we show that mice deficient for S6 kinase 1, an effector of the phosphatidylinositide-3-OH kinase signalling pathway, are hypoinsulinaemic and glucose intolerant. Whereas insulin resistance is not observed in isolated muscle, such mice exhibit a sharp reduction in glucose-induced insulin secretion and in pancreatic insulin content. This is not due to a lesion in glucose sensing or insulin production, but to a reduction in pancreatic endocrine mass, which is accounted for by a selective decrease in beta-cell size. The observed phenotype closely parallels those of preclinical type 2 diabetes mellitus, in which malnutrition-induced hypoinsulinaemia predisposes individuals to glucose intolerance.

Animals↗

PubMed1996

Dietary fish oil normalize dyslipidemia and glucose intolerance with unchanged insulin levels in rats fed a high sucrose diet.

The aim of this study was to investigate the relationship between the lipid-lowering effects of fish oils and concomitant consequences on glucose tolerance and insulin sensitivity in an experimental animal model of hypertriglyceridemia induced by high sucrose intake. To achieve this goal, male Wistar rats were fed a semi-synthetic sucrose rich diet (SRD) (w/w: 62.3% sucrose, 8% corn oil, 17% protein) for 90 days. At the time, a well established and permanent hypertriglyceridemia accompanied by glucose intolerance was present. After that, one half of the animals continued on the SRD up to 120 days. The other half received an SRD in which the source of fat was substituted by cod liver oil (w/w 7% CLO plus 1% corn oil) from day 90 to 120 (SRD+CLO). Control rats were fed a semi-synthetic diet (CD) (w/w: 62.5% corn starch, 8% corn oil, 17% protein) throughout the 120 days experimental period. Results obtained after the experimental period show that the hypertriglyceridemia and glucose intolerance ensuing long term feeding normal rats with a sucrose-rich diet could be completely reversed mediating no change in circulating insulin levels by shifting the source of fat in the diet from corn oil to cod liver oil. These findings suggest that manipulation of dietary fats may play a role in the management of the lipid disorders associated with glucose intolerance and insulin resistance.

Animals↗

PubMed2000

A cross-sectional study of dietary patterns with glucose intolerance and other features of the metabolic syndrome.

Previous epidemiological studies have demonstrated relationships between individual nutrients and glucose intolerance and type 2 diabetes, but the association with the overall pattern of dietary intake has not previously been described. In order to characterize this association, 802 subjects aged 40-65 years were randomly selected from a population-based sampling frame and underwent a 75 g oral glucose-tolerance test. Principal component analysis was used to identify four dietary patterns explaining 31.7% of the dietary variation in the study cohort. These dietary patterns were associated with other lifestyle factors including socio-economic group, smoking, alcohol intake and physical activity. Component 1 was characterized by a healthy balanced diet with a frequent intake of raw and salad vegetables, fruits in both summer and winter, fish, pasta and rice and low intake of fried foods, sausages, fried fish, and potatoes. This component was negatively correlated with central obesity, fasting plasma glucose, 120 min non-esterified fatty acid and triacylglycerol, and positively correlated with HDL-cholesterol. It therefore appears to be protective for the metabolic syndrome. Component 1 was negatively associated with the risk of having undiagnosed diabetes, and this association was independent of age, sex, smoking and obesity. The findings support the hypothesis that dietary patterns are associated with other lifestyle factors and with glucose intolerance and other features of the metabolic syndrome. The results provide further evidence for the recommendation of a healthy balanced diet as one of the main components of chronic disease prevention.

Adult↗

PubMed1989

Glucose tolerance and insulin response to glucose load before and after enzyme inducing therapy in subjects with glucose intolerance and patients with NIDDM having hyperinsulinemia or relative insulin deficiency.

We evaluated the role of insulin availability in the induction therapy of non-insulin dependent diabetes mellitus (NIDDM). Plasma glucose (BG) and insulin (IRI) response to glucose loading (OGTT) was investigated before and after placebo and phenobarbitone (PB) therapy in patients with glucose intolerance and NIDDM treated with diet only, sulphonylureas (SU) plus metformin (M) or insulin. The antipyrine test was used to reflect the liver mixed function oxidase system. Therapy with PB, but not placebo, reduced fasting IRI and BG in subjects with glucose intolerance and improved the glucose tolerance, insulin response to glucose and antipyrine metabolism. The effects of PB on patients with NIDDM were dependent on the insulin availability and duration of the disease. Best responses were seen in hyperinsulinemic patients at the early phase of the disease. They had lowered fasting BG and IRI values, improved glucose tolerance, insulin response to OGTT and antipyrine metabolism after PB therapy. The SU plus M treated patients responded beneficially if they had high fasting and postglucose IRI values and were non-responders if they had relative insulin deficiency. Antipyrine metabolism improved among the responders and non-responders. The hyperglycemic patients treated with insulin showed improved glucose metabolism, an improved C-peptide response and antipyrine metabolism. The subjects could be classified into responders and non-responders by calculating the ratio of areas above the fasting level curve of insulin and glucose (sigma delta I-OGTT/sigma delta G-OGTT). These values for the former were 0.2-0.4 and the latter 0.03-0.04, as compared to healthy volunteers (1.0) and subjects with glucose intolerance (1.4). A PB type inducer improves insulin sensitivity but does not alter its production or secretion. The outcome of glucose metabolism is therefore dependent on insulin availability.

Adult↗

PubMed2006

Glucose intolerance and insulin resistance in extremely premature newborns, and implications for nutritional management.

UNLABELLED: Glucose intolerance and postnatal growth retardation are commonly seen in low-gestation newborns. In contrast to the nutrient compositions of parenteral and enteral nutrition, fetuses at equivalent gestational ages receive much more amino acids (protein) but less glucose and lipids through placental transfer. CONCLUSION: A nutrition regime that simulates placental nutrient delivery would potentially minimize glucose intolerance and facilitate early attainment of normal growth velocity with normal body composition after preterm birth.

Glucose Intolerance↗

PubMed2004

Long-term effects of a reduced fat diet intervention on cardiovascular disease risk factors in individuals with glucose intolerance.

The long-term effects on cardiovascular disease risk factors of a reduced fat (RF), ad libitum diet were compared with usual diet (control, CD) in glucose intolerance individuals. Participants were 136 adults aged > or =40 years with 'glucose intolerance' (2h blood glucose 7-11.0 mmol/l) detected at a Diabetes Survey who completed at 1 year intervention study of reduced fat, ad libitum diet versus usual diet. They were re-assessed at 2, 3 and 5 years. Main outcome measures were blood pressure, serum concentrations of total cholesterol, HDL and LDL cholesterol, total cholesterol:HDL ratio, triglycerides and body weight. The reduced fat diet lowered total cholesterol (P<0.01), LDL cholesterol (P< or =0.05), total cholesterol:HDL ratio (P< or =0.05), body weight (P<0.01) and systolic blood pressure (P< or =0.05) initially and diastolic blood pressure (P<0.01) long-term. No significant changes occurred in HDL cholesterol or triglycerides. In the more compliant 50% of the intervention group, systolic and diastolic blood pressure levels and body weight were lower at 1, 2 and 3 years (P<0.05). It was concluded that a reduced fat ad libitum diet has short-term benefits for cholesterol, body weight and systolic blood pressure and long-term benefits for diastolic blood pressure without significantly effecting HDL cholesterol and triglycerides despite participants regaining their lost weight.

Blood Pressure↗

PubMed2005

HMG-CoA reductase inhibitors do not improve glucose intolerance in spontaneously diabetic Goto-Kakizaki rats.

We examined whether 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) improve glucose intolerance in spontaneously diabetic Goto-Kakizaki (GK) rats or not. The fasting blood glucose, plasma insulin, and serum cholesterol levels were significantly higher in GK rats than those in age-matched Wistar rats. All rats were given orally once a day 0.5% carboxymethylcellulose, pravastatin 8 mg/kg, simvastatin 8 mg/kg, or atorvastatin 8 mg/kg. An oral glucose tolerance test (OGTT) was performed before and 3, 6 and 12 weeks after statin treatments. The hyperglycemic response to OGTT in GK rats significantly exceeded that in Wistar rats. The plasma insulin level in GK rats increased with age until 14-week-old (treated for 6 weeks), and then decreased. Glucose intake significantly increased the plasma insulin in almost all rats. The increment of plasma insulin due to OGTT in GK rats appeared to be less than that in Wistar rats, because the basal level was already high in GK rats. Pravastatin, simvastatin, and atorvastatin did not modify changes in blood glucose and plasma insulin induced by glucose intake. In conclusion, long-term treatments of GK rats with statins did not improve glucose intolerance observed during OGTT.

Animals↗

PubMed1992

Beneficial effect of intravenous bolus of corticotropin-releasing factor on glucose intolerance of genetically obese (fa/fa) rats.

The effect of an ovine corticotropin-releasing factor (oCRF) bolus administered intravenously at the onset of glucose ingestion during oral glucose tolerance tests (OGTTs) was evaluated in conscious lean (FA/FA) and genetically obese (fa/fa) rats. When the amount of oCRF was purposely small to not stimulate the hypothalamo-pituitary-adrenal (HPA) axis, it normalized the glucose intolerance of genetically obese rats as tested during OGTTs and decreased their insulin output, whereas it had no effect in lean rats. In obese rats, plasma xylose levels measured after the ingestion of a xylose load were unaltered by the intravenous oCRF bolus, indicating that the beneficial effect of oCRF on glucose intolerance of fa/fa rats was unlikely to be dependent on glucose absorption. When the intravenous bolus of oCRF was doubled at the onset of OGTTs, it stimulated the HPA axis and produced a worsening of glucose intolerance in obese rats together with an increase in their insulin response. Again, it had no effect in lean rats. The abnormal intravenous glucose tolerance of obese rats was unaffected by the administration of an oCRF bolus: This is in keeping with previous data showing that bypassing the oral cavity fails to elicit several sensory reflexes that markedly influence subsequent glucose clearance. It has been suggested that obese rats may have deficient oropharyngeal reflexes that could be reactivated by the oCRF bolus, thereby being responsible for the normalization of their impaired OGTT, which lies in the hepatic glucose production process.

Animals↗

PubMed1994

[Usefulness of hemoglobin A1c and fructosamine for screening of glucose intolerance in community adults].

The usefulness of hemoglobin A1c and fructosamine for screening of glucose intolerance were compared in 383 semi-urban residents ranging from 35 to 88 years of age. Both the sensitivity and specificity of the indices for screening of those with 110 mg/dl and over of fasting blood glucose were examined. The results showed that hemoglobin A1c was better than fructosamine for screening for glucose intolerance.

Adult↗

PubMed2007

Temporal and dietary fat content-dependent islet adaptation to high-fat feeding-induced glucose intolerance in mice.

The high fat-fed mouse is an experimental model for studies of islet dysfunction as a mechanism for glucose intolerance and for evaluation of therapeutic targets. This model is, however, dynamic with a temporal and dietary fat content-dependent impact on islet function and glucose tolerance, the details of which are unknown. This study therefore examined the time course of changes in the insulin response to intravenous glucose (1 g/kg) in relation to glucose tolerance in female mice after 1, 3, 8, or 16 weeks of feeding with diets containing 11% fat (normal diet [ND]), 30% fat (medium-fat diet [MFD]), or 58% fat (high-fat diet [HFD]; by energy). High-fat diet increased body weight and body fat content, whereas MFD did not. The insulin response (postglucose suprabasal mean 1- and 5-minute insulin) was impaired after 1 week on MFD (481+/- 33 pmol/L) or HFD (223 +/- 31 pmol/L) compared with ND (713 +/- 46 pmol/L, both P < .001). This was accompanied by impaired glucose elimination compared with ND (both P < .001). Over the 16-week study period, the insulin response adaptively increased in the groups fed with HFD and MFD, to be not significantly different from ND after 16 weeks. This compensation normalized glucose tolerance in MFD, whereas the glucose tolerance was still below normal in HFD. Insulin clearance, as judged by elimination of intravenous human insulin, was not altered in HFD, suggesting that the observed changes in insulin responses to glucose are due to changes in insulin secretion rather than to changes in insulin clearance. We conclude that time- and dietary fat-dependent dynamic adaptive islet compensation evolves after introducing HFD in mice and that MFD-fed mice is a novel nonobese model of glucose intolerance.

Adipose Tissue↗

PubMed2005

Common variants in the ATP-sensitive K+ channel genes KCNJ11 (Kir6.2) and ABCC8 (SUR1) in relation to glucose intolerance: population-based studies and meta-analyses.

AIMS: To evaluate the relation between common variants in the ATP-sensitive K+ channel genes and glucose intolerance. METHODS: We conducted a meta-analysis of reported association studies in Caucasian populations for common variants in the ABCC8 (exons 16 and 18) and the KCNJ11 (E23K) gene and examined sources of heterogeneity in the results. The meta-analysis was based on 7768-10216 subjects (depending on the gene variant), and included two new population-based studies in the Netherlands with 725 cases and 742 controls. RESULTS: For the KCNJ11 variant, the summary odds ratio (OR) for glucose intolerance was 1.12 (1.01-1.23, P=0.03) for the EK genotype and 1.44 (1.17-1.78, P=0.0007) for the KK genotype, as compared with the EE genotype. For the ABCC8 exon 16 variant, the OR was 1.06 (0.94-1.19, P=0.34) for ct and 0.93 (0.71-1.20, P=0.56) for tt, as compared with the cc genotype. For ABCC8 exon 18, the OR was 1.20 (0.97-1.49, P=0.10) for CT/TT, as compared with the CC genotype. Studies of the ABCC8 variants that were published first or had smaller sample sizes (for the exon 18 variant) showed stronger associations, which may indicate publication bias. For the ABCC8 exon 18 and the KCNJ11 variant, associations were stronger for studies of clinical diabetes than newly detected glucose intolerance. The population attributable risk for clinical Type 2 diabetes was 6.2% for the KCNJ11 KK genotype and 10.1% for the KCNJ11 EK and KK genotype combined. CONCLUSIONS: The common KCNJ11 E23K gene variant, but not the ABCC8 exon 16 or exon 18 variant, was consistently associated with Type 2 diabetes.

ATP-Binding Cassette Transporters↗

PubMed2002

Comparing fasting plasma glucose against two-hour post-load glucose concentrations for the diagnosis of diabetes mellitus and glucose intolerance in Singaporean hospital patients.

INTRODUCTION: Several studies have assessed the impact of the 1997 American Diabetes Association (ADA) recommendation, of using fasting plasma glucose (FPG) concentration, to diagnose diabetes mellitus in population-based cohorts. However, data concerning the impact of this recommendation in the hospital setting are limited. As the performance characteristics of diagnostic tests vary depending on the prevalence of diabetes in the population studied, we have examined the clinical impact of adopting the ADA recommendations in comparison to the traditional 2-hour post-load glucose (2HPG) concentration used by the World Health Organisation (WHO) in diagnosing diabetes and other categories of glucose intolerance in Singaporean hospital patients. MATERIALS AND METHODS: We analysed the results of the standard 75 g oral glucose tolerance test (OGTT) performed on 625 patients in our hospital from 1994 to 1999. RESULTS: The prevalence of diabetes amongst these 625 patients was 36.8% (230) based on the ADA recommendation of using FPG, 42.8% (263) on using the 2HPG and 52.0% (325) on using the full 1998 WHO criteria. The degree of agreement (kappa) in establishing the diagnosis of diabetes between the FPG and 2HPG cut-offs was 0.48. Ninety-five (15.2%) individuals had diabetes based on the 2HPG alone, 62 (9.9%) based on the FPG alone and 168 (26.9%) based on both the FPG and 2HPG. Eighty-six (13.8%) individuals had impaired fasting glucose (IFG) and 123 (19.7%) had impaired glucose tolerance (IGT). The kappa-value between IFG and IGT was 0.08. CONCLUSION: Fasting plasma glucose concentration was an inadequate parameter in diagnosing diabetes and intermediate categories of glucose intolerance in our cohort of subjects. Our findings suggest that the OGTT remains an important diagnostic tool for classifying glucose tolerance in our hospital patients.

Adolescent↗