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Results for “Glucose Intolerance”

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PubMed1998

One-year treatment with ethyl esters of n-3 fatty acids in patients with hypertriglyceridemia and glucose intolerance: reduced triglyceridemia, total cholesterol and increased HDL-C without glycemic alterations.

n-3 Fatty acids in the form of ethyl esters (EE) allow lower daily doses and improved compliance. Administration of n-3 fatty acids to patients with glucose intolerance has led to controversial findings, some studies indicating worsening of the disorder, others no effect, or an improvement. A total of 935 patients with hypertriglyceridemia, associated with additional cardiovascular risk factors, i.e. glucose intolerance, NIDDM and/or arterial hypertension were entered a double blind (DB) protocol lasting 6 months with n-3 EE versus placebo, followed by a further 6 months of open study (n = 868) on 2 g a day of n-3 EE. At the end of the DB period, triglyceridemia in the total group was reduced significantly more by n-3 EE, without alterations in glycemic parameters. In the 6 months open follow up, patients on n-3 EE with type IIB hyperlipoproteinemia showed a significant reduction of total cholesterol, both in cases with (-4.15% vs. the 6 month levels) and without NIDDM (-3.8%). HDL-cholesterol had an overall mean rise of 7.4%, maximal in type IV patients with (+9.1%) and without (+10.1%) NIDDM. No alterations in glycemic parameters were detected in treated patients. Administration of n-3 EE to patients with hypertriglyceridemia associated with NIDDM or impaired glucose tolerance appears safe and effective.

Aged↗

PubMed1998

Role of hyperinsulinemia and glucose intolerance in the pathogenesis of nonalcoholic fatty liver in patients with normal body weight.

OBJECTIVES: The pathogenesis of nonalcoholic fatty liver in non-obese persons is poorly understood. We aimed to elucidate whether hyperinsulinemia and glucose intolerance are associated with development of fatty liver in patients with normal body weight. METHODS: Forty-seven patients with fatty liver were divided into non-obese (n = 25) and obese groups (n = 22) according to age adjusted body mass index. Inclusion criteria were as follows: (1) elevated transaminase levels during more than 3 months of follow up period, (2) no detectable HBsAg or anti-HCV in the serum, (3) alcohol consumption less than 40 gm/week, (4) no use of potential hepatotoxic drugs within 3 months and (4) sonographic evidence of fatty liver(moderate to severe degree). Baseline insulin levels and oral glucose tolerance test using 75gm of glucose were performed and the results were compared in each group of patients. RESULTS: Mean baseline insulin levels were elevated in both groups above the reference value, 9.3 +/- 3.5 microU/L in non-obese group and 9.9 +/- 3.5 microU/L in obese group (p = 0.26). Seventeen of non-obese patients (68%) had elevated basal insulin level and 16 of obese patients (73%) had elevated basal insulin level (p = 0.39). In oral glucose tolerance test, there was no difference in glucose level between non-obese and obese groups from O minute to 180 minutes (p > 0.05). Eleven patients from the non-obese group (44%) and 8 patients from the obese group (36%) had either impaired glucose tolerance or diabetes (p = 0.29). CONCLUSION: Our data suggest that hyperinsulinemia and glucose intolerance may play a role in the pathogenesis of fatty liver in patients with normal body weight as well as in patients with obesity.

Adult↗

PubMedDate not supplied

Relative importance of maternal constitutional factors and glucose intolerance of pregnancy in the development of newborn macrosomia.

The purpose of this case-control study was to determine the relative importance of various predictors of newborn macrosomia, with particular reference to maternal constitutional factors and glucose intolerance of pregnancy. Macrosomia was defined by both absolute birthweight > or = 4,000 g and birthweight > or = 90th centile for gestational age. One thousand mother/newborn pairs [209 macrosomic (cases) and 791 non-macrosomic newborns (controls)] were recruited. Mothers with pre-gestational diabetes mellitus were excluded. Data on pregnancy and pregnancy variables were collected by review of prenatal, labour, and delivery and newborn assessment records and interview with the mother. Predictors that entered the stepwise multiple regression model in order of significance were: previous history of macrosomia, increasing maternal weight, nonsmoking status, multiparity, male newborn gender, gestational age of 40-42 weeks, North American Aboriginal ethnicity, maternal birthweight > 4,000 g, maternal height and maternal age < 17 years. Glucose screen positive/100-g oral glucose tolerance test (GTT) negative status was a significant predictor for macrosomia as defined by birthweight greater than the 90th percentile for gestational age, but not for absolute birthweight over 4,000 g. It was the least significant of all the factors examined. Treated gestational diabetes was not a significant predictor. By multivariate analysis, maternal constitutional factors are more powerful predictors of newborn macrosomia than maternal mild glucose intolerance. Treatment of mothers with GDM may be masking the effect of more pronounced carbohydrate intolerance.

Adolescent↗

PubMed1997

Effect of acarbose on glucose intolerance in patients with non-insulin-dependent diabetes mellitus.

We evaluated the effect of acarbose, an alpha-glucosidase inhibitor, on glucose intolerance in patients with non-insulin-dependent diabetes mellitus (NIDDM). Acarbose was given orally (300 mg/day) for 24 weeks to 20 NIDDM patients. Data in an oral glucose tolerance test (OGTT) were evaluated before and after 24 weeks of treatment using principal component analysis. Acarbose administration significantly reduced the postprandial plasma glucose level over 24 weeks of treatment. Principal component analysis suggested that the patients were separated into responders and non-responders. There was a significant improvement of fasting and postprandial glucose levels after 12 and 24 weeks in the responders, but not in the non-responders. Plasma glucose level following the OGTT improved significantly after 24 weeks of treatment in the responders (Hotelling T2 value = 47.098, P = 0.022500), but not in the non-responders. The immunoreactive insulin level did not change in either group. Results thus suggest that acarbose improved insulin resistance in some patients with NIDDM (responders as classified by principal component analysis).

Acarbose↗

PubMed1997

Glucose intolerance induced by oligemic brain hypoxia: the effect of terguride.

Two series of experiments were performed. In the first one experiments were carried out in Koletsky genetically hypertensive lean female rats and in the normotensive female rats of Wistar strain. Glucose intolerance was induced by oligemic brain hypoxia (4 hours of occlusion of both common carotid arteries followed by 44 hours reperfusion). Brain water content were used as a marker of brain edema. Changes in insulinemia and specific insulin binding were used as expression of regulative mechanisms participating in modification of glucose tolerance. The effect of terguride (trans-dihydro-lisuride) was tested. Brain hypoxia induced glucose intolerance in both strains of rat but brain edema was found only in the normotensive females. Both abnormalities were alleviated by terguride treatment. Basal glycaemia was not changed either by the brain hypoxia or by terguride treatment, except normotensive female where brain hypoxia induced hyperglycaemia. The second series of experiments were carried out in the normotensive females. The arrangement of experiments was the same as in first series except omission of the final glucose tolerance test. Brain hypoxia causes increase in brain water content. The mentioned elevation of brain water content was alleviated by terguride treatment. Insulin binding to erythrocytes was not influenced by brain hypoxia. Terguride treatment shows decrease of insulin binding to erythrocytes. Brain hypoxia elevates insulinemia which was not alleviated by terguride treatment.

Animals↗

PubMed1991

Hyperinsulinaemia in obesity is not accompanied by an increase in serum proinsulin/insulin ratio in groups of human subjects with and without glucose intolerance.

Serum proinsulin is disproportionately elevated compared to insulin in Type 2 (non-insulin-dependent) diabetes mellitus. We studied the effect of obesity on serum proinsulin with varying degrees of glucose intolerance. Serum proinsulin and insulin were measured during a 75 g oral glucose tolerance test in 73 obese and 74 non-obese subjects with normal, borderline or diabetic-type glucose tolerance. Proinsulin was assayed by a direct radioimmunoassay using proinsulin-specific antiserum. Fasting serum proinsulin and insulin and the summed values of proinsulin and insulin during oral glucose tolerance test were significantly, or tended to be, higher in obese subjects than in those without obesity in each category of glucose tolerance. However, the molar ratio of proinsulin to insulin was nearly the same between obese and non-obese groups with a similar degree of glucose tolerance. On the other hand, the proinsulin/insulin ratio increased progressively with the deterioration of glucose tolerance. We conclude that proinsulin secretion is disproportionately increased in the presence of glucose intolerance but not by obesity itself. Each Beta cell seems to function normally in obese subjects while glucose tolerance remains normal.

Blood Glucose↗

PubMed1994

Hyperinsulinemia in glucose intolerance: is it true?

To evaluate whether beta-cell hyperfunction characterizes glucose intolerant states per se independent of fasting glycemia, we conducted a case-control study among 430 subjects who were classified, by NDGG criteria, as having normal glucose tolerance (n = 230, 130M/130F), nondiagnostic tolerance (NDT, n = 100, 50M/50F) and impaired glucose tolerance (IGT, n = 100, 50M/50F). Thirty-four subjects (17M/17F) with normal glucose tolerance were matched by age, sex, body mass index (BMI), waist-to-hip ratio (WHR), fasting glucose and HbA1c with 30 NDT (15M/15F) and 30 IGT (15M/15F) subjects. The continuous and significant increase in insulin and C-peptide levels across categories of glucose tolerance (from normal to NDT to IGT) was no longer evident in the case-control study: at a fasting plasma glucose ranging from 5.2-5.5 mmol/L (HbA1c was 5%) the concentration of fasting C-peptide was 0.793 +/- 225 nmol/L (mean +/- SD) in subjects with normal glucose tolerance, 0.805 +/- 200 nmol/L in NDT and 0.807 +/- 231 nmol/L in IGT subjects (p = NS). Similarly, plasma concentrations of triglycerides and blood pressure values were similar when subjects of different categories were compared at the same level of glycemia. Sixteen normal subjects were rendered mildly hyperglycemic by a 24-h glucose infusion to match the fasting glucose level of NDT (1 mg/kg/min) and IGT (2 mg/kg/min) subjects. At the same fasting glucose level, normal subjects presented elevations of fasting C-peptide significantly (p < 0.01) higher than subjects belonging to the NDT and IGT categories.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Glucose intolerance in critically ill surgical patients: relationship to total parenteral nutrition and severity of illness.

The authors evaluated the relative influence of severity of illness and total parenteral nutrition (TPN) on glucose intolerance in critically ill surgical patients. Records of TPN administration, serum glucose measurements, and the simplified acute physiology score (SAPS) were extracted from the surgical intensive care unit (SICU) and hospital clinical information systems (CIS) for all patients admitted to the SICU from October 1, 1989 through March 31, 1990. Critical hyperglycemia was defined as glucose > 400 mg/dL and critical hypoglycemia as < 40 mg/dL. During the study period, 1,129 patients received 3,054 days of care, including 88 patients who received 705 days of TPN. Of 4,985 glucose determinations performed during the study period, 48 (0.96%) were critically abnormal. Critical hyperglycemia occurred in 1.7 per cent of blood samples from TPN patients, compared to 0.7 per cent in non-TPN patients (P < 0.005). However, the mean admission and daily and maximum severity of illness scores were significantly higher in TPN patients compared to non-TPN patients (all P < 0.0005). Mean glucose levels rose with increasing SAPS in both TPN and non-TPN patients. When stratified by severity of illness, TPN patients did not have significantly higher glucose levels than non-TPN patients except for the SAPS = 15 category. The authors conclude that the glucose intolerance noted in critically ill TPN patients reflects their underlying severity of illness rather than TPN administration per se.

Aged↗

PubMed2000

Trends in pulmonary function in patients with cystic fibrosis correlate with the degree of glucose intolerance at baseline.

In patients with cystic fibrosis, CF-related diabetes mellitus (CFRD) has been associated with increased morbidity and mortality. Whether glucose intolerance is also associated with poor outcomes is unclear. To better define these relationships we prospectively followed a group of 152 patients with CF without diabetes for 4 yr. Patients were classified as having normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or CFRD without fasting hyperglycemia (CFRD-No FH). FEV(1), FVC, and body mass index (BMI) were measured at baseline and quarterly. At baseline 45% of the patients had NGT, 38.8% had IGT, and 15.8% had CFRD-No FH. FEV(1), FVC, and BMI at baseline were comparable among these groups (all p > 0.1). After 4 yr an overall decline in FEV(1) and FVC occurred, with no change in BMI. The rates of decline for FEV(1) and FVC correlated with the glucose tolerance groups, with the highest rates of decline occurring among the CFRD-No FH group. In addition, patients in the lowest quartile for insulin production at baseline experienced the highest rates of pulmonary function decline over time, suggesting a relationship between insulin deficiency and clinical deterioration. We conclude that the degree of glucose intolerance is a strong determinant of future lung function decline in patients with CF.

Adolescent↗

PubMed1991

Hepatic dearterialisation induces glucose intolerance and inhibits insulin secretion in patients with liver malignancy.

Intermittent hepatic dearterialisation is used in palliation of liver malignancy. In rats hepatic dearterialisation is accompanied by glucose intolerance and impaired insulin secretion, but it is not known if similar effects occur in man. Six patients with nonresectable liver malignancy were subjected to an intravenous glucose (50 g) challenge before dearterialisation (control challenge), during a 1-hour dearterialisation period, and in the immediate reperfusion phase after the end of 1-hour dearterialisation. Insulin secretion, as judged by the plasma levels of both insulin and C peptide, was inhibited during the 1-hour dearterialisation, while the glucose elimination rate was delayed (both p less than 0.03). Contrastingly, in the immediate reperfusion phase both insulin secretion and glucose elimination did not differ from values after the control challenge. We therefore conclude that hepatic dearterialisation in patients with liver malignancy is accompanied by inhibited insulin secretion and glucose intolerance, both readily reversible.

Aged↗

PubMed1991

Abrogation of dominant glucose intolerance in SJL mice by a growth hormone transgene.

Glucose tolerance was studied in transgenic mice (SJL x C57BL/6) expressing human GH under the control of a housekeeping promoter. Parental SJL mice were found to harbour a dominant allele, termed here glid, determining glucose intolerance in pure-bred animals and in F1 hybrids with glucose-tolerant C57BL/6 mice. Blood glucose levels in transgenic SJL x C57BL/6 hybrid mice were well controlled following glucose challenge, whereas non-transgenic hybrids failed to control their glucose adequately. Pancreatic morphology was normal in all animals. In confirmation of a physiological role for GH in glucose regulation. GH-deficient lit/lit mice were pathologically sensitive to glucose.

Alleles↗

PubMed1998

Bromocriptine reduces obesity, glucose intolerance and extracellular monoamine metabolite levels in the ventromedial hypothalamus of Syrian hamsters.

We examined whether reductions in body fat stores and insulin resistance in Syrian hamsters induced by bromocriptine are associated with reductions in daily norepinephrine (NE) and serotonin activities as indicated by their extracellular metabolite levels in the ventromedial hypothalamus (VMH). High levels of these monoamines within the VMH have been suspected to induce obesity and insulin resistance. Microdialysate samples from the VMH of freely moving obese male hamsters (BW: 208 +/- 5 g) were collected hourly over a 25-hour period before bromocriptine treatment, during the first day of and after 2 weeks of bromocriptine treatment (800 microg/animal daily, i.p.), and body composition and glucose tolerance analyses were conducted before and after 2 weeks of treatments. The microdialysate samples were analyzed by HPLC for metabolites of serotonin: 5-hydroxy-indoleacetic acid (5-HIAA), NE: 3-methoxy-4-hydroxy-phenylglycol (MHPG), and dopamine: homovanillic acid (HVA). Bromocriptine treatment for 14 days significantly reduced body fat by 60% and areas under the glucose and insulin curves during a glucose tolerance test by 50 and 46%, respectively. Concurrently, extracellular VMH contents of 5-HIAA, MHPG, and HVA were reduced by 50, 29 and 66%, respectively (p < 0.05). Similarly, VMH 5-HIAA and MHPG contents were 48 and 44% less, respectively (p < 0.05), in naturally glucose-tolerant hamsters compared with naturally glucose-intolerant hamsters. Bromocriptine induced reductions of body fat, and improvements in glucose intolerance may result in part from its ability to decrease serotonin and NE activities in the VMH.

Adipose Tissue↗

PubMed1991

Nifedipine vs. enalapril in treatment of hypertensive patients with glucose intolerance.

To compare the metabolic effects of nifedipine and enalapril, we studied 21 obese patients (BMI of 31.6 +/- 1.1) with mild-to-moderate hypertension and glucose intolerance. None of the patients were receiving insulin or hypoglycemic agents. After a washout period of 15 days, blood pressure was recorded and fasting blood glucose, insulin, and lipid concentrations were determined. At random, 11 patients were started on nifedipine and 10 patients on enalapril. At the 90th day of treatment, clinical and laboratory tests were again performed. Both of the drugs reduced blood pressure values comparably. No significant variation of metabolic parameters was found after 90 days of treatment in the enalapril group. In the nifedipine group, the fasting insulin level was decreased and the glucose/insulin ratio was significantly increased, suggesting an improvement in insulin sensitivity; moreover, total plasma cholesterol was significantly reduced. Enalapril and nifedipine seem to be effective and safe drugs in the treatment of hypertensive subjects with obesity and glucose intolerance. Nifedipine can ameliorate insulin resistance and the lipid state.

Blood Glucose↗

PubMed2004

Glucose intolerance, as reflected by hemoglobin A1c level, is associated with the incidence and severity of transplant coronary artery disease.

OBJECTIVES: The possible effect of plasma hemoglobin A(1c) (HbA(1c)) on the development of transplant coronary artery disease (TxCAD) was investigated. BACKGROUND: Glucose intolerance is implicated as a risk factor for TxCAD. However, a relationship between HbA(1c) and TxCAD has not been demonstrated. METHODS: Plasma HbA(1c) was measured in 151 adult patients undergoing routine annual coronary angiography at a mean period of 4.1 years after heart transplantation. Intracoronary ultrasound (ICUS) was also performed in 42 patients. Transplant CAD was graded by angiography as none, mild (stenosis in any vessel < or =30%), moderate (31% to 69%), or severe (> or =70%) and was defined by ICUS as a mean intimal thickness (MIT) > or =0.3 mm in any coronary artery segment. The association between TxCAD and established risk factors was examined. RESULTS: Plasma HbA(1c) increased with the angiographic grade of TxCAD (5.6%, 5.8%, 6.4%, and 6.2% for none, mild, moderate, and severe disease, respectively; p < 0.05 for none vs. moderate or severe) and correlated with disease severity (r = 0.24, p < 0.05). The HbA(1c) level was higher in patients with MIT > or =0.3 mm than in those with MIT <0.3 mm (6.4% vs. 5.7%, p < 0.05). Multivariate logistic regression analysis identified HbA(1c) as an independent predictor of TxCAD, as detected by angiography or ICUS (odds ratios 1.9 and 2.4, 95% confidence intervals 1.5 to 6.3 [p = 0.010] and 1.3 to 4.2 [p < 0.005], respectively). CONCLUSIONS: Persistent glucose intolerance, as reflected by plasma HbA(1c), is associated with the occurrence of TxCAD and may play an important role in its pathogenesis.

Adolescent↗

PubMed2007

Prevalence of glucose intolerance in primary hyperparathyroidism and the benefit of parathyroidectomy.

BACKGROUND: Increased prevalence of diabetes mellitus (DM) in primary hyperparathyroidism (PHPT) is established, but not glucose intolerance (GI), nor benefit from parathyroidectomy on GI. We determined these during management of a continuous series of patients with PHPT routinely followed after surgery. PATIENTS AND METHODS: WHO criteria classified 75 g oral glucose tolerance tests (OGTT) in 51/54 consecutively proven PHPT patients, into normal glucose tolerance (NGT), DM, impaired glucose tolerance (IGT) or impaired fasting glucose (IFG); GI was derived by adding those with DM and IGT/IFG. OGTT were repeated after parathyroidectomy (mean follow up 2.4 +/- SD 1.6 years). Paired student t tests were used to compare fasting and 2-h plasma glucose (PG). RESULTS: At presentation 32/54 patients (59%) had NGT, 10 IGT/IFG (19%) and 12 type 2 DM (22%), nine newly diagnosed. Before parathyroidectomy 17/35 patients had NGT (49%), 18 GI (51%), 12 DM (34%) and 6 IGT/IFG (17%). Five out of six patients with IGT/IFG had NGT, one with NGT developed IGT. At completion 23 patients (66%) had NGT, 12 GI (34%), 4 IGT/IFG (11%) and 8 DM (23%). After parathyroidectomy fasting and 2-h. PG fell in 30/34 normocalcaemic patients not on hypoglycaemic agents, 5.6 +/- 1.0 to 5.4 +/- 0.8 mmol/l, 7.2 +/- 3.0 to 6.3 +/- 3.1 mmol/l (p < 0.05, p < 0.01). CONCLUSIONS: 1. At presentation with PHPT, OGTT commonly identifies Type 2 DM and GI.2. After successful parathyroidectomy fasting and 2-h. PG fall significantly (p < 0.05, p < 0.01). DM and IGT/IFG often ameliorates to IGT or NGT, persistently.

Adult↗

PubMed2006

Mechanism of glucose intolerance in mice with dominant negative mutation of CEACAM1.

Mice with liver-specific overexpression of dominant negative phosphorylation-defective S503A-CEACAM1 mutant (L-SACC1) developed chronic hyperinsulinemia resulting from blunted hepatic clearance of insulin, visceral obesity, and glucose intolerance. To determine the underlying mechanism of altered glucose homeostasis, a 2-h hyperinsulinemic euglycemic clamp was performed, and tissue-specific glucose and lipid metabolism was assessed in awake L-SACC1 and wild-type mice. Inactivation of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) caused insulin resistance in liver that was mostly due to increased expression of fatty acid synthase and lipid metabolism, resulting in elevated intrahepatic levels of triglyceride and long-chain acyl-CoAs. Whole body insulin resistance in the L-SACC1 mice was further attributed to defects in insulin-stimulated glucose uptake in skeletal muscle and adipose tissue. Insulin resistance in peripheral tissues was associated with significantly elevated intramuscular fat contents that may be secondary to increased whole body adiposity (assessed by (1)H-MRS) in the L-SACC1 mice. Overall, these results demonstrate that L-SACC1 is a mouse model in which chronic hyperinsulinemia acts as a cause, and not a consequence, of insulin resistance. Our findings further indicate the important role of CEACAM1 and hepatic insulin clearance in the pathogenesis of obesity and insulin resistance.

Acyl Coenzyme A↗

PubMed1996

Effect of estrogen on hyperprolactinemia-induced glucose intolerance in SHN mice.

The effects of prolactin (PRL) on circulating levels of glucose and insulin, and of estradiol on hyperprolactinemia-induced glucose intolerance of tissues were studied in pituitary-grafted SHN mice (PG mice) and sham-operated controls. Pituitary grafting (PG) decreased blood glucose levels in male mice at 1 and 3 months after the operation but did not alter those in females. PG had little effect on serum insulin levels in males, but increased those in females. In female mice at 2 months after PG, blood glucose levels were significantly higher at 1, 2, and 4 hr after glucose load when compared with those in controls. In contrast, there was no significant difference in blood glucose levels after glucose load between male PG and control mice. The rate at which blood glucose levels decreased was slower in female PG mice than in controls during the 30 min after insulin injection, whereas there was no difference in the rate after insulin injection between male PG and control mice. In ovariectomized (Ovx) mice, no significant difference was found in the blood glucose levels after a glucose load between PG and control groups at 2 months after PG. In Ovx mice treated daily with estrogen, however, a PG-dependent high level of blood glucose was observed after glucose load. These results suggest that hyperprolactinemia decreases glucose tolerance via an increase in insulin resistance in female SHN mice and that estrogen is essential to the expression of the PRL effect.

Animals↗

PubMed2006

Activation of cannabinoid CB1 receptors induces glucose intolerance in rats.

Recent reports have described the presence of cannabinoid CB1 receptors in pancreatic islets. Here we show that administration of the endogenous cannabinoid anandamide or the selective cannabinoid CB1 receptor agonist Arachidonyl-2'-chloroethylamide (ACEA) results in glucose intolerance after a glucose load. This effect is reversed by the selective cannabinoid CB1 receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251). These results suggest that targeting cannabinoid CB1 receptors may serve as new therapeutic alternatives for metabolic disorders such as diabetes.

Animals↗