Effect Of Glycemia Research Articles

Understanding persistent gender gaps in STEM.

Does achievement matter differently for men and women?

Non-invasive evaluation of retinal vascular remodeling and hypertrophy in humans: intricate effect of ageing, blood pressure and glycaemia.

Ageing, hypertension and diabetes have an intricate effect on microvascular structure. In the retina, the respective contribution of remodeling and hypertrophy in such process is still unclear. We aimed at disentangling age, blood pressure and glycaemia effects onretinal microcirculation using the non-invasive adaptive optics ophthalmoscopy (AOO). We included 429 subjects, distributed into 4 groups according to normal (nBP) or high blood pressure (hBP) and/or normal (nGly) or high fasting glycaemia (hGly). The nBP/nGly group was stratified in age tertiles to isolate theeffect of ageing. AOO was used to measure arteriolar wall thickness (WT, µm), arteriolar (aID, µm) and venular internal diameter (vID, µm) and calculate arteriolar wall-to-lumen ratio (WLR), wall cross-sectional area (WCSA, µm2). One-way ANOVA for parametric variables and Kruskal-Wallis test for non-parametric variables were used for comparison among groups. A multivariate regression analysis including age, gender, BP, hGly and antihypertensive treatment was performed to calculate independent predictors of retinal remodeling. WT was increased with ageing (tertile1: 22.5 ± 3.2, tertile2: 24.2 ± 3.5, tertile 3: 25.2 ± 3.8, p = 0.001) and BP (hBP: 25.2 ± 4.1 vs nBP: 23.9 ± 3.7, p = 0.003). aID decreased with BP (hBP: 90.2 ± 13.4 vs nBP: 93.6 ± 11.6, p = 0.013) and increased with glycaemia (hGly: 97.7 ± 12.5 vs nGly: 93.6 ± 11.6, p = 0.002). Amultivariate analysis showed independent association of hBPwithWLR; hGly withWCSA; ageing with WLR and WCSA. AOO non-invasively identifies retinal structural changes in human confirming that microvascular remodeling is exclusively related to hypertension, whereas vascular growth is related to ageing and hyperglycaemia.

The Effect of Glycemia on Choroidal Thickness in Different Stages of Diabetic Retinopathy

Objective: The purpose of this study was to evaluate the influence of renal and glycemic parameters on choroidal thickness (CT) in patients with diabetes with and without diabetic retinopathy (DR). Methods: This cross-sectional study included patients with and without diabetes. Patients underwent comprehensive ocular examination. CT was obtained using spectral-domain optical coherence tomography (SD-OCT) with enhanced depth imaging (EDI) mode. Clinical parameters were body mass index, mean arterial pressure, glycated hemoglobin, fasting plasma glucose, estimated glomerular filtration rate, and capillary plasma glucose (CPG) a few minutes before EDI-SD-OCT. Results: The study included 275 participants: 42 with diabetes and no DR, 43 with mild nonproliferative diabetic retinopathy (NPDR), 46 with moderate NPDR, 39 with severe NPDR, 24 with proliferative diabetic retinopathy (PDR), 40 with previous panretinal photocoagulation (PRP) treatment for DR, and 41 without diabetes. The diabetic patients had thinner subfoveal CT than the nondiabetic participants (280.5 ± 83.4 vs. 327.1 ± 48.8 µm, p < 0.001). After multivariable adjustment, CT was significantly correlated with age, DR stage, and CPG. In patients with mild and moderate NPDR, a higher level of CPG was associated with thicker CT. This relationship was not found in patients with PDR. Conclusion: CPG had the strongest correlation with CT in patients with NPDR (mild, moderate, and severe), but not in PDR and PRP PDR patients. Our study suggests that the glucose level at the time of the test should be aggregated to other systemic and ocular parameters, such as age and axial length, when studying the choroid using SD-OCT.

Effects of Glycemia on Immediate Complications Followings Cabg

ObjectiveWe investigated the relationship between postoperative glucose levels (days 1 through 3) and immediate outcomes in patients who underwent isolated coronary artery bypass grafting (CABG). MethodsWe conducted a retrospective study of 2,558 consecutive patients who had isolated CABG. Patients were stratified into 3 groups based on their pre-operative mortality risk (MR), using Society of Thoracic Surgeons’ criteria. Average glucose levels for the first 3 days following surgery were determined. Glucose levels for each group were divided into quartiles and related to relevant outcomes. Odds ratios assessing changes in outcomes as functions of increased glucose exposure were determined for postoperative days 1, 2, and 3 and for postoperative days 1 and 2 and 1 through 3. ResultsThe number of patients in each MR group (1 through 3; low, medium, and high) was 1,233, 852, and 473, respectively. Mean ± SD quartile glucose levels for days 1 and 2 were 133 ± 8.2, 150.4 ± 4.7, 167.2 ± 6.89, and 205.9 ± 24.9 mg/dL. The proportion of patients with a glucose level <70 mg/dL was 6.4%, <60 mg/dL was 2.7%, and <50 mg/dL was 1.1%.The most consistent and significant correlations between glucose quartiles and outcomes were observed for MR group 1, and they were most significant for the first 2 days following surgery. Glycemic control was not correlated with mortality, but it was correlated with total complications. ConclusionHyperglycemia during the first two days after CABG adversely affected total complications in patients who were in the low and medium MR groups, but it did not significantly affect hospital mortality. (Endocr Pract. 2013;19:928-936)

Effect of Glycemia on Plasma Incretins and the Incretin Effect During Oral Glucose Tolerance Test

The incretin effect, reflecting the enhancement of postprandial insulin secretion by factors including the intestinal hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, increases in proportion to meal size. However, it is unknown whether the incretin effect is dependent on ambient glucose. The goal of this study was to determine the effect of plasma glycemia on the incretin effect. Thirteen healthy subjects consumed 50 g oral glucose solution mixed with d-xylose during fixed hyperglycemia at 8 and 10.5 mmol/L, on 3 separate days, twice at lower glycemia (LOW) and once at higher values (HIGH). The relative increase in insulin release after glucose ingestion at fixed hyperglycemia, a surrogate for the incretin effect, was similar among all three studies. The GLP-1 response to oral glucose was significantly lower at higher plasma glycemia, as was the appearance of d-xylose after the meal. Between the two LOW studies, the reproducibility of insulin release in response to intravenous glucose alone and intravenous plus ingested glucose was similar. These findings indicate that the incretin contribution to postprandial insulin release is independent of glycemia in healthy individuals, despite differences in GLP-1 secretion. The incretin effect is a reproducible trait among humans with normal glucose tolerance.

O-03 Comparison of two different glycaemia protocols for coronary artery surgery on postoperative cognitive dysfunction

Postoperative cognitive dysfunction is a well known phenomenon after cardiac surgery [1]. Tight glycaemic control has been shown to improve survival and to reduce morbidity in coronary surgery [2]. The effects of glycaemia on neurological outcome are quite limited except for focal neurological injury of this surgical population. The aim of this study was to compare two different glycaemia protocols, tight or liberal, on postoperative cognitive function.

Contributions of dysglycaemia, obesity, and insulin resistance to impaired endothelium‐dependent vasodilation in humans

Individual effects of hyperglycaemia and obesity to impair vascular health are recognized. However, the relative contributions of dysglycaemia versus other obesity-related traits to vascular dysfunction have not been systematically evaluated. We undertook a cross-sectional evaluation of factors contributing to vascular function in 271 consecutive subjects, categorized as non-obese normal glucose tolerant (n = 115), non-obese dysglycaemic (n = 32), obese normal glucose tolerant (n = 57), obese dysglycaemic (n = 38), or type 2 diabetic (n = 29). Vascular function was measured invasively as leg blood flow responses to methacholine chloride, an endothelium-dependent vasodilator. Categorical and continuous analyses were carried out to assess the contributions of hyperglycaemia to vascular dysfunction. Even among normoglycaemic subjects, obese subjects had impaired vascular function compared to non-obese subjects (p = 0.004). Vascular function was also impaired in non-obese dysglycaemic subjects (p = 0.04 versus non-obese normoglycaemic subjects), to a level comparable to normoglycaemic obese subjects. Within obese subject groups, gradations of dysglycaemia including the presence of diabetes were not associated with further worsening of these vascular responses beyond the effect of obesity alone (p = not significant comparing all obese groups, p < 0.001 versus lean normoglycaemic subjects). After univariate and multivariable modelling analyses we found that effects of glycaemia were less powerful than effects of insulin resistance and obesity on vascular dysfunction. Dysglycaemia contributes to impaired vascular function in non-obese subjects, but obesity and insulin resistance are more important determinants of vascular function in obese and diabetic subjects.

Effect of glycemia and blood-lipid in patients with type 2 diabetes educated by diabetes conversation map

Objective To observe the effect of diabetes conversation map in treatment of patients with type 2 diabetes (T2DM). Methods From Sep 2009 to July 2010, 110 patients with T2DM were randomly classified into two groups, which observation group were educated with diabetes conversation map and control group with traditional models. The fasting blood glucose (FBG), postal blood glucose(PBG), HbA1c and bloodlipid were observed between the two groups. Results Compared with pre-education, the FPG, PBG and HbA1c were significantly decreased (P ＜0. 05) after education in both groups. Compared with traditional model group,LDL-C were significantly decreased (P ＜0. 05) after education by diabetes conversation map. The TC、TG and HDL-C were no statistically significant (P ＞ 0. 05); FBG、 PBG、 HbA1c、 LDL-C were statistically significant (P ＜0. 05 or P ＜ 0. 01) after education in both groups. Conclusions Diabetes conversation map education model can decrease glycemia, improve the dyslipidemia, and was an effective education model in T2DM. Key words: Diabetes conversation map; Diabetes,2 type; Glycemia; Blood-lipid

The Association Between Glycemia and Endothelial Function in Nondiabetic Individuals: The Importance of Body Weight

The aim of this study was to examine the association between glycemia and markers of early atherosclerosis in healthy nondiabetic individuals. In 309 individuals without diabetes or symptomatic cardiovascular disease, we assessed long-term glycemia by glycosylated hemoglobin (HbA1c) and endothelial function by flow-mediated dilatation (FMD) in the brachial artery. HbA1c was negatively associated with FMD (r = -0.162, P = 0.004). Multivariate linear regression analysis after adjusting for common risk factors of cardiovascular disease showed that BMI was an effect modifier of the association between HbA1c and FMD (P = 0.034 for the HbA1c x BMI interaction). We stratified the FMD outcome data into two groups separated by the median BMI (group 1: BMI < or = 26.1 kg/m(2) and group 2: BMI > 26.1 kg/m(2)). In the lower BMI group, HbA1c was an independent predictor of FMD even when adjusted for confounding factors associated with impaired glucose metabolism (r = -0.215, P = 0.009), but in the higher BMI group HbA1c was not associated with FMD (r = -0.051, P = 0.5). In a nondiabetic population, long-term glycemia was associated with endothelial dysfunction only in lean individuals. In the overweight individuals, this association was not apparent, possibly because some of the mechanisms that mediate the effect of glycemia on vascular function are shared by obesity.

High Incidence of Glucose Intolerance in Asian-Indian Subjects With Acute Coronary Syndrome

The risk of diabetes and coronary heart disease is high in Asian Indians. In this study, we aim to assess 1) the prevalence of hyperglycemia in incident acute coronary syndrome (ACS), 2) the effect of glycemia on the outcome, and 3) the association of plasma levels of insulin and proinsulin with ACS. A total of 146 nondiabetic subjects (121 men, 25 women) with ACS admitted to two hospitals in 1 year were enrolled. Random blood glucose at admission and a standard oral glucose tolerance test within 3 days were done. Glucose tolerance was categorized as normal glucose tolerance, impaired glucose tolerance (IGT) or impaired fasting glucose, and diabetes. Diabetes was arbitrarily classified further as undiagnosed (HbA1c [A1C] >6.0%) or possibly stress diabetes (A1C <6.0%). Subjects not on antidiabetic treatment were reassessed with a glucose tolerance test between 1 and 2 months. Fasting plasma specific insulin, proinsulin, their molar ratios, and insulin resistance (homeostasis model assessment) were estimated at baseline. Mean age of the cohort was 55 +/- 10.6 (SD) years. At baseline, 24 (16.4%) had normal glucose tolerance, 67 (45.9%) had IGT or impaired fasting glucose, and 55 (37%) had diabetes (35 [24%] were undiagnosed and 20 [13.7%] had stress diabetes). At follow-up, 53 of 92 responders (57.6%) continued to have IGT or diabetes. Mean baseline plasma insulin, proinsulin and its ratios, and insulin resistance were higher than normal in all subgroups. Nondiabetic Asian Indians showed a high prevalence of hyperglycemia following ACS. ACS was associated with insulin resistance and increased levels of specific insulin, proinsulin, and high proinsulin-to-insulin ratios.

Effect of glycemia on mortality in Pima Indians with type 2 diabetes.

The effect of plasma glucose concentration on overall and cause-specific mortality was examined in 1,745 Pima Indians (725 men, 1,020 women) > or = 15 years old with type 2 diabetes. During a median follow-up of 10.6 years (range 0.1-24.8), 533 subjects (275 men, 258 women) died; 113 of the deaths were attributable to cardiovascular disease, 96 to diabetes-related diseases (diabetic nephropathy for 92 of these), 249 to other natural causes, and 75 to external causes. After adjusting for age, sex, duration of diabetes, and BMI in a generalized additive proportional hazards model, higher baseline 2-h postload plasma glucose concentration predicted deaths from cardiovascular disease (P = 0.007) and diabetes-related diseases (P = 0.003), but not from other natural causes (P = 0.73). An increment of 5.6 mmol/l (100 mg/dl) in the 2-h plasma glucose concentration was associated with 1.2 times (95% CI 1.1-1.4) the death rate from cardiovascular disease, 1.3 times (95% CI 1.1-1.5) the death rate from diabetes-related diseases, and almost no change in the death rate from other natural causes (rate ratio = 1.0; 95% CI 0.94-1.1). In Pima Indians with type 2 diabetes, higher plasma glucose concentration predicts deaths from cardiovascular and diabetes-related diseases but has little or no effect on deaths from other natural or external causes.

Effects of glycaemia on glucose transport in isolated skeletal muscle from patients with NIDDM: in vitro reversal of muscular insulin resistance

Effects of glycaemia on glucose transport in isolated skeletal muscle from patients with NIDDM: in vitro reversal of muscular insulin resistance

Effects of glycaemia on glucose transport in isolated skeletal muscle from patients with NIDDM: in vitro reversal of muscular insulin resistance

We investigated the influence of altered glucose levels on insulin-stimulated 3-0-methylglucose transport in isolated skeletal muscle obtained from NIDDM patients (n = 13) and non-diabetic subjects (n = 23). Whole body insulin sensitivity was 71% lower in the NIDDM patients compared to the non-diabetic subjects (p < 0.05), whereas, insulin-mediated peripheral glucose utilization in the NIDDM patients under hyperglycaemic conditions was comparable to that of the non-diabetic subjects at euglycaemia. Following a 30-min in vitro exposure to 4 mmol/l glucose, insulin-stimulated 3-0-methylglucose transport (600 pmol/l insulin) was 40% lower in isolated skeletal muscle strips from the NIDDM patients when compared to muscle strips from the non-diabetic subjects. The impaired capacity for insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle was normalized following prolonged (2h) exposure to 4 mmol/l, but not to 8 mmol/l glucose. Insulin-stimulated 3-0-methylglucose transport in the NIDDM skeletal muscle exposed to 8 mmol/l glucose was similar to that of the non-diabetic muscle exposed to 5 mmol/l glucose, but was decreased by 43% (p < 0.01) when compared to non-diabetic muscle exposed to 8 mmol/l glucose. Despite the impaired insulin-stimulated 3-0-methylglucose transport capacity demonstrated by skeletal muscle from the NIDDM patients, skeletal muscle glycogen content was similar to that of the non-diabetic subjects. Kinetic studies revel a Km for 3-0-methylglucose transport of 9.7 and 8.8 mmol/l glucose for basal and insulin-stimulated conditions, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of glycemia on breathing movements and plasmaprostaglandin E concentrations in the sheep fetus

The purpose of this study was to determine the roles of fetal plasma glucose and prostaglandin E in controlling fetal breathing movements. Five late pregnant ewes with catheterized twin fetuses were fasted for 48 hours; one fetus was kept normoglycemic (by glucose infusion) and the other allowed to become hypoglycemic during this period. Fetal breathing movement and fetal and maternal plasma prostaglandin E and glucose concentrations were measured throughout. Data were analyzed by paired and unpaired t tests. The mean incidence of fetal breathing movement was significantly greater in the normoglycemic fetuses that in the hypoglycemic twins at the end of the fast (p less than 0.05), whereas plasma prostaglandin E levels increased significantly (p less than 0.05) and to the same extent in both groups of fetuses. The reduced incidence of ovine fetal breathing movement that occurs during maternal fasting appears to be primarily caused by fetal hypoglycemia and does not directly involve changes in fetal plasma prostaglandin E.

Effect of glycemia and nonesterified fatty acids on forearm glucose uptake in normal humans

The purpose of this study was to examine the effect of physiological plasma nonesterified fatty acid (NEFA) levels on insulin-stimulated forearm and whole body glucose uptake and substrate oxidation during euglycemia and hyperglycemia. Seven healthy men received Intralipid and heparin for 210 min in two studies, with saline as control in two further studies. Insulin (0.05 U.kg-1.h-1) was infused from 60 min, and euglycemia was maintained during lipid (EL) and control (EC) studies, and hyperglycemia was maintained in the other studies (HL and HC). Forearm NEFA uptake was comparable in the lipid studies (+61 +/- 10 and +52 +/- 8 nmol.100 ml forearm-1.min-1, EL and HL) and was suppressed in the controls. With Intralipid, forearm glucose uptake decreased during euglycemia but not during hyperglycemia (+3.85 +/- 0.34 vs. +3.34 +/- 0.25 mumol.100 ml forearm-1.min-1, EC vs. EL, P less than 0.02), with comparable changes in whole body glucose uptake. Glucose oxidation and forearm alanine release decreased with Intralipid at both blood glucose levels, with no significant change in the rates of nonoxidative glucose disposal. These observations support the operation of the glucose-fatty acid cycle at physiological plasma NEFA levels at both blood glucose concentrations, but this was associated with a decrease in peripheral insulin sensitivity only during euglycemia.

Hyperinsulinemia, upper body adiposity, and cardiovascular risk factors in non-diabetics

Previous studies have suggested that hyperinsulinemia and upper body adiposity are each separately associated with elevated BP and triglyceride (TG) levels, and with lower high density lipoprotein (HDL) cholesterol levels. The joint effect of hyperinsulinemia and upper body adiposity on lipids, lipoproteins, and BP, however, has not been previously studied. We hypothesized that the effect of body fat distribution on cardiovascular risk factors might be mediated through hyperinsulinemia. We measured BP, lipids and lipoproteins, HDL subfractions, and insulin and glucose concentrations as part of the San Antonio Heart Study, a population-based study of diabetes and cardiovascular risk factors. Insulinemia and glycemia were assessed as the sum of the fasting, half-hour, one-hour, and two-hour insulin and glucose levels, respectively, measured during a standardized oral glucose tolerance test. Individuals who had diabetes according to National Diabetes Data Group criteria were excluded from the analyses. In univariate analyses, both hyperinsulinemia and waist-to-hip ratio (WHR), a measure of upper body adiposity, were positively associated with TG and negatively associated with total HDL and HDL 2 cholesterol levels. However, when the effects of glycemia and insulinemia were controlled for by analysis of variance, WHR was no longer significantly related to TG levels. By contrast, WHR continued to be inversely related to total HDL and HDL 2 cholesterol even after adjustment for glycemia and insulinemia. Hyperinsulinemia was only weakly related to HDL cholesterol. These results suggest that insulinemia and glycemia might mediate the effects of upper body adiposity on TG, although not on HDL and HDL 2 cholesterol. Hyperinsulinemia was also positively associated with diastolic and systolic BP in men.

Vagal glucoreceptors in the small intestine of the cat.

1. In anaesthetized cats, the unitary activity of seventy-eight sensory vagal neurones was recorded in nodose ganglia by means of extracellular glass microelectrodes. 2. These neurones were stimulated by perfusion of the small intestine (duodenum and first part of jejunum) with glucose or other different carbohydrates at concentrations of 1--20 g/l. (i.e. 55--1100 m-osmole/l.). 3. The neurones were slowly adapting to stimulation and their discharge frequency was always low (1--30 Hz). 4. The activity of these neurones depended on the particular carbohydrate used and on its concentration: the discharge frequency generally increased when the concentration rose. 5. The neurones were of the C type (conduction velocities: 0.8--1.4 m/sec; mean, 1.1 m/sec). 6. In contrast with the known neurones connected to the gastro-intestinal tension receptors, they were not obviously activated by intestinal contractions or distensions. 7. In the same way, the stimuli which produced the response of other known endings, i.e. the mucosal receptors, were not effective; these stimuli included in particular stroking of the mucosa, over-distension of the bowel, intestinal perfusion with alkaline or acid solutions. On the other hand, the use of substances other than glucose (KCl and NaCl of the same osmolarity) showed that the osmotic pressure was not directly related to the receptor activation. 8. Therefore it is proposed to call the endings corresponding to these neurones 'glucoreceptors'. 9. The effect of glycaemia and intestinal motility were also studied. These variables acted presumably by changing the intestinal absorption rate. 10. The functional characteristics of the glucoreceptors (in particular the short latency of their response) strongly suggested that they were located close to the intestinal epithelium. 11. An ultrastructural study was performed in an attempt to identify the histological site of the receptors. Many non-medullated fibres were observed in the villi, especially beneath the epithelial layer. They gave complex branchings with abundant swellings. Some of them, at least, belonged to the vagal sensory component, because they were less numerous after unilateral selective sensory vagotomy. Therefore these complex endings could serve as the vagal glucoreceptors. 12. The roles of vagal intestinal glucoreceptors are discussed. Their functional characteristics as well as the clinical and experimental data suggest that they may be involved in the regulation of different types of alimentary behaviour (hunger, thirst, alliesthesia) and energy balance.