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PubMed1991

Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression.

Evidence is emerging for a direct role of glucose, independent of changes in insulin, in the regulation of cellular glucose transport and glucose utilization in vivo. In this study we investigate potential cellular and molecular mechanisms for this regulatory effect of glucose by determining how normalization of glycemia without insulin therapy in diabetic rats influences 3-O-methylglucose transport and the expression and translocation of two genetically distinct species of glucose transporters (GTs) in adipose cells. These results are compared with alterations in glucose disposal in vivo measured by euglycemic clamp. In rats rendered diabetic by 90% pancreatectomy, insulin-stimulated glucose transport in adipose cells is decreased 50% in parallel with reduced insulin-mediated glucose disposal in vivo. Levels of adipose/muscle GTs measured by immunoblotting are decreased in adipose cell subcellular membrane fractions, as are the corresponding mRNA levels assessed by Northern blotting of total adipose cell RNA. Normalization of blood glucose in diabetic rats with phlorizin, which impairs renal tubular glucose reabsorption and thus enhances glucose excretion, restores insulin-stimulated glucose transport in adipose cells and insulin-mediated glucose disposal in vivo. Importantly, levels of the adipose/muscle GT protein remain 43% reduced in the low-density microsomes in the basal state and 46% reduced in the plasma membranes in the insulin-stimulated state. Adipose/muscle GT mRNA levels remain approximately 50% depressed. Levels of the HepG2/brain GT protein and mRNA are unaltered by diabetes or phlorizin treatment. Thus, changes in ambient glucose independent of changes in ambient insulin can regulate the glucose transport response to insulin in isolated adipose cells and changes in responsiveness parallel alterations in glucose uptake in vivo. Since this effect can occur without alteration in the expression of the two species of glucose transporters present in adipose cells or in their translocation to the plasma membrane in response to insulin, it may result from changes in GT functional activity.

Adipose Tissue↗
PubMed2003

Glucose sensors and the alternate site testing-like phenomenon: relationship between rapid blood glucose changes and glucose sensor signals.

In the last few years blood glucose meters have been developed allowing glucose measurements in capillary blood samples collected at sites other than the fingertips. The main reason for establishing this so-called alternate site testing (AST) was to sample blood from locations with reduced pain perception. It is well known that capillary blood glucose is closely correlated to systemic (i.e., arterial) glucose levels and that under steady-state conditions, glucose values measured in blood samples collected from alternate sites are virtually identical to those collected from the fingertip. However, during rapid changes in blood glucose levels, glucose concentrations in capillary blood samples from the fingertips can differ considerably in both domains (time and concentration) from those determined in capillary blood from alternate sites (i.e., the so-called AST phenomenon). Such differences can have serious clinical consequences (e.g., risky delays in hypoglycemia detection). There is evidence that all skin sites exhibiting a reduced blood flow (in comparison with the fingertip) within the superficial skin layers are prone to this AST phenomenon. Nearly all glucose sensors having been developed so far or being currently under development measure glucose levels at alternate sites and also in another compartment [e.g., interstitial fluid (ISF)] than blood. So, in principle they might be prone to an AST-like phenomenon (i.e., rapid changes in systemic blood glucose levels may also result in delayed ISF glucose readings). Our knowledge about the impact of an AST-like phenomenon on the performance of glucose monitoring systems is presently very limited. Glucose kinetics in the different compartments during dynamic systemic blood glucose changes have not been fully elucidated yet. If an AST-like phenomenon plays a role with glucose sensors should therefore be studied. Depending on the measurement technology used for the individual type of glucose monitoring system probably this phenomenon has a variable impact on the results obtained.

Abdomen↗
PubMed1993

Heterogeneity in glucose sensitivity among pancreatic beta-cells is correlated to differences in glucose phosphorylation rather than glucose transport.

Rat beta-cells differ in their individual rates of glucose-induced insulin biosynthesis and release. This functional heterogeneity has been correlated with intercellular differences in metabolic redox responsiveness to glucose. The present study compares glucose metabolism in two beta-cell subpopulations that have been separated on the basis of the presence (high responsive) or absence (low responsive) of a metabolic redox shift at 7.5 mM glucose. Mean rates of glucose utilization and glucose oxidation in high responsive beta-cells were 2- to 4-fold higher than in low responsive beta-cells, whereas their leucine and glutamine oxidation was only 10-50% higher. This heterogeneity in glucose metabolism cannot be attributed to differences in GLUT2 mRNA levels or in glucose transport. In both cell subpopulations, the rates of glucose transport (13-19 pmol/min/10(3) beta-cells) were at least 50-fold higher than corresponding rates of glucose utilization. On the other hand, rates of glucose phosphorylation (0.3-0.7 pmol/min/10(3) beta-cells) ranged within those of total glucose utilization (0.2-0.4 pmol/min/10(3) beta-cells). High responsive beta-cells exhibited a 60% higher glucokinase activity than low responsive beta-cells and their glucokinase mRNA level was 100% higher. Furthermore, glucose phosphorylation via low Km hexokinase was detected only in the high responsive beta-cell subpopulation. Heterogeneity in glucose sensitivity among pancreatic beta-cells can therefore be explained by intercellular differences in glucose phosphorylation rather than in glucose transport.

Amino Acids↗
PubMed2001

Type I diabetes mellitus does not alter initial splanchnic glucose extraction or hepatic UDP-glucose flux during enteral glucose administration.

AIMS/HYPOTHESIS: Our aim was to determine whether an alteration in splanchnic glucose metabolism could contribute to postprandial hyperglycaemia in people with Type I (insulin-dependent) diabetes mellitus. METHODS: Splanchnic glucose extraction, hepatic glycogen synthesis and endogenous glucose production were compared in 8 Type I diabetic patients and in 11 control subjects. Endogenous hormone secretion was inhibited with somatostatin while insulin (approximately 550 pmol/l) and glucagon (approximately 130 ng/l) concentrations were matched with exogenous hormone infusions. Glucose containing [3-3H] glucose was infused into the duodenum at a rate of 20 micromol.kg(-1).min(-1). Plasma glucose concentrations were maintained at about 8.5 mmol/l in both groups by means of a separate variable intravenous glucose infusion. RESULTS: Initial splanchnic glucose uptake, calculated by subtracting the systemic rate of appearance of [3-3H] glucose from the rate of infusion of [3-3H] glucose into the duodenum, did not differ in the diabetic and non-diabetic patients (4.1 +/- 0.8 vs 3.0 +/- 1.0 micromol/kg/min). In addition, hepatic glycogen synthesis, measured using the acetaminophen glucuronide method did not differ (10.7 +/- 2.4 vs 10.1 +/- 2.7 micromol.kg(-1).min(-1)). On the other hand, suppression of endogenous glucose production, measured by an intravenous infusion of [6,6-2H2] glucose, was greater (p < 0.05) in the diabetic than in the non-diabetic subjects (1.7 +/- 1.6 vs 5.8 +/- 1.9 micromol.kg(-1).min(-1)). CONCLUSION/INTERPRETATION: When glucose, insulin and glucagon concentrations are matched in individuals with relatively good chronic glycaemic control, Type I diabetes does not alter initial splanchnic glucose uptake of enterally delivered glucose or hepatic glycogen synthesis. Alterations in splanchnic glucose metabolism are not likely to contribute to postprandial hyperglycaemia in people with well controlled Type I diabetes.

Blood Glucose↗
PubMed2002

C-reactive protein is more strongly related to post-glucose load glucose than to fasting glucose in non-diabetic subjects; the Insulin Resistance Atherosclerosis Study.

AIMS: It has been suggested that cardiovascular disease may be more strongly related to post-challenge glycaemia than to fasting glucose concentrations. We hypothesized that subclinical inflammation, as indicated by elevated serum levels of C-reactive protein (CRP), may partially explain the association of cardiovascular disease with post-challenge glycaemia. METHODS: We studied the relationship of CRP (measured with a highly sensitive immunoassay) with fasting glucose and 2-h glucose concentrations during an oral glucose tolerance test in non-diabetic subjects from the Insulin Resistance Atherosclerosis Study. RESULTS: Spearman correlation analyses and multiple linear regression analyses showed a significant association of both fasting glucose and 2-h glucose concentrations with CRP levels, after adjusting for demographic covariates (age, sex, ethnicity, clinical centre; Spearman correlation coefficients: r = 0.18 for fasting glucose, r = 0.27 for 2-h glucose, both P < 0.0001). However, after additional adjustment for body mass index and waist-hip ratio only 2-h glucose (and not fasting glucose) was significantly related to CRP (r = 0.03 for fasting glucose, P = NS; r = 0.14 for 2-h glucose, P < 0.0001). Adding insulin sensitivity to the multivariate models further weakened the relationship of CRP to 2-h glucose (r = 0.07, P < 0.05). CRP mean values increased by 2-h glucose category (normal vs. impaired glucose tolerance vs. isolated post-challenge hyperglycaemia). CONCLUSIONS: Chronic, subclinical inflammation, as indicated by elevated circulating CRP levels, is more strongly associated with post-challenge glycaemia than with fasting glucose levels in non-diabetic subjects. This association is partially independent of body fat and insulin resistance.

Adipose Tissue↗
PubMed1992

Assessment of glucose turnover rates in euglycaemic clamp studies using primed-constant [3-3H]-glucose infusion and labelled or unlabelled glucose infusates.

Underestimation of glucose turnover rates has been a problem in clamp studies using primed-constant [3-3H]-glucose infusion technique. Due to slow mixing in interstitial compartments concealed specific activity gradients may arise between plasma and interstitial compartments during intravenous unlabelled glucose infusion. Such specific activity gradients, however, can be prevented if plasma specific activity is maintained constant. Two euglycaemic clamp studies (insulin infusion 40 mU m-2 min-1) were performed in six lean normal subjects. Using conventional unlabelled glucose infusates plasma specific activity declined by 74%, tracer determined glucose appearance was smaller than actual glucose infusion rates (317 +/- 11 vs 366 +/- 15 mg m-2 min-1, p < 0.001), and erroneous negative values were calculated for glucose production (- 49 +/- 7 mg m-2 min-1). Average underestimation during the first 2 h correlated with glucose infusion rates (r = 0.88, p < 0.02). In contrast, when plasma specific activity was maintained constant, using appropriately labelled glucose infusates, tracer determined glucose appearance and glucose infusion rates were similar (385 +/- 16 vs 385 +/- 17 mg m-2 min-1), and negative errors for glucose production were avoided. In conclusion, using unlabelled glucose infusates, as in previous studies, suppression of glucose production is overestimated and stimulation of glucose utilization is underestimated. As errors were greater with larger glucose infusions, the mistakes may have been greatest in insulin sensitive control subjects, and smaller in insulin resistant subjects. Therefore, re-evaluation of hepatic insulin sensitivity seems appropriate in diabetes, obesity, and other insulin resistant states.

Adult↗
PubMed2000

Enhanced stimulation of glucose uptake by insulin increases exercise-stimulated glucose uptake in skeletal muscle in humans: studies using [15O]O2, [15O]H2O, [18F]fluoro-deoxy-glucose, and positron emission tomography.

In vitro studies have shown that insulin and exercise stimulate glucose uptake in part via distinct mechanisms. We determined whether a high rate of insulin-stimulated glucose uptake (good insulin sensitivity) is associated with an enhanced ability of exercise to increase glucose uptake in vivo in humans. In our study, 22 normal subjects performed one-legged isometric exercise for 105 min (45-150 min) under intravenously maintained euglycemic-hyperinsulinemic conditions (0-150 min). Rates of oxygen consumption, blood flow, and glucose uptake were quantitated simultaneously in skeletal muscle of both legs using [15O]O2, [15O]H2O, [18F]fluoro-deoxy-glucose, and positron emission tomography. The one-legged exercise, performed at an intensity of 11% of maximal isometric force, was designed to induce similar increases in oxygen consumption in both groups. In the entire group, exercise increased oxygen consumption from 2.3 +/- 0.3 ml x kg(-1) muscle x min(-1) (insulin) to 34.2 +/- 3. ml x kg(-1) muscle x min(-1) (insulin and exercise) (P < 0.001) and muscle glucose uptake from 60 +/- 6 pmol x kg(-1) muscle x min(-1) (insulin) to 220 +/- 22 micromol x kg(-1) muscle x min(-1) (insulin and exercise) (P < 0.001). The exercise-induced increase in glucose uptake was due to marked increases in blood flow (36 +/- 5 ml x kg(-1) muscle x min(-1) [insulin] vs. 262 +/- 20 ml x kg(-1) muscle x min(-1) [insulin and exercise], P < 0.001) rather than glucose extraction, which decreased from 2.0 +/- 0.2 mmol/l (insulin) to 1.0 +/- 0.1 mmol/1 (insulin and exercise) (P < 0.001). The subjects were classified according to their mean rate of whole-body insulin-stimulated glucose uptake into those with high (49 +/- 3 micromol x kg(-1) x min(-1)) and normal (27 +/- 2 micromol x kg(-1) x min(-1)) rates of insulin-stimulated glucose uptake. Both insulin-stimulated (2.4 +/- 1.1 vs. 2.3 +/- 1.2 ml x kg(-1) muscle x min(-1), normal vs. high insulin sensitivity) and exercise- and insulin-stimulated (33 +/- 6 vs. 34 +/- 4 ml x kg(-1) muscle x min(-1)) rates of oxygen consumption were comparable between the groups. Exercise increased glucose uptake more in the group with high insulin sensitivity (195 +/- 25 pmol x kg(-1) muscle x min(-1)) than in the group with normal insulin sensitivity (125 +/- 19 micromol x kg(-1) muscle x min(-1)) (P < 0.05). Muscle blood flow was closely correlated with the rate of oxygen consumption (r = 0.91, P < 0.0001), and insulin-stimulated (30 +/- 5 vs. 35 +/- 6 ml x kg(-1) muscle x min(-1)) and exercise-induced increments (222 +/- 31 vs. 228 +/- 23 ml x kg(-1) muscle x min(-1)) in muscle blood flow were similar between the groups. Glucose extraction remained higher in the group with high insulin sensitivity (1.2 +/- 0.2 mmol/l) than in the group with normal insulin sensitivity (0.7 +/- 0.1 mmol/l, P < 0.05). We conclude that whereas acute exercise per se increases glucose uptake via increasing glucose delivery, good insulin sensitivity modulates exercise-induced increases in glucose uptake by enhancing cellular glucose extraction.

Adult↗
PubMed1988

Over-estimation of glucose-6-phosphatase activity in brain in vivo. Apparent difference in rates of [2-3H]glucose and [U-14C]glucose utilization is due to contamination of precursor pool with 14C-labeled products and incomplete recovery of 14C-labeled metabolites.

Significant dephosphorylation of glucose 6-phosphate due to glucose-6-phosphatase activity in rat brain in vivo was recently reported (Huang, M., and Veech, R.L. (1982) J. Biol. Chem. 257, 11358-11363). The evidence was an apparent more rapid 3H than 14C loss from the glucose pool and faster [2-3H]glucose than [U-14C]glucose utilization following pulse labeling of the brain with [2-3H,U-14C]glucose. Radiochemical purity of the glucose and quantitative recovery of the labeled products of glucose metabolism isolated from the brain were obviously essential requirements of their study, but no evidence for purity and recovery was provided. When we repeated these experiments with the described isolation procedures, we replicated the results, but found that: 1) the precursor glucose pool contained detritiated, 14C-labeled contaminants arising from glucose metabolism, particularly 2-pyrrolidone-5-carboxylic acid derived from [14C]glutamine; 2) [14C]glucose metabolite were not quantitatively recovered; 3) the procedure used to isolate the glucose itself produced detritiated, 14C-labeled derivatives of [2-3H,U-14C]glucose. These deficiencies in the isolation procedures could fully account for the observations that were interpreted as evidence of significant glucose 6-phosphate dephosphorylation by glucose-6-phosphatase activity. When glucose was isolated by more rigorous procedures and its purity verified in the present studies, no evidence for such activity in rat brain was found.

Animals↗
PubMed1991

Glucose regulates both glucose transport and the glucose transporter gene expression in a hamster-derived pancreatic beta-cell line (HIT).

We studied the effect of chronic exposure to high glucose on the glucose transport regulation in hamster pancreatic Beta cells in permanent culture (HIT). Cells were exposed to either 5.5 mmol/l or 16.7 mmol/l glucose for 48 h and then glucose transport was studied by measuring the (3H)-2-deoxyglucose uptake for 5 and 10 min at 37 degrees C. The 2-deoxyglucose uptake was lower in cells pre-exposed to glucose 16.7 mmol/l for 48 h compared to cells pre-exposed to 5.5 (12.0 +/- 1.6 vs 19.1 +/- 1.2 nmol/0.1 mg after 5 min, and 22.2 +/- 2.6 vs 39.0 +/- 2.9 after 10 min respectively, mean +/- SEM, n = 5, p less than 0.01). In order to investigate the mechanism(s) for glucose impairment of glucose transport, we studied the glucose carrier gene expression in the same cells by Northern and slot-blot analysis. When total RNA was extracted from HIT cells cultured at either 5.5 or 16.7 mmol/l glucose and then hybridized to 32P-labelled cDNA probes for the glucose transporter 1, the glucose transporter 2 and beta-actin, a significant reduction of both glucose transporter 1 (-63.9 +/- 4.1%, mean +/- SEM, n = 3) and glucose transporter 2 (-48.9 +/- 3.2%) mRNA was observed in HIT cells cultured with high glucose. In the same experiments no change of beta-actin mRNA was observed, suggesting that the effect of high glucose was specific on the glucose-transporter mRNAs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Preservation of glucose tolerance and insulin secretory response to repeated glucose levels by the feeding of minimal glucose during prolonged fasting.

The facilitation of glucose disposal (Staub-Traugott effect) and potentiation of serum insulin (IRI) concentration normally occurring after closely spaced intravenous glucose loads, are known to disappear after prolonged starvation. To study the effects of minimal amounts of glucose during fasting upon the insulin response and disposal of repeated intravenous glucose tolerance tests, obese volunteers were fasted for a mean of 25 +/- 2 days, while receiving either 8 or 16 gm of oral glucose every 6 hr, and compared to totally fasted subjects without glucose supplementation. Weight loss rate and the fall in basal IRI and glucose levels were similar to those of totally fasted subjects. However, the Staub-Traugott effect and insulin secretory dynamics after stimulation by repetitive intravenous glucose loading were preserved by this glucose modified fast, while baseline serum glucagon levels (IRG) were significantly lower, and the basal IRI/IRG ratios were thus unchanged from the fed state. IRG and free fatty acid suppression were similar in the fed and glucose modified fasted states. Lactic acid levels increased as expected after the repeated glucose injections in the fed state, but failed to do so after the prolonged modified fast until the second and third repetitive glucose loads, in which a significant rise coincided with accelerated glucose disposal. It is suggested that minimal amounts of carbohydrate during fasting preserve the insulin potentiating action of glucose, preferentially sparing a delayed releasable pool of insulin, while protecting the glucose utilization mechanisms, including increased glycolysis, responsible for the Staub-Traugott effect.

Adult↗
PubMed1996

Epinephrine exerts opposite effects on peripheral glucose disposal and glucose-stimulated insulin secretion. A stable label intravenous glucose tolerance test minimal model study.

Epinephrine (EPI) plays a pivotal role in regulating glucose metabolism both in splanchnic and peripheral tissues. Nevertheless, previous studies did not clarify the mechanisms by which EPI affect both glucose disposal processes in peripheral tissues and beta-cell secretion. The aim of this study was to investigate, in six normal volunteers, the effects of elevated EPI concentration on peripheral glucose disposal and insulin secretion by using the stable labeled (either [6,6-2H2] or [2-2H1]glucose) intravenous glucose tolerance test (IVGTT) in conjunction with the minimal models of labeled glucose disappearance and C-peptide secretion. Elevated plasma EPI concentration significantly decreased glucose effectiveness (SG*) by 29% (0.0059 +/- 0.0013 vs. 0.0083 +/- 0.0011 min-1, P < 0.05), and even more, 61%, insulin sensitivity (SI*); (22 +/- 6 x 10(4) vs. 54 +/- 20 x 10(4) min-1.pmol.l-1; P < 0.01). These findings are not due to an isotopic effect induced by an enhanced glycogen breakdown, because the [2-2H1]glucose tracer, which is not incorporated into glycogen, gave results similar to those of [6,6-2H2]glucose tracer. No differences were observed in first phase cell sensitivity, phi 1, in the EPI study (199 +/- 91 vs. 245 +/- 144 10(9), NS), but there was a significant increase in the second-phase cell sensitivity to glucose phi 2, (15.2 +/- 1.7 vs. 17.7 +/- 4.4 10(9).min-1, P < 0.05). In conclusion, EPI selectively impairs peripheral glucose metabolism because of its unique ability to simultaneously and independently decrease glucose effectiveness and insulin sensitivity. Furthermore, EPI enhances phi 2, the ratio between the C-peptide amount secreted during the second phase and the area under the curve of the glucose signal, indicating that the observed increase of C-peptide concentration is due not only to the augmented glucose signal but also to a specific EPI-mediated enhancement of beta-cell responsivity to glucose.

Adult↗
PubMed1979

Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Glucose-turnover values and futile-cycle activities obtained with 14C- and 3H-labelled glucose.

1. A trace amount of glucose labelled with 14C uniformly and with 3H at position 2, 3 or 6 was injected intravenously into starved rats to measure the turnover rate of blood glucose. 2. Reliable estimates were made based on the semilogarithmic plot of specific radioactivity of the glucose contained in whole blood samples taken from the tail vein. 3. Glucose turned over more rapidly in hyperthyroid and more slowly in hypothyroid than in euthyroid rats. The percentage contribution of glucose recycling (determined from the difference in replacement rates between [U-14C]glucose and [6-3H]glucose) to the glucose utilization increased on induction of hyperthyroidism. 4. Futile cycles between glucose and glucose 6-phosphate (determined from the difference between replacement rates of [2-3H]glucose and [6-3H]glucose) were activated and inactivated by induction of hyperthyroid and hypothyroid states respectively. 5. The hepatic content of glycogen was much lower in hyper- and hypo-thyroid than in euthyroid rats. The enhanced glucose production in hyperthyroid rats resulted from not only activationof hepatic gluconeogenesis but also diversion of the final product of gluconeogenesis from liver glycogen to blood glucose. In hypothyroidism, the inhibition of gluconeogensis led to suppression of both glucose production and glycogenesis in the liver.

Animals↗
PubMed1992

Dissociated effects of 2-deoxy-D-glucose on D-[2-3H]glucose and D-[5-3H]glucose conversion into 3HOH in rat erythrocytes.

When rat erythrocytes were preincubated with 2-deoxy-D-glucose, the generation of both 3H-labelled acidic metabolites and 3HOH from D-[5-3H]glucose, the total production of L-lactate, and the generation of 14CO2, 14C-labelled acidic metabolites and 14C-labelled lactate from D-[1-14C]glucose or D-[U-14C]glucose were all lower than in erythrocytes preincubated in the absence of a hexose or in the presence of 3-O-methyl-D-glucose. However, preincubation with 2-deoxy-D-glucose failed to decrease the generation of 3H-labelled acidic metabolites and L-[3-3H]lactate from D-[2-3H]glucose, while decreasing the production of 3HOH more severely from D-[2-3H]glucose than from D-[5-3H]glucose. This may be attributable not solely to inhibition of D-glucose phosphorylation by 2-deoxy-D-glucose and 2-deoxy-D-glucose 6-phosphate, but also to inhibition by 2-deoxy-D-glucose 6-phosphate of hexose 6-phosphate interconversion in the reaction catalysed by phosphoglucoisomerase, as also observed with the purified enzyme. The generation of 3HOH from D-[2-3H]glucose should therefore be considered as a tool to assess the efficiency of interconversion of hexose 6-phosphates in the reaction catalysed by phosphoglucoisomerase, rather than to estimate D-glucose phosphorylation rate.

Animals↗
PubMed2002

Glucose monitoring at the thenar: evaluation of upper dermal blood glucose kinetics during rapid systemic blood glucose changes.

OBJECTIVE: We compared blood glucose measurements at the thenar with those at the fingertip during glucose increase and decrease that was rapid enough to induce glucose differences between the forearm and the fingertip. METHODS: A rapid glucose increase was induced by oral glucose; subsequently, a rapid glucose decrease was induced by intravenous insulin in 16 insulin-treated patients with diabetes. Capillary samples were taken in parallel from the thenar and fingertip. Different glucose monitors (FreeStyle, OneTouch Ultra, Soft-Sense) were used. Additional samples were taken from the forearm (n = 10 patients) in order to demonstrate that the blood glucose change achieved was rapid enough to principally induce glucose differences at alternative sites. RESULTS: Neither blood glucose at baseline (135 +/- 34 vs. 136 +/- 41 mg/dl, p = 0.86) nor glucose amplitude during increase (190 +/- 35 vs. 188 +/- 41 mg/dl, p = 0.65) or decrease (255 +/- 32 vs. 257 +/- 45 mg/dl, p = 0.83) differed significantly between the fingertip and the thenar. Intra-individual average thenar-fingertip glucose difference was - 2 +/- 12 (p = 1.00) and + 5 +/- 9 mg/dl (p = 0.11). In the subgroup, intra-individual average forearm-finger difference was - 50 +/- 19 (p < 0.01) and + 45 +/- 11 mg/dl (p < 0.01) during glucose-increase and decrease, respectively. There were no obvious device-specific differences. CONCLUSIONS: Blood glucose measurements at the thenar are a safe alternative to measurements at the fingertip at steady state as well as during blood glucose change that is sufficiently rapid to induce clinically relevant differences between forearm and fingertip.

Adolescent↗
PubMed2003

The 75-gram glucose load in pregnancy: relation between glucose levels and anthropometric characteristics of infants born to women with normal glucose metabolism.

OBJECTIVE: To investigate, in pregnant women without gestational diabetes mellitus (GDM), the relation among obstetric/demographic characteristics; fasting, 1-h, and 2-h plasma glucose values resulting from a 75-g glucose load; and the risk of abnormal neonatal anthropometric features and then to verify the presence of a threshold glucose value for a 75-g glucose load above which there is an increased risk for abnormal neonatal anthropometric characteristics. RESEARCH DESIGN AND METHODS: The study group consisted of 829 Caucasian pregnant women with singleton pregnancy who had no history of pregestational diabetes or GDM, who were tested for GDM with a 75-g, 2-h glucose load, used as a glucose challenge test, in two periods of pregnancy (early, 16-20 weeks; late, 26-30 weeks), and who did not meet the criteria for a GDM diagnosis. In the newborns, the following abnormal anthropometric characteristics were considered as outcome measures: cranial/thoracic circumference (CC/TC) ratio </=10th percentile for gestational age (GA), ponderal index (birth weight/length(3) x 100) >/=90th percentile for GA, and macrosomia (birth weight >/=90th percentile for GA), on the basis of growth standard development for our population. For the first part of the objective, logistic regression models were used to identify 75-g glucose load values as well as obstetric and demographic variables as markers for abnormal neonatal anthropometric characteristics. For the second part, the receiver operating characteristic (ROC) curve was performed for the 75-g glucose load values to determine the plasma glucose threshold value that yielded the highest combined sensitivity and specificity for the prediction of abnormal neonatal anthropometric characteristics. RESULTS: In both early and late periods, maternal age >35 years was a predictor of neonatal CC/TC ratio </=10th percentile and macrosomia, with fasting 75-g glucose load values being independent predictors of neonatal CC/TC ratio </=10th percentile. In both periods, 1-h values gave a strong association with all abnormal neonatal anthropometric characteristics chosen as outcome measures, with maternal age >35 years being an independent predictor for macrosomia. The 2-h, 75-g glucose load values were significantly associated in both periods with neonatal CC/TC ratio </=10th percentile and ponderal index >/=90th percentile, whereas maternal age >35 years was an independent predictor of both neonatal CC/TC ratio </=10th percentile and macrosomia. In the ROC curves for the prediction of neonatal CC/TC ratio </=10th percentile for GA in both early and late periods of pregnancy, inflection points were identified for a 1-h, 75-g glucose load threshold value of 150 mg/dl in the early period and 160 mg/dl in the late period. CONCLUSIONS: This study documented a significant association, seen even in the early period of pregnancy, between 1-h, 75-g glucose load values and abnormal neonatal anthropometric features, and provided evidence of a threshold relation between 75-g glucose load results and clinical outcome. Our results would therefore suggest the possibility of using a 75-g, 1-h oral glucose load as a single test for the diagnosis of GDM, adopting a threshold value of 150 mg/dl at 16-20 weeks and 160 mg/dl at 26-30 weeks.

Blood Glucose↗
PubMed1987

Memory improvement by glucose, fructose, and two glucose analogs: a possible effect on peripheral glucose transport.

The memory-improving action of post-training, noncontingent injections of glucose was investigated in a series of experiments which examined the effects of several substances that interact with glucose metabolism on the retention of a conditioned emotional response and on blood glucose levels in male hooded rats. Although post-training glucose injections of 1, 2, and 3 g/kg all produced similar increases in blood glucose, only 2 g/kg improved retention, suggesting that attainment of a particular blood glucose level is not critical for memory improvement. Post-training injections of a range of insulin doses (0.25-4 IU/kg) failed to affect retention. Post-training injection of fructose (the same doses as were used for glucose) had no effect on blood glucose levels and, as with glucose, only the 2 g/kg dose improved retention. This finding suggests that blood glucose levels are not critical for the memory-improving effect, that glucose and fructose may act on the same substrate and, because fructose does not act directly on the brain, it raises the possibility that both substances act peripherally. Post-training injections of 2-deoxyglucose and 3-O-methylglucose both improved retention. The fact that these mostly nonmetabolized glucose analogs were effective suggests that the memory-improving action of glucose may depend on the activation of a membrane glucose transport mechanism. The implications of the possible action of glucose on peripheral transport mechanisms for understanding the effect of reinforcers on memory are discussed.

3-O-Methylglucose↗
PubMed2006

[Characteristics of the daily blood glucose profiles of impaired glucose tolerance and type 2 diabetes mellitus subjects by continuous glucose monitoring system].

OBJECTIVE: To investigate the characteristics of daily glucose profiles of the impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) subjects by continuous glucose monitoring system (CGMS) so as to instruct the development of rational programs of treatment. METHODS: The CGMS data of 6 normal glucose tolerance (NGT), 10 IGT, and 20 newly diagnosed T2DM subjects were analyzed. RESULTS: (1) The values of average blood glucose, standard deviation of blood glucose, total time of plasma glucose > or = 7.8 mmol/L (T(PG) > or = 7.8 mmol/L) of the T2DM subjects were all significantly higher than those of IGT subjects (all P < 0.05), and these values of the IGI subjects were all significantly higher than those of the NGT subjects (all P < 0.05). The CGMS blood glucose profile excursion were also more and more fluctuant with the deterioration of glucose tolerance. (2) In the IGT group, the time of PG reaching peak was 109 minutes +/- 32 minutes and the daily time of PG > or = 7.8 mmol/L was 3.0 hours +/- 0.8 hours. In the newly diagnosed T2DM group, the time of PG reaching peak was 92 minutes +/- 22 minutes, and the daily time of PG > or = 11.1 mmol/L was 12.6 hours +/- 1.3 hours. The blood glucose increased more quickly and more sharply, and continued for more time after breakfast. CONCLUSIONS: (1) CGMS data accurately display the characteristics of daily 24 h blood glucose profiles of the IGT and newly diagnosed T2DM subjects, and CGMS examination helps instruct the development of rational treatment program. (2) In daily life, the time of PG > or = 7.8 mmol/L in IGT subjects was nearly 3 hours. (3) With the deterioration of glucose tolerance, the postprandial glucose peak is elevated higher and more rapidly, and the daily blood glucose profile excursion becomes more and more fluctuant.

Blood Glucose↗
PubMed2000

Regulation of the glucose-6-phosphatase gene by glucose occurs by transcriptional and post-transcriptional mechanisms. Differential effect of glucose and xylitol.

To understand how glucose regulates the expression of the glucose-6-phosphatase gene, the effect of glucose was studied in primary cultures of rat hepatocytes. Glucose-6-phosphatase mRNA levels increased about 10-fold when hepatocytes were incubated with 20 mm glucose. The rate of transcription of the glucose-6-phosphatase gene increased about 3-fold in hepatocytes incubated with glucose. The half-life of glucose-6-phosphatase mRNA was estimated to be 90 min in the absence of glucose and 3 h in its presence. Inhibition of the oxidative and the nonoxidative branches of the pentose phosphate pathway blocked the stimulation of glucose-6-phosphatase expression by glucose but not by xylitol or carbohydrates that enter the glycolytic/gluconeogenic pathways at the level of the triose phosphates. These results indicate that (i) the glucose induction of the mRNA for the catalytic unit of glucose-6-phosphatase occurs by transcriptional and post-transcriptional mechanisms and that (ii) xylitol and glucose increase the expression of this gene through different signaling pathways.

Animals↗