Glucose Infusion (glucose + infusion)

Distribution by Scientific Domains

Terms modified by Glucose Infusion

  • glucose infusion rate

  • Selected Abstracts


    Impact of glucose infusion on the structural and functional characteristics of adipose tissue and on hypothalamic gene expression for appetite regulatory neuropeptides in the sheep fetus during late gestation

    THE JOURNAL OF PHYSIOLOGY, Issue 1 2005
    B. S. Mühlhäusler
    In the present study, our aim was to determine whether intrafetal glucose infusion increases fetal adiposity, synthesis and secretion of leptin and regulates gene expression of the ,appetite regulatory' neuropeptides neuropepetide Y (NPY), agouti-related peptide (AGRP), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and receptors (leptin receptor (OB-Rb) and melancortin 3 receptor (MC3R)) within the fetal hypothalamus. Glucose (50% dextrose in saline) or saline was infused (7.5 ml h,1) into fetal sheep between 130 and 140 days gestation (term = 150 ± 3 days gestation). Glucose infusion increased circulating glucose and insulin concentrations, mean lipid locule size (532.8 ± 3.3 ,m2versus 456.7 ± 14.8 ,m2) and total unilocular fat mass (11.7 ± 0.6 g versus 8.9 ± 0.6 g) of the perirenal fat depot. The expression of OB-Rb mRNA was higher in the ventromedial nucleus compared to the arcuate nucleus of the hypothalamus in both glucose and saline infused fetuses (F= 8.04; P < 0.01) and there was a positive correlation between expression of OB-Rb and MC3R mRNA in the arcuate nucleus (r= 0.81; P < 0.005). Glucose infusion increased mRNA expression for POMC, but not for the anorectic neuropeptide CART, or the orexigenic neuropeptides NPY and AGRP, in the arcuate nucleus of the fetal hypothalamus. These findings demonstrate that increased circulating glucose and insulin regulate gene expression of the neuropeptides within the fetal hypothalamus that are part of the neural network regulating energy balance in adult life. [source]


    The circulating IGF system and its relationship with 24-h glucose regulation and insulin sensitivity in healthy subjects

    CLINICAL ENDOCRINOLOGY, Issue 6 2003
    Jan Frystyk
    Summary objective and design It has been suggested that circulating free IGF-I participates in glucose homeostasis and that IGFBP-1 reflects changes in insulin sensitivity. To study this further, we examined 10 healthy, nonobese subjects under standardized conditions for 24 h with and without an intravenous infusion of glucose, the latter in order to augment insulin sensitivity. Serum was collected every 2 h for analysis of free and total IGFs, IGFBP-1, , 2 and , 3 and the acid labile subunit (ALS). Insulin sensitivity was estimated at the end of each 24-h study period by use of the hyperinsulinaemic euglycaemic clamp technique. results Glucose infusion resulted in mild hyperglycaemia (P < 0·0001), a reduction in IGFBP-1 by approximately 40% (P < 0·0003), and increased insulin and C-peptide levels (P < 0·0001). Glucose infusion also increased insulin sensitivity (P < 0·003). However, despite the reduction in IGFBP-1, glucose infusion did not increase free IGF-I over the control level, and free IGF-II was slightly reduced (P < 0·02). Irrespective of glucose infusion, free IGF-I and -II remained stable during daytime (i.e. they were unresponsive to meal-related changes in plasma glucose), but both free fractions decreased during the night, reaching nadir at 04·00 h. None of the other members of the IGF system showed any relationship with plasma glucose levels. Finally, we failed to observe any relationship between changes in insulin sensitivity and the circulating IGF system. conclusion We found no evidence that the circulating IGF system is involved in meal-related blood glucose regulation or that it reflects short-term changes in insulin sensitivity in healthy, nonobese subjects. However, we cannot preclude that the observed changes in circulating IGFBP-1 may affect the glucose-lowering effect of IGF-I and -II at the local tissue level. [source]


    Glucose infusions into peripheral veins in the management of neonatal hypoglycemia , 20% instead of 15%?

    ACTA PAEDIATRICA, Issue 3 2010
    T Vanhatalo
    Abstract Aim: To establish whether peripheral intravenous 20% glucose solutions would cause less local irritation, fewer cannulation changes and less weight gain than 15% glucose in newborn infants. Methods: A total of 121 newborn infants with hypoglycemia were randomized to receive either 20% (group 20%, 60 infants) or 15% (group 15%, 61 infants) glucose infusions, which were initiated at 8 mg/kg/min rates and tapered according to the blood glucose levels. When the cannulation site had to be changed, signs of phlebitis at the previous cannulation site were scored (0,3). Number of cannulation site changes, durations of infusions and the infants' daily weights were recorded. Results: The median durations of infusions in groups 20 and 15% were 4 (range 2,7) days versus 4 (range 2,8) days and the median number of cannulation site changes were 1 (range 0,6) versus 1 (range 0,5), respectively. Thirty-six infants in group 20% and 37 in group 15% developed some phlebitis, median severity scores being 1 (range 0,7) versus 15% 1 (range 0,8). The weights during the treatment were also similar. Conclusion:, 20% and 15% glucose solutions can be infused equally safely into peripheral veins in neonates. [source]


    The role of intramuscular lipid in insulin resistance

    ACTA PHYSIOLOGICA, Issue 4 2003
    B. D. Hegarty
    Abstract There is interest in how altered lipid metabolism could contribute to muscle insulin resistance. Many animal and human states of insulin resistance have increased muscle triglyceride content, and there are now plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic glucose,fatty acid cycle. We postulate that muscle cytosolic accumulation of the metabolically active long-chain fatty acyl CoAs (LCACoA) is involved, leading to insulin resistance and impaired insulin signalling or impaired enzyme activity (e.g. glycogen synthase or hexokinase) either directly or via chronic translocation/activation of mediators such as a protein kinase C (particularly PKC , and ,). Ceramides and diacylglycerols (DAGs) have also been implicated in forms of lipid-induced muscle insulin resistance. Dietary lipid-induced muscle insulin resistance in rodents is relatively easily reversed by manipulations that lessen cytosolic lipid accumulation (e.g. diet change, exercise or fasting). PPAR agonists (both , and ,) also lower muscle LCACoA and enhance insulin sensitivity. Activation of AMP-activated protein kinase (AMPK) by AICAR leads to muscle enhancement (especially glycolytic muscle) of insulin sensitivity, but involvement of altered lipid metabolism is less clear cut. In rodents there are similarities in the pattern of muscle lipid accumulation/PKC translocation/altered insulin signalling/insulin resistance inducible by 3,5-h acute free fatty acid elevation, 1,4 days intravenous glucose infusion or several weeks of high-fat feeding. Recent studies extend findings and show relevance to humans. Muscle cytosolic lipids may accumulate either by increased fatty acid flux into muscle, or by reduced fatty acid oxidation. In some circumstances muscle insulin resistance may be an adaptation to optimize use of fatty acids when they are the predominant available energy fuel. The interactions described here are fundamental to optimizing therapy of insulin resistance based on alterations in muscle lipid metabolism. [source]


    Is postprandial hypertriglyceridaemia in relatives of type 2 diabetic subjects a consequence of insulin resistance?

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2005
    A. Kriketos
    Abstract Background, Higher postprandial triglyceride responses reported in first degree relatives of people with type 2 diabetes (REL) were postulated to be the result of an early, possibly intrinsic, defect in oral lipid handling. The postprandial triglyceride response to high fat meals (HFM) in normal subjects is reduced by the insulin response to dietary carbohydrate (CHO) in the meal. The aims of this study were to examine whether (1) insulin resistance is associated with an intrinsic defect in triglyceride handling in insulin-resistant REL and (2) insulin resistance is associated with altered triglyceride handling after HFM with high CHO content. Materials and methods, Postprandial responses to a HFM in normolipidaemic, normoglycaemic REL were compared with subjects without a family history of diabetes mellitus (CON). Over 6 h, the insulin, glucose, triglyceride and nonesterified fatty acid (NEFA) responses after a high fat (80 g fat), low CHO (HFM-LC; 20 g CHO, 4250 kJ) meal and a high fat, high CHO (HFM-HC; 100 g CHO, 5450 kJ) meal were examined. Results, The 10 (7F/3M) REL were significantly more insulin-resistant, determined by glucose infusion during a hyperinsulinaemic euglycaemic clamp than the 10 (5F/5M) CON (glucose infusion rate 44·6 ± 4·9 vs. 60·0 ± 4·8 µmol min,1 kg FFM,1, P = 0·037). Subjects were similar for age and body mass index (BMI). The triglyceride increments after the HFM-LC were similar in both, peaking at 180,240 min (,0·77 ± 0·11 mmol L,1), demonstrating no postprandial defect in REL, despite insulin resistance. There was a significantly lower postprandial triglyceride response in CON following the HFM-HC compared with the HFM-LC, but not in REL. In contrast, the higher insulin level during the HFM-HC was associated with significantly greater NEFA level suppression than in the HFM-LC (2·13 ± 0·51 vs. 0·70 ± 0·35 mmol L,1, P = 0·03), only in the REL. Conclusions, These results are inconsistent with a primary aetiological role for postprandial hypertriglyceridaemia in already insulin resistant type 2 diabetic REL, but raise the possibility that this potentially atherogenic manifestation is secondary to insulin resistance lessening VLDL production and/or release from the liver. [source]


    An insulin-resistant hypertriglyceridaemic normotensive obese dog model: assessment of insulin resistance by the euglycaemic hyperinsulinaemic clamp in combination with the stable isotope technique

    JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 3-4 2003
    E. Bailhache
    Summary Many studies have shown that in humans insulin resistance (IR) is associated with obesity and hypertriglyceridaemia. The aim of our study was to develop slowly dietary-induced obesity in dogs through long-term overfeeding of a high-fat diet, and to characterize this IR, hypertriglyceridaemic and normotensive model. Insulin resistance was assessed by the euglycaemic hyperinsulinaemic clamp technique. The contribution of hepatic glucose production during the clamp was evaluated using a constant stable-isotope-labelled glucose infusion. Overfeeding a high-fat diet for 7 months was associated with a 43 ± 5% body weight increase. Insulin resistance was characterized by hyperinsulinaemia in the unfed state (10 ± 1 vs. 24 ± 1 ,U/ml, in healthy and obese dogs, respectively, p < 0.02) and by a reduction of the insulin-mediated glucose uptake (28 ± 3 vs. 16 ± 1 mg/kg/min, p < 0.02). Hepatic glucose production suppression under insulin infusion allowed to conclude that this reduced glucose uptake resulted from a decrease of insulin sensitivity in obese dogs. Furthermore, animals remained normotensive and exhibited a marked hypertriglyceridaemia (0.26 ± 0.04 vs. 0.76 ± 0.15 mmol/l, in healthy and obese dogs, respectively, p < 0.02). Because hypertriglyceridaemia is the most common lipid abnormality in insulin-resistant humans, this dog with slowly induced obesity may constitute a good model to study the consequences of IR in lipid metabolism independently of vascular changes. [source]


    On the reliability of 13C metabolic modeling with two-compartment neuronal-glial models

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 15 2007
    Alexander A. Shestov
    Abstract Metabolic modeling of 13C NMR spectroscopy (13C MRS) data using two-compartment neuronal-glial models enabled non-invasive measurements of the glutamate-glutamine cycle rate (VNT) in the brain in vivo. However, the reliability of such two-compartment metabolic modeling has not been examined thoroughly. This study uses Monte-Carlo simulations to investigate the reliability of metabolic modeling of 13C positional enrichment time courses measured in brain amino acids such as glutamate and glutamine during [1- 13C]- or [1,6- 13C2]glucose infusion. Results show that the determination of VNT is not very precise under experimental conditions typical of in vivo NMR studies, whereas the neuronal TCA cycle rate VTCA(N) is determined with a much higher precision. Consistent with these results, simulated 13C positional enrichment curves for glutamate and glutamine are much more sensitive to the value of VTCA(N) than to the value of VNT. We conclude that the determination of the glutamate-glutamine cycle rate VNT using 13C MRS is relatively unreliable when fitting 13C positional enrichment curves obtained during [1- 13C] or [1,6- 13C2]glucose infusion. Further developments are needed to improve the determination of VNT, for example using additional information from 13C- 13C isotopomers and/or using glial specific substrates such as [2- 13C]acetate. © 2007 Wiley-Liss, Inc. [source]


    In vivo 13C magnetic resonance spectroscopy of human brain on a clinical 3 T scanner using [2- 13C]glucose infusion and low-power stochastic decoupling

    MAGNETIC RESONANCE IN MEDICINE, Issue 3 2009
    Shizhe Li
    Abstract This study presents the detection of [2- 13C]glucose metabolism in the carboxylic/amide region in the human brain, and demonstrates that the cerebral metabolism of [2- 13C]glucose can be studied in human subjects in the presence of severe hardware constraints of widely available 3 T clinical scanners and with low-power stochastic decoupling. In the carboxylic/amide region of human brain, the primary products of 13C label incorporation from [2- 13C]glucose into glutamate, glutamine, aspartate, ,-aminobutyric acid, and N-acetylaspartate were detected. Unlike the commonly used alkanyl region where lipid signals spread over a broad frequency range, the carboxylic carbon signal of lipids was found to be confined to a narrow range centered at 172.5 ppm and present no spectral interference in the absence of lipid suppression. Comparison using phantoms shows that stochastic decoupling is far superior to the commonly used WALTZ sequence at very low decoupling power at 3 T. It was found that glutamine C1 and C5 can be decoupled using stochastic decoupling at 2.2 W, although glutamine protons span a frequency range of ,700 Hz. Detailed specific absorption rate analysis was also performed using finite difference time domain numerical simulation. Magn Reson Med, 2009. © 2009 Wiley-Liss, Inc. [source]


    Intermittent hypoxia reverses the diurnal glucose rhythm and causes pancreatic ,-cell replication in mice

    THE JOURNAL OF PHYSIOLOGY, Issue 3 2008
    Takuya Yokoe
    Obstructive sleep apnoea (OSA) and type 2 diabetes frequently co-exist and potentially interact haemodynamically and metabolically. However, the confounding effects of obesity have obscured the examination of any independent or interactive effects of the hypoxic stress of OSA and the hyperglycaemia of type 2 diabetes on haemodynamic and metabolic outcomes. We have developed a chronically catheterized, unhandled, lean murine model to examine the effects of intermittent hypoxic (IH) exposure and exogenous glucose infusion on the diurnal pattern of arterial blood pressure and blood glucose, as well as pancreatic ,-cell growth and function. Four experimental groups of adult male C57BL/J mice were exposed to 80 h of (1) either IH (nadir of inspired oxygen 5,6% at 60 cycles h,1 for 12 h during light period) or intermittent air (IA; control) and (2) continuous infusion of either 50% dextrose or saline (control). IH exposure during saline infusion caused a sustained increase in arterial blood pressure of 10 mmHg (P < 0.0001), reversed the normal diurnal rhythm of blood glucose (P < 0.03), doubled corticosterone levels (P < 0.0001), and increased replication of pancreatic ,-cells from 1.5 ± 0.3 to 4.0 ± 0.8% bromodeoxyuridine (BrdU)-positive) ,-cells. The combined stimulus of IH exposure and glucose infusion attenuated the hypertension, exacerbated the reversed diurnal glucose rhythm, and produced the highest rates of apoptosis in ,-cells, without any additive effects on ,-cell replication. We conclude that, in contrast to the development of sustained hypertension, IH impaired glucose homeostasis only during periods of hypoxic exposure. IH acted as a stimulus to pancreatic ,-cell replication, but the presence of hyperglycaemia may increase the hypoxic susceptibility of ,-cells. This model will provide a basis for future mechanistic studies as well as assessing the metabolic impact of common comorbities in OSA, including obesity, insulin resistance and type 2 diabetes. [source]


    Impact of glucose infusion on the structural and functional characteristics of adipose tissue and on hypothalamic gene expression for appetite regulatory neuropeptides in the sheep fetus during late gestation

    THE JOURNAL OF PHYSIOLOGY, Issue 1 2005
    B. S. Mühlhäusler
    In the present study, our aim was to determine whether intrafetal glucose infusion increases fetal adiposity, synthesis and secretion of leptin and regulates gene expression of the ,appetite regulatory' neuropeptides neuropepetide Y (NPY), agouti-related peptide (AGRP), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and receptors (leptin receptor (OB-Rb) and melancortin 3 receptor (MC3R)) within the fetal hypothalamus. Glucose (50% dextrose in saline) or saline was infused (7.5 ml h,1) into fetal sheep between 130 and 140 days gestation (term = 150 ± 3 days gestation). Glucose infusion increased circulating glucose and insulin concentrations, mean lipid locule size (532.8 ± 3.3 ,m2versus 456.7 ± 14.8 ,m2) and total unilocular fat mass (11.7 ± 0.6 g versus 8.9 ± 0.6 g) of the perirenal fat depot. The expression of OB-Rb mRNA was higher in the ventromedial nucleus compared to the arcuate nucleus of the hypothalamus in both glucose and saline infused fetuses (F= 8.04; P < 0.01) and there was a positive correlation between expression of OB-Rb and MC3R mRNA in the arcuate nucleus (r= 0.81; P < 0.005). Glucose infusion increased mRNA expression for POMC, but not for the anorectic neuropeptide CART, or the orexigenic neuropeptides NPY and AGRP, in the arcuate nucleus of the fetal hypothalamus. These findings demonstrate that increased circulating glucose and insulin regulate gene expression of the neuropeptides within the fetal hypothalamus that are part of the neural network regulating energy balance in adult life. [source]


    The circulating IGF system and its relationship with 24-h glucose regulation and insulin sensitivity in healthy subjects

    CLINICAL ENDOCRINOLOGY, Issue 6 2003
    Jan Frystyk
    Summary objective and design It has been suggested that circulating free IGF-I participates in glucose homeostasis and that IGFBP-1 reflects changes in insulin sensitivity. To study this further, we examined 10 healthy, nonobese subjects under standardized conditions for 24 h with and without an intravenous infusion of glucose, the latter in order to augment insulin sensitivity. Serum was collected every 2 h for analysis of free and total IGFs, IGFBP-1, , 2 and , 3 and the acid labile subunit (ALS). Insulin sensitivity was estimated at the end of each 24-h study period by use of the hyperinsulinaemic euglycaemic clamp technique. results Glucose infusion resulted in mild hyperglycaemia (P < 0·0001), a reduction in IGFBP-1 by approximately 40% (P < 0·0003), and increased insulin and C-peptide levels (P < 0·0001). Glucose infusion also increased insulin sensitivity (P < 0·003). However, despite the reduction in IGFBP-1, glucose infusion did not increase free IGF-I over the control level, and free IGF-II was slightly reduced (P < 0·02). Irrespective of glucose infusion, free IGF-I and -II remained stable during daytime (i.e. they were unresponsive to meal-related changes in plasma glucose), but both free fractions decreased during the night, reaching nadir at 04·00 h. None of the other members of the IGF system showed any relationship with plasma glucose levels. Finally, we failed to observe any relationship between changes in insulin sensitivity and the circulating IGF system. conclusion We found no evidence that the circulating IGF system is involved in meal-related blood glucose regulation or that it reflects short-term changes in insulin sensitivity in healthy, nonobese subjects. However, we cannot preclude that the observed changes in circulating IGFBP-1 may affect the glucose-lowering effect of IGF-I and -II at the local tissue level. [source]


    The relationship between peripheral glucose utilisation and insulin sensitivity in the regulation of hepatic glucose production: studies in normal and alloxan-diabetic dogs

    DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2006
    M. J. Christopher
    Abstract Background Hepatic glucose overproduction (HGP) of diabetes could be primary or could occur in response to the metabolic needs of peripheral (skeletal muscle (SkM)) tissues. This question was tested in normal and diabetic dogs. Methods HGP, SkM glucose uptake (Rdtissue), metabolic clearance of glucose (MCRg) and glycolytic flux (GFexog), and SkM biopsies were measured in the same dogs before and after alloxan-induced diabetes. Normal dogs were exposed to (1) an extended 20-h fast, (2) low- and high-dose glucose infusions (GINF) at basal insulinaemia, and chronic diabetic dogs were exposed to (3) hyperglycaemia, (4) phlorizin-induced normoglycaemia, and (5) poor and good diabetic control. Results (1) Prolonged fast: HGP, Rdtissue, and GFexog fell in parallel (p < 0.05). (2) Low-dose GINF: plasma glucose, insulin, Rdtissue, MCRg, and GFexog were unchanged, but HGP fell by ,40%, paralleling the supplemental GINF. (3) High-dose GINF at basal insulin: plasma glucose doubled and synchronous changes in HGP, Rdtissue, MCRg, and GFexog occurred; ICglucose, G6P, and glycogen were unchanged. (4) Hyperglycaemic diabetes: HGP was raised (p < 0.05), matching urinary glucose loss (UGL) and decreased MCRg, and maintaining normal basal Rdtissue and GFexog. SkM ICglucose was increased and glycogen decreased (both p < 0.05). (5) Phlorizin-induced normoglycaemia in diabetic dogs: HGP rose, matching the increased UGL, while maintaining normal Rdtissue and GFexog. Intramuscular substrates normalised. (6) Whole body and SkM metabolism normalised with correction of the insulin resistance and good diabetic control. Conclusion HGP reflects whether SkM is in a state of relative glucose ,excess' or absolute/relative glucose ,deprivation'. Copyright © 2005 John Wiley & Sons, Ltd. [source]


    Prehospital management of diabetic emergencies , a population-based intervention study

    ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2003
    A. Holstein
    Background: Diabetes-related emergencies are frequent and potentially life-threatening. A study was performed to obtain reliable data about the prevalence of diabetic emergencies and to improve the quality of prehospital care of patients with diabetes-related emergencies. Methods: A prospective population-based study in a German emergency medical service district in the period from 1997 to 2000 was conducted. After initial diabetes training for the entire emergency team, a standardized protocol was introduced for prehospital emergency therapy of severe hypoglycaemia (SH) and severe hyperglycaemic disorders. A rapid blood glucose test was performed on all emergency patients with the exception of resuscitations and deaths. Indicators of treatment quality before and after these interventions were compared. Results: A rapid blood glucose test was performed in 6631 (85%) of the 7804 emergencies that occurred during the period investigated. The prevalence of acute diabetic complications was 3.1%, and 213 cases of SH and 29 severe hyperglycaemic disorders were recorded. Education of the emergency team led to a significant improvement in the quality of treatment. Larger volumes of iv 40% glucose solution (50 ± 20 ml (1997,2000) vs. 25 ± 17 ml (1993,96); P < 0.0001) were administered to patients with SH. Insulin-treated patients who were well educated about their diabetes were more often treated only at the emergency scene, after SH (25% vs. 8%; P = 0.007), and without complications. In 50 patients who experienced sulfonylurea-induced SH, the mandatory additional glucose infusions and hospitalization for further observation reduced mortality from 4.9% to 0% (P = 0.2). Conclusion: Training of the emergency team is an effective and efficient intervention to improve quality of treatment and prognosis outcome for patients with diabetic emergencies. Treatment of SH at the emergency scene only was demonstrated to be safe in type 1 diabetic patients who had previously received structured patient education. [source]


    Role of glial metabolism in diabetic encephalopathy as detected by high resolution 13C NMR

    NMR IN BIOMEDICINE, Issue 6-7 2003
    María A. García-Espinosa
    Abstract The roles of glial energetics and of the glutamine cycle in diabetic encephalopathy have been investigated ex vivo by 13C NMR in extracts of adult rat brain. Streptozotocin-induced diabetic or euglycemic animals received intravenous infusions of (1- 13C) glucose in the absence and presence of trifluoroacetic acid or methionine sulfoximine, two selective inhibitors of the glial tricarboxylic acid cycle or of glutamine synthase, respectively. (1- 13C) glucose infusions resulted in smaller 13C incorporation in all carbons of cerebral glutamate, glutamine and GABA in the diabetic animals. Co-infusion of trifluoroacetic acid with (1- 13C) glucose further reduced the 13C enrichments in cerebral glutamate and glutamine, the decrease being larger in the diabetic animals than in the corresponding euglycemic controls. Methionine sulfoximine decreased to undetectable levels the fractional 13C enrichment in the carbons of cerebral glutamine in both groups and had no significant effect on 13C incorporation in glutamate and GABA, suggesting that glutamine is not the main precursor of glutamate and GABA. Additional animals were infused with (1,2- 13C2) acetate, a major substrate of glial metabolism. In this case, (1,2- 13C2) acetate infusions resulted in increased 13C incorporation in all carbons of glutamate, glutamine and GABA in the diabetic animals. Together, these results reveal that diabetic encephalopathy has an important effect in astroglial metabolism, decreasing glucose transport and metabolism and increasing the relative contribution of glial oxidative metabolism to the support of glutamatergic and GABAergic neurotransmissions. Copyright © 2003 John Wiley & Sons, Ltd. [source]


    Glucose infusions into peripheral veins in the management of neonatal hypoglycemia , 20% instead of 15%?

    ACTA PAEDIATRICA, Issue 3 2010
    T Vanhatalo
    Abstract Aim: To establish whether peripheral intravenous 20% glucose solutions would cause less local irritation, fewer cannulation changes and less weight gain than 15% glucose in newborn infants. Methods: A total of 121 newborn infants with hypoglycemia were randomized to receive either 20% (group 20%, 60 infants) or 15% (group 15%, 61 infants) glucose infusions, which were initiated at 8 mg/kg/min rates and tapered according to the blood glucose levels. When the cannulation site had to be changed, signs of phlebitis at the previous cannulation site were scored (0,3). Number of cannulation site changes, durations of infusions and the infants' daily weights were recorded. Results: The median durations of infusions in groups 20 and 15% were 4 (range 2,7) days versus 4 (range 2,8) days and the median number of cannulation site changes were 1 (range 0,6) versus 1 (range 0,5), respectively. Thirty-six infants in group 20% and 37 in group 15% developed some phlebitis, median severity scores being 1 (range 0,7) versus 15% 1 (range 0,8). The weights during the treatment were also similar. Conclusion:, 20% and 15% glucose solutions can be infused equally safely into peripheral veins in neonates. [source]