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Intravenous Glucose (intravenous + glucose)
Terms modified by Intravenous Glucose Selected AbstractsReactive hypoglycaemia following GLP-1 infusion in pancreas transplant recipientsDIABETES OBESITY & METABOLISM, Issue 8 2010M. R. Rickels The aim of the study was to determine whether reactive hypoglycaemia in pancreas transplant recipients that followed administration of glucagon-like peptide-1 (GLP-1) was associated with excessive insulin, insufficient glucagon, or both. Methodology involved six portally drained pancreas recipients who received GLP-1 (1.5 pmol/kg/min) or placebo infusion on randomized occasions during glucose-potentiated arginine testing. The second subject developed symptomatic hypoglycaemia [plasma glucose (PG) 42 mg/dl] 1 h after GLP-1 administration; subsequent subjects received intravenous glucose following GLP-1, but not placebo, infusion for PG levels <65 mg/dl. Following GLP-1 vs. placebo infusion, PG was lower (58 ± 4 vs. 76 ± 5 mg/dl; p < 0.05) despite administration of intravenous glucose. During hypoglycaemia, insulin levels and the insulin-to-glucagon ratio were greater after GLP-1 vs. placebo infusion (p < 0.05), while glucagon did not vary. It can be concluded from the study that GLP-1 can induce reactive hypoglycaemia in pancreas transplant recipients through excessive insulin secretion associated with an increased insulin-to-glucagon ratio. [source] No reactive hypoglycaemia in Type 2 diabetic patients after subcutaneous administration of GLP-1 and intravenous glucoseDIABETIC MEDICINE, Issue 2 2001T. Vilsbøll SUMMARY Aims It has previously been shown that intravenous and subcutaneous administration of glucagon-like peptide (GLP)-1 concomitant with intravenous glucose results in reactive hypoglycaemia in healthy subjects. Since GLP-1 is also effective in Type 2 diabetic patients and is presently being evaluated as a therapeutic agent in this disease, it is important to investigate whether GLP-1 can cause hypoglycaemia in such patients. Methods Eight Type 2 diabetic patients (age 54 (49,67) years; body mass index 31 (27,38) kg/m2; HbA1c 9.4 (7.0,12.5)%) and seven matched non-diabetic subjects (HbA1c 5.5 (5.2,5.8)%, fasting plasma glucose 5.4 (5.0,5.7) mmol/l) were given a subcutaneous injection of 1.5 nmol GLP-1/kg body weight (maximally tolerated dose), and 15 min later, plasma glucose (PG) was raised to 15 mmol/l with an intravenous glucose bolus. Results Hypoglycaemia with a PG at or below 2.5 mmol/l was seen in five of the seven healthy subjects after 60,70 min, but PG spontaneously increased again, reaching 3.7 (3.3,4.0) mmol/l at 90 min. In the patients, PG fell slowly and stabilized at 8.6 (4.2,12.1) mmol/l after 80 min. In both groups, glucagon levels initially decreased, but later increased, exceeding basal levels in healthy subjects, in spite of persistent, high concentrations of GLP-1 (P < 0.02). Conclusions Subcutaneous GLP-1 plus intravenous glucose induced reactive hypoglycaemia in healthy subjects, but not in Type 2 diabetic patients. Therefore, a GLP-1-based therapy would not be expected to be associated with an increased risk of hypoglycaemia in Type 2 diabetes mellitus. [source] Watchful waiting: A management protocol for maternal glycaemia in the peripartum periodAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 2 2009Helen Lorraine BARRETT Background: It is accepted that tight glycaemic control is necessary during labour in women with pregestational or gestational diabetes mellitus (GDM). Although policies vary, routine use of intravenous glucose and insulin remains a standard practice in some institutions. We present a retrospective review of a more conservative approach. Briefly, regardless of planned delivery method, maternal blood sugar level (BSL) is monitored during delivery and only if outside 4,7 mmol/L is action taken. We report the results of an audit of this practice. Methods: A retrospective (August 2001,July 2004) review of 137 singleton, term deliveries of women with diabetes (23 pregestational, 114 GDM). Predetermined outcomes reported were BSL achieved prior to delivery, first neonatal BSL and/or admission to neonatal intensive care unit (NICU) for hypoglycaemia. Results: With our management practice, most women had a BSL between 4 and 8 mmol/L prior to delivery (17 (74%) diabetes mellitus (DM), 37 (93%) diet-controlled GDM, 55 (89%) insulin-requiring GDM). Neonatal hypoglycaemia (< 2.6 mmol/L) was common (n= 30 (22%)). However, most neonatal hypoglycaemia occurred in infants born to mothers with BSL 4,8 mmol/L (n= 26 (87%)). Neonatal hypoglycaemia requiring NICU admission (n= 13) was predominantly in infants born to mothers with BSL < 8mmol/L prior to delivery (n= 10 (77%)). Three of eight maternal BSLs > 8 mmol/L occurred prior to emergency caesarean section in women with pregestational diabetes. Conclusion: These results suggest that our current practice, particularly in women with GDM, may offer an alternative to more aggressive regimes. [source] Rosiglitazone improves insulin sensitivity and glucose tolerance in subjects with impaired glucose toleranceCLINICAL ENDOCRINOLOGY, Issue 1 2005Yi-Jen Hung Summary Objective, This study was designed to evaluate the effects of rosiglitazone (ROS) on insulin sensitivity, ,-cell function, and glycaemic response to glucose challenge and meal in subjects with impaired glucose tolerance (IGT). Methods, Thirty patients with IGT (ages between 30 and 75 years and BMI (body mass index) , 27 kg/m2) were randomly assigned to receive either placebo (n = 15) or ROS (4 mg/day) (n = 15). All participants underwent a 75-g oral glucose tolerance test (OGTT), meal test, and frequently sampled intravenous glucose tolerance test (FSIGT) before and after the 12-week treatment. Results, After 12 weeks of ROS treatment, there were significant increases in total cholesterol (TC) (4·25 ± 0·22 vs 4·80 ± 0·17 mmol/l, P < 0·001), high-density lipoprotein cholesterol (HDL-C) (1·25 ± 0·07 vs 1·43 ± 0·06 mmol/l, P < 0·05), and low-density lipoprotein cholesterol (LDL-C) (2·70 ± 0·15 vs 3·37 ± 0·17 mmol/l, P < 0·05) without changes in triglyceride concentration, TC/HDL-C and LDL-C/HDL-C ratio. Although the acute insulin response (AIR) to intravenous glucose and disposition index (measured as the ability of pancreatic ,-cell compensation in the presence of insulin resistance) remained unchanged, the insulin sensitivity (SI) and glucose effectiveness (SG) were remarkably elevated (0·38 ± 0·06 vs 0·54 ± 0·09 × 10,5 min,1/pmol, P < 0·05; 0·017 ± 0·002 vs 0·021 ± 0·001 min,1, P < 0·05, respectively) in the ROS group. The glucose, insulin, and c-peptide areas under curve (AUC) in response to OGTT and the glucose and insulin AUC during meal were significantly ameliorated in the ROS group. Five out of 15 (33%) and two out of 15 (13%) subjects treated with ROS and placebo, respectively, reversed to normal response during OGTT (P < 0·05). Conclusion, Rosiglitazone treatment significantly improved insulin resistance and reduced postchallenge glucose and insulin concentrations in patients with impaired glucose tolerance without remarkable effects on ,-cell secretory function. [source] |