Effect of Halothane Anesthesia on Glucose Utilization and Production in Adolescents 

1995 ◽  
Vol 82 (5) ◽  
pp. 1154-1159 ◽  
Author(s):  
Dounia Sbai ◽  
Philippe Jouvet ◽  
Anne Soulier ◽  
Luc Penicaud ◽  
Jacques Merckx ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Blood Glucose Concentration ◽  
Glucose Infusion ◽  
Plasma Glucose Concentration ◽  
Whole Body ◽  
Metabolic Clearance ◽  
Halothane Anesthesia ◽  
Plasma Insulin Concentration

Background It should be possible to avoid variations in plasma glucose concentration during anesthesia by adjusting glucose infusion rate to whole-body glucose uptake. To study this hypothesis, we measured glucose utilization and production, before and during halothane anesthesia. Methods After an overnight fast, six adolescents between 12 and 17 yr of age were infused with tracer doses of [6,6-2H2]glucose for 2 h before undergoing anesthesia, and the infusion was continued after induction, until the beginning of surgery. Plasma glucose concentration was monitored throughout, and free fatty acids, lactate, insulin, and glucagon concentrations were measured before and during anesthesia. Results Despite the use of a glucose-free maintenance solution, plasma glucose concentration increased slightly but significantly 5 min after induction (5.3 +/- 0.4 vs. 4.5 +/- 0.4 mmol.l-1, P < 0.05). This early increase corresponded to a significant increase in endogenous glucose production over basal conditions (4.1 +/- 0.4 vs. 3.6 +/- 0.2 mg.kg-1.min-1, P < 0.05), with no concomitant change in peripheral glucose utilization. Fifteen minutes after induction, both glucose utilization and production rates decreased steadily and were 20% less than basal values by 35 min after induction (2.9 +/- 0.3 vs. 3.6 +/- 0.2 mg.kg-1.min-1, P < 0.05). Similarly, glucose metabolic clearance rate decreased by 25% after 35 min. Despite the increase in blood glucose concentration, anesthesia resulted in a significant decrease in plasma insulin concentration. Conclusions These data suggest that halothane anesthesia per se affects glucose metabolism. The decrease in peripheral glucose utilization and metabolic clearance rates and the blunted insulin release question the relevance of glucose infusion in these clinical settings.

Muscle glucose utilization during sustained swimming in the carp (Cyprinus carpio)

1994 ◽  
Vol 267 (5) ◽  
pp. R1226-R1234 ◽  
Author(s):  
T. G. West ◽  
C. J. Brauner ◽  
P. W. Hochachka
Keyword(s):  
Muscle Mass ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Plasma Glucose Concentration ◽  
Whole Body ◽  
Control Fish ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Red Muscle

The involvement of circulatory glucose in the energy provision of skeletal muscle and heart of swimming carp was examined. Plasma glucose concentration varied from 3 to 17 mM among individual carp, and estimates of glucose turnover rate (RT) were positively correlated with plasma glucose level in resting fish (range 1.6-6.3 mumol.min-1.kg-1) and in swimming fish (range 4.2-10.7 mumol.min-1.kg-1). Carp that were exercised at 80% of their critical swimming speed displayed a twofold higher RT at any given plasma glucose concentration. Metabolic clearance rate also doubled in swimming carp (1.0 +/- 0.1 ml.min-1.kg-1) relative to resting controls (0.5 +/- 0.1 ml.min-1.kg-1). Indexes of muscle glucose utilization (GUI), determined with 2-deoxy-D-[14C]glucose, indicated that glucose utilization in red muscle was not dependent on plasma glucose concentration; however, glucose utilization in this muscle mass was threefold higher in swimming fish than in resting control fish. On the basis of whole body aerobic scope measurements in carp, it was estimated that circulatory glucose potentially comprised 25-30% of the total fuel oxidation in the active red muscle mass. GUI in heart was positively correlated with plasma glucose concentration, and it is possible that glucose availability had considerable influence on the pattern of myocardial substrate oxidation in resting and active carp. Carp are somewhat more reliant than rainbow trout on glucose for locomotor energetics, correlating with species differences in swimming capability and with the greater capacity of omnivorous carp to tolerate dietary glucose.

Insulin does not mediate the attenuation of fatigue associated with glucose infusion in rat plantaris muscle

2003 ◽  
Vol 95 (1) ◽  
pp. 330-335 ◽  
Author(s):  
Antony D. Karelis ◽  
François Péronnet ◽  
Phillip F. Gardiner
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Plasma Glucose Concentration ◽  
Muscle Performance ◽  
Insulin Concentration ◽  
Dynamic Force ◽  
Plantaris Muscle ◽  
Plasma Insulin Concentration

Glucose infusion attenuates fatigue in rat plantaris muscle stimulated in situ, and this is associated with a better maintenance of electrical properties of the fiber membrane (Karelis AD, Péronnet F, and Gardiner PF. Exp Physiol 87: 585–592, 2002). The purpose of the present study was to test the hypothesis that elevated plasma insulin concentration due to glucose infusion (∼900 pmol/l), rather than high plasma glucose concentration (∼10–11 mmol/l), could be responsible for this phenomenon, because insulin has been shown to stimulate the Na+-K+ pump. The plantaris muscle was indirectly stimulated (50 Hz, for 200 ms, 5 V, every 2.7 s) via the sciatic nerve to perform concentric contractions for 60 min, while insulin (8 mU · kg-1 · min-1: plasma insulin ∼900 pmol/l) and glucose were infused to maintain plasma glucose concentration between 4 and 6 [6.2 ± 0.4 mg · kg-1 · min-1: hyperinsulinemic-euglycemic (HE)] or 10 and 12 mmol/l [21.7 ± 1.1 mg · kg-1 · min-1: hyperinsulinemic-hyperglycemic clamps (HH)] (6 rats/group). The reduction in submaximal dynamic force was significantly ( P < 0.05) less with HH (-53%) than with HE and saline only (-66 and -70%, respectively). M-wave characteristics were also better maintained in the HH than in HE and control groups. These results demonstrate that the increase in insulin concentration is not responsible for the increase in muscle performance observed after the elevation of circulating glucose.

Glucose clamp technique: a method for quantifying insulin secretion and resistance.

1979 ◽  
Vol 237 (3) ◽  
pp. E214 ◽  
Author(s):  
R A DeFronzo ◽  
J D Tobin ◽  
R Andres
Keyword(s):  
Negative Feedback ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Plasma Glucose Concentration ◽  
Plasma Insulin Concentration ◽  
Clamp Technique ◽  
Hyperglycemic Clamp ◽  
Tissue Sensitivity

Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique) are described. Hyperglycemic clamp technique. The plasma glucose concentration is acutely raised to 125 mg/dl above basal levels by a priming infusion of glucose. The desired hyperglycemic plateau is subsequently maintained by adjustment of a variable glucose infusion, based on the negative feedback principle. Because the plasma glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism. Under these conditions of constant hyperglycemia, the plasma insulin response is biphasic with an early burst of insulin release during the first 6 min followed by a gradually progressive increase in plasma insulin concentration. Euglycemic insulin clamp technique. The plasma insulin concentration is acutely raised and maintained at approximately 100 muU/ml by a prime-continuous infusion of insulin. The plasma glucose concentration is held constant at basal levels by a variable glucose infusion using the negative feedback principle. Under these steady-state conditions of euglycemia, the glucose infusion rate equals glucose uptake by all the tissues in the body and is therefore a measure of tissue sensitivity to exogenous insulin.

Contribution of cortisol to glucose counterregulation in humans

1989 ◽  
Vol 257 (1) ◽  
pp. E35-E42 ◽  
Author(s):  
P. De Feo ◽  
G. Perriello ◽  
E. Torlone ◽  
M. M. Ventura ◽  
C. Fanelli ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Hepatic Glucose Production ◽  
Hormone Secretion ◽  
Glucose Production ◽  
Plasma Free Fatty Acid ◽  
Normal Subjects ◽  
Plasma Glucose Concentration ◽  
Cortisol Increase

To test the hypothesis that cortisol secretion plays a counterregulatory role in hypoglycemia in humans, four studies were performed in eight normal subjects. In all studies, insulin (15 mU.m-2.min-1) was infused subcutaneously (plasma insulin 27 +/- 1 microU/ml). In study 1, plasma glucose concentration and glucose fluxes [( 3-3H]glucose), substrate, and counterregulatory hormone concentrations were simply monitored, and plasma glucose decreased from 89 +/- 2 to 52 +/- 2 mg/dl for 12 h. In study 2, (pituitary-adrenal-pancreatic clamp), insulin and counterregulatory hormone secretion (except for catecholamines) was prevented by somatostatin (0.5 mg/h, iv) and metyrapone (0.5 g/4 h, per os), and glucagon, cortisol, and growth hormone were infused to reproduce the concentrations of study 1. In study 3 (lack of cortisol increase), the pituitary-adrenal-pancreatic clamp was performed with maintenance of plasma cortisol at basal levels, and glucose was infused, whenever needed, to reproduce plasma glucose concentration of study 2. Study 4 was identical to study 3, but exogenous glucose was not infused. Isolated lack of cortisol increase caused a approximately 22% decrease in hepatic glucose production (P less than 0.01) and a approximately 15% increase in peripheral glucose utilization (P less than 0.01), which resulted in greater hypoglycemia (37 +/- 2 vs. 52 +/- 2 mg/dl, P less than 0.01) despite compensatory increases in plasma epinephrine. Lack of cortisol response also reduced plasma free fatty acid, beta-hydroxybutyrate, and glycerol concentrations approximately 50%. We conclude that cortisol normally plays an important counterregulatory role during hypoglycemia by augmenting glucose production, decreasing glucose utilization, and accelerating lipolysis.

Importance of blood glucose concentration in regulating lipolysis during fasting in humans

1990 ◽  
Vol 258 (1) ◽  
pp. E32-E39 ◽  
Author(s):  
S. Klein ◽  
O. B. Holland ◽  
R. R. Wolfe
Keyword(s):  
Blood Glucose ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Glucose Infusion ◽  
Short Term ◽  
Epinephrine Infusion ◽  
Isotopic Studies ◽  
Fasting Plasma Insulin

The importance of the decline in blood glucose concentration on lipolysis and the lipolytic effect of epinephrine was evaluated during short-term fasting. Lipolytic rates were determined by infusing [2H5]glycerol and [1-13C]palmitic acid. Five volunteers were studied after 12 h of fasting before and during epinephrine infusion and after 84 h of fasting, before and during glucose infusion when plasma glucose was restored to postabsorptive values, and during glucose plus epinephrine infusion. In another protocol, five volunteers were given glucose intravenously throughout fasting to maintain plasma glucose at postabsorptive levels and isotopic studies were performed after 12 and 84 h of fasting before and during epinephrine infusion. Glucose infusion after 84 h of fasting restored glucose and insulin concentrations and lipolytic rates toward 12-h fasting values. When euglycemia was maintained throughout fasting, plasma insulin still declined (P less than 0.05) and lipolytic rates still increased (P less than 0.05). Despite similar glucose concentrations, the lipolytic response to epinephrine infusion was greater after 84 h than after 12 h of fasting in both protocols (P less than 0.05). These studies demonstrate that the decline in plasma glucose contributes to, but is not required for, the increase in lipolysis during fasting. The increase in epinephrine-stimulated lipolysis that occurs during fasting is not dependent on a decrease in plasma glucose concentration.

scholarly journals Orally administered, insulin-loaded amidated pectin hydrogel beads sustain plasma concentrations of insulin in streptozotocin-diabetic rats

2000 ◽  
Vol 164 (1) ◽  
pp. 1-6 ◽  
Author(s):  
CT Musabayane ◽  
O Munjeri ◽  
P Bwititi ◽  
EE Osim
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Plasma Concentrations ◽  
Diabetic Rats ◽  
Plasma Glucose Concentration ◽  
Pharmacokinetic Parameters ◽  
Plasma Insulin Concentration ◽  
Hydrogel Beads ◽  
Concomitant Reduction

We report successful oral administration of insulin entrapped in amidated pectin hydrogel beads in streptozotocin (STZ)-diabetic rats, with a concomitant reduction in plasma glucose concentration. The pectin-insulin (PI) beads were prepared by the gelation of humilin-pectin solutions in the presence of calcium. Separate groups of STZ-diabetic rats were orally administered two PI beads (30 micrograms insulin) once or twice daily or three beads (46 micrograms) once daily for 2 weeks. Control non-diabetic and STZ-diabetic rats were orally administered pectin hydrogel drug-free beads. By comparison with control non-diabetic rats, untreated STZ-diabetic rats exhibited significantly low plasma insulin concentration (0.32+/-0. 03 ng/ml, n=6, compared with 2.60+/-0.44 ng/ml in controls, n=6) and increased plasma glucose concentrations (25.84+/-1.44 mmol/l compared with 10.72+/- 0.52 mmol/l in controls). Administration of two PI beads twice daily (60 micrograms active insulin) or three beads (46 micrograms) once a day to STZ-diabetic rats increased plasma insulin concentrations (0.89+/-0.09 ng/ml and 1.85+/- 0.26 ng/ml, respectively), with a concomitant reduction in plasma glucose concentration (15.45+/-1.63 mmol/l and 10.56+/-0.26 mmol/l, respectively). However, a single dose of PI beads (30 micrograms) did not affect plasma insulin concentrations, although plasma glucose concentrations (17.82+/-2.98 mmol/l) were significantly reduced compared with those in untreated STZ-diabetic rats. Pharmacokinetic parameters in STZ-diabetic rats show that the orally administered PI beads (30 micrograms insulin) were more effective in sustaining plasma insulin concentrations than was s.c. insulin (30 micrograms). The data from this study suggest that this insulin-loaded amidated pectin hydrogel bead formulation not only produces sustained release of insulin, but may also reduce plasma glucose concentration in diabetes mellitus.

Glucose intolerance following chronic metabolic acidosis in man.

1979 ◽  
Vol 236 (4) ◽  
pp. E328 ◽  
Author(s):  
R A DeFronzo ◽  
A D Beckles
Keyword(s):  
Metabolic Acidosis ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Glucose Infusion ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Chronic Metabolic Acidosis ◽  
Tissue Sensitivity

The effect of chronic metabolic acidosis (0.1 g/(kg . day) X 3 days) on carbohydrate metabolism was examined with the glucose-clamp technique in 16 healthy volunteers. Hyperglycemic clamp. Plasma glucose concentration is acutely raised and maintained 125 mg/dl above the basal level. Because the glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism (M). Following NH4Cl, M decreased from 8.95 +/- 1.12 to 7.35 +/- 0.76 (P less than 0.05) despite an increased plasma insulin concentration (I) 23 +/- 9%, P less than 0.05). Consequently the M/I ratio, an index of tissue sensitivity to insulin, decreased by 32 +/- 5% (P less than 0.005). Euglycemic clamp. Plasma insulin concentration is acutely raised and maintained 101 +/- 3 microU/ml above basal and plasma glucose is held constant at the fasting level by a variable glucose infusion (M). Following NH4Cl both M and M/I decreased by 15 +/- 4% (P = 0.005) and 15 +/- 5% (P = 0.01), respectively. Metabolic acidosis had no effect on basal [3-3H]glucose production or the percent of decline (91 +/- 4%) following hyperinsulinemia. Both hyperglycemic and euglycemic clamp studies indicate that impaired glucose metabolism following metabolic acidosis results from impaired tissue sensitivity to insulin.

scholarly journals Postprandial glucose and insulin profiles following a glucose-loaded meal in cats and dogs

2011 ◽  
Vol 106 (S1) ◽  
pp. S101-S104 ◽  
Author(s):  
Adrian K. Hewson-Hughes ◽  
Matthew S. Gilham ◽  
Sarah Upton ◽  
Alison Colyer ◽  
Richard Butterwick ◽  
...  
Keyword(s):  
Body Weight ◽  
Plasma Glucose ◽  
Test Meal ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Plasma Glucose Concentration ◽  
Insulin Concentration ◽  
Metabolic Adaptation ◽  
Plasma Insulin Concentration ◽  
High Blood Glucose

Data from intravenous (i.v.) glucose tolerance tests suggest that glucose clearance from the blood is slower in cats than in dogs. Since different physiological pathways are activated following oral administration compared with i.v. administration, we investigated the profiles of plasma glucose and insulin in cats and dogs following ingestion of a test meal with or without glucose. Adult male and female cats and dogs were fed either a high-protein (HP) test meal (15 g/kg body weight; ten cats and eleven dogs) or a HP+glucose test meal (13 g/kg body-weight HP diet+2 g/kg body-weight d-glucose; seven cats and thirteen dogs) following a 24 h fast. Marked differences in plasma glucose and insulin profiles were observed in cats and dogs following ingestion of the glucose-loaded meal. In cats, mean plasma glucose concentration reached a peak at 120 min (10·2, 95 % CI 9·7, 10·8 mmol/l) and returned to baseline by 240 min, but no statistically significant change in plasma insulin concentration was observed. In dogs, mean plasma glucose concentration reached a peak at 60 min (6·3, 95 % CI 5·9, 6·7 mmol/l) and returned to baseline by 90 min, while plasma insulin concentration was significantly higher than pre-meal values from 30 to 120 min following the glucose-loaded meal. These results indicate that cats are not as efficient as dogs at rapidly decreasing high blood glucose levels and are consistent with a known metabolic adaptation of cats, namely a lack of glucokinase, which is important for both insulin secretion and glucose uptake from the blood.

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