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.

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.

scholarly journals IMPLICATIONS OF HYPERGLYCEMIA FOR POST-EXERCISE RESYNTHESIS OF GLYCOGEN IN TROUT SKELETAL MUSCLE

1994 ◽  
Vol 189 (1) ◽  
pp. 69-84 ◽  
Author(s):  
T West ◽  
P Schulte ◽  
P Hochachka
Keyword(s):  
Skeletal Muscle ◽  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Glucose Concentration ◽  
Plasma Glucose Level ◽  
White Muscle ◽  
Glucose Utilization ◽  
Glucose Turnover ◽  
Red Muscle ◽  
Glucose Availability

Rates of whole-body glucose turnover and muscle-specific glucose utilization were determined in rainbow trout (Oncorhynchus mykiss) at rest and at intervals during recovery from burst swimming. Plasma glucose level was high in the experimental animals (range 6­38 mmol l-1), but hyperglycemia was not related specifically to exercise. Estimated glucose turnover, 19.3±2.6 (rest) and 15.8±3.9 µmol min-1 kg-1 (recovery), was also highly variable, but was linearly associated with plasma glucose concentration (turnover=0.97[glucose]+0.57, r=0.93) in both resting and recovering fish. While utilization of glucose in the whole animal was clearly responsive to plasma glucose availability, estimated total skeletal muscle disposal of glucose accounted for less than 15 % of glucose turnover, indicating that glucose was utilized largely by tissues other than locomotory muscle. Rates of glucose utilization in white muscle (range 0.5­4 nmol min-1 g-1) provide direct evidence that glucose, regardless of plasma concentration, accounted for less than 10 % of glycogen repletion during exercise recovery. In red muscle, glucose uptake was influenced by plasma glucose level below 10­12 mmol l-1 (utilization range 1­15 nmol min-1 g-1), but was independent of glucose concentration above about 12 mmol l-1 (utilization plateaued at 15­20 nmol min-1 g-1). Trout red muscle is similar to mammalian white muscle in the sense that glucose is estimated to account incompletely for glycogen restoration (25­60 %), suggesting dependence on both glycogenesis and glyconeogenesis during recovery. It is concluded that hyperglycemia may be important to the pattern of substrate incorporation into red muscle glycogen and to the rate of repletion observed, but glucose availability has, as predicted from earlier indirect studies, little relevance to white muscle glycogen restoration. The regulatory mechanisms that govern apparently very high glucose turnover rates during extreme hyperglycemia, concomitant with low disposal rates in skeletal muscle, require further investigation.

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.

scholarly journals Autoradiographic Determination of Cerebral Glucose Content, Blood Flow, and Glucose Utilization in Focal Ischemia of the Rat Brain: Influence of the Plasma Glucose Concentration

1988 ◽  
Vol 8 (1) ◽  
pp. 100-108 ◽  
Author(s):  
Maiken Nedergaard ◽  
Johannes Jakobsen ◽  
Nils Henrik Diemer
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Plasma Glucose Concentration ◽  
Glucose Content ◽  
Border Areas ◽  
Ischemic Core

Focal cerebral ischemia was produced by occlusion of the middle cerebral artery in rats. Cerebral blood flow measured with [14C]iodoantipyrine was severely reduced in the lateral portion of neostriatum. This area of dense ischemia was sharply demarcated against the surroundings. The adjacent cortex was perfused at one-third of normal, whereas blood flow in the medial neostriatum was only slightly reduced. This pattern of perfusion was independent of the plasma glucose concentration of the animal. In contrast, the glucose utilization calculated from the 2-[3H]deoxyglucose accumulation depended on the plasma glucose concentration. Enhanced glucose utilization was evident in the border areas surrounding the ischemic focus in normoglycemic animals. Neither acutely nor chronically diabetic animals had such an increase of metabolism in the borderzone. Moderately hyperglycemic rats had a narrow rim of enhanced glucose utilization immediately surrounding the ischemic core, whereas animals with plasma glucose values above 22 mmol/L had no such rim. In mild hypoglycemia (2–4 mmol/L), the glucose utilization was slightly enhanced in the border areas, but during severe hypoglycemia (<2.5 mmol/L), the glucose utilization declined gradually toward the ischemic core. Glucose content, and thereby the lumped constant (measured by 3-0-[14C]methylglucose) showed little regional variation, except in the ischemic core. These findings indicate that blood flow alterations after occlusion of the middle cerebral artery in rats are not influenced by the plasma glucose utilizations. In contrast, glucose utilization depends on a combination of plasma glucose concentration and blood flow instead of blood flow per se.

Steady state glucose kinetics and their relation to plasma glucose concentration in the premature and full term neonatal piglet

1981 ◽  
Vol 59 (10) ◽  
pp. 1069-1072 ◽  
Author(s):  
P. A. Flecknell ◽  
R. Wootton ◽  
Muriel John ◽  
J. P. Royston
Keyword(s):  
Steady State ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Turnover Rate ◽  
Full Term ◽  
Plasma Glucose Concentration ◽  
Human Infant ◽  
Glucose Turnover ◽  
Glucose Kinetics ◽  
Neonatal Piglet

Steady state glucose kinetics were measured in 19 premature and 16 full-term piglets. Bodyweight, plasma glucose concentration, total body glucose turnover rate, and glucose pool size were not significantly different between the two groups. This suggests that the premature piglet is capable of maintaining glucose homeostasis during the first 24 h of life. Although there appeared to be a correlation between glucose turnover and plasma glucose concentration, analysis of covariance showed that it was spurious, suggesting that glucose utilization proceeds independently of the glucose concentration in plasma.Glucose turnover rate in the premature piglet is closely comparable with that reported in the premature human infant. These findings encourage the use of the neonatal piglet as an animal model for the study of the problems of the neonatal human.

Adrenocortical functions in a macropodid marsupial Thylogale billardierii

1986 ◽  
Vol 110 (3) ◽  
pp. 471-480 ◽  
Author(s):  
I. K. Martin ◽  
I. R. McDonald
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Plasma Cortisol ◽  
Tammar Wallaby ◽  
Cortisol Concentration ◽  
Plasma Glucose Concentration ◽  
Metabolic Clearance ◽  
Acth Stimulation ◽  
Plasma Cortisol Concentration ◽  
Red Kangaroo

ABSTRACT In a study of adrenocortical functions in macropodid marsupials, measurements were made of the effects of ACTH infusion, ether stress and adrenaline infusion on plasma corticosteroid and glucose concentrations in wallabies (Thylogale billardierii) provided with indwelling venous catheters. The mean plasma total glucocorticoid concentration in undisturbed males and females was 80 ± 5 (s.e.m.) μg/l, of which more than 90% was cortisol. This fraction declined to 68% of the total at the highest ACTH-stimulated concentration of 225 μg/l, due to an increase in the contribution by 11-deoxycortisol. Although maximal ACTH stimulation (4·5 i.u./kg per h) caused a five- to sixfold increase in cortisol secretion rate, as measured by isotope dilution during constant-rate tracer infusion, plasma cortisol concentration rose only two- to threefold, due to a marked increase in metabolic clearance. Plasma glucose concentration did not change significantly during either short-term (1 h) i.v. infusion or long-term (8 days) i.m. injection of ACTH, even though plasma cortisol concentration was significantly increased. Ether anaesthesia caused a marked hyperglycaemia that preceded an increase in plasma cortisol concentration and was not sustained while plasma cortisol concentration continued to increase. Infusion of adrenaline i.v. at rates sufficient to cause a similar hyperglycaemia had no significant effect on plasma cortisol concentration. A marked hyperglycaemia during xylazine anaesthesia was not associated with an increase in plasma cortisol concentration and was attributable to suppression of insulin secretion. It is concluded that, as in the red kangaroo (Macropus rufus) and the quokka (Setonix brachyurus) and in contrast to the reported effects in the tammar wallaby (Macropus eugenii), neither ACTH, nor the increase in plasma glucocorticoid concentration caused by ACTH administration, influence plasma glucose concentration in Thylogale billardierii. J. Endocr. (1986) 110, 471–480

scholarly journals Dapagliflozin Lowers Plasma Glucose Concentration and Improves β-Cell Function

2015 ◽  
Vol 100 (5) ◽  
pp. 1927-1932 ◽  
Author(s):  
Aurora Merovci ◽  
Andrea Mari ◽  
Carolina Solis ◽  
Juan Xiong ◽  
Giuseppe Daniele ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Cell Function ◽  
Plasma Glucose Concentration ◽  
Concentration Curve ◽  
Whole Body ◽  
Β Cell ◽  
C Peptide ◽  
Insulin Clamp ◽  
Β Cell Function

Abstract Background: β-Cell dysfunction is a core defect in T2DM, and chronic, sustained hyperglycemia has been implicated in progressive β-cell failure, ie, glucotoxicity. The aim of the present study was to examine the effect of lowering the plasma glucose concentration with dapagliflozin, a glucosuric agent, on β-cell function in T2DM individuals. Research Design and Methods: Twenty-four subjects with T2DM received dapagliflozin (n = 16) or placebo (n = 8) for 2 weeks, and a 75-g oral glucose tolerance test (OGTT) and insulin clamp were performed before and after treatment. Plasma glucose, insulin, and C-peptide concentrations were measured during the OGTT. Results: Dapagliflozin significantly lowered both the fasting and 2-hour plasma glucose concentrations and the incremental area under the plasma glucose concentration curve (ΔG0–120) during OGTT by −33 ± 5 mg/dL, −73 ± 9 mg/dL, and −60 ± 12 mg/dL · min, respectively, compared to −13 ± 9, −33 ± 13, and −18 ± 9 reductions in placebo-treated subjects (both P &lt; .01). The incremental area under the plasma C-peptide concentration curve tended to increase in dapagliflozin-treated subjects, whereas it did not change in placebo-treated subjects. Thus, ΔC-Pep0–120/ΔG0–120 increased significantly in dapagliflozin-treated subjects, whereas it did not change in placebo-treated subjects (0.019 ± 0.005 vs 0.002 ± 0.006; P &lt; .01). Dapagliflozin significantly improved whole-body insulin sensitivity (insulin clamp). Thus, β-cell function, measured as ΔC-Pep0–120/ ΔG0–120 ÷ insulin resistance, increased by 2-fold (P &lt; .01) in dapagliflozin-treated vs placebo-treated subjects. Conclusion: Lowering the plasma glucose concentration with dapagliflozin markedly improves β-cell function, providing strong support in man for the glucotoxic effect of hyperglycemia on β-cell function.

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