Effects of Plasma Glucose Concentration on Glucose Utilization and Glucose Clearance in Normal Man

Diabetes ◽  
1981 ◽  
Vol 30 (6) ◽  
pp. 535-537 ◽  
Author(s):  
C. A. Verdonk ◽  
R. A. Rizza ◽  
J. E. Gerich
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Plasma Glucose Concentration ◽  
Glucose Clearance ◽  
Normal Man

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.

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 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.

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.

scholarly journals The Lumped Constant of the Deoxyglucose Method in Hypoglycemia: Effects of Moderate Hypoglycemia on Local Cerebral Glucose Utilization in the Rat

1990 ◽  
Vol 10 (4) ◽  
pp. 499-509 ◽  
Author(s):  
Sumio Suda ◽  
Mami Shinohara ◽  
Makoto Miyaoka ◽  
Giovanni Lucignani ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Plasma Glucose Concentration ◽  
Local Cerebral Glucose Utilization ◽  
Cerebral Glucose Utilization ◽  
Lumped Constant ◽  
Arterial Plasma ◽  
The Brain ◽  
Deoxyglucose Method

The applicability of the [14C]deoxyglucose method for measuring local cerebral glucose utilization (lCMRglc) has been extended for use in hypoglycemia by determination of the values of the lumped constant to be used in rats with plasma glucose concentrations ranging from approximately 2 to 6 m M. Lumped constant values were higher in hypoglycemia and declined from a value of 1.2 at the lowest arterial plasma glucose level (1.9 m M) to about 0.48 in normoglycemia. The distribution of glucose, and therefore also of the lumped constant, was found to remain relatively uniform throughout the brain at the lowest plasma glucose levels studied. lCMRglc in moderate, insulin-induced hypoglycemia (mean arterial plasma glucose concentration ± SD of 2.4 ± 0.3 m M) was determined with the appropriate lumped constant corresponding to the animal's plasma glucose concentration and compared with the results obtained in six normoglycemic rats. The weighted average rate of glucose utilization for the brain as a whole was significantly depressed by 14% in the hypoglycemic animals, i.e., 61 μmol/100 g/min in hypoglycemia compared to 71 μmol/100 g/min in the normoglycemic controls ( p < 0.05). lCMRglc was lower in 47 of 49 structures examined but statistically significantly below the rate in normoglycemic rats in only six structures ( p < 0.05) by multiple comparison statistics. Regions within the brainstem were most prominently affected. The greatest reductions, statistically significant or not, occurred in structures in which glucose utilization is normally high, suggesting that glucose delivery and transport to the tissue became rate-limiting first in those structures with the greatest metabolic demands for glucose.

scholarly journals Anti-inflammatory salicylate treatment alters the metabolic adaptations to lactation in dairy cattle

2013 ◽  
Vol 305 (2) ◽  
pp. R110-R117 ◽  
Author(s):  
Jaymelynn K. Farney ◽  
Laman K. Mamedova ◽  
Johann F. Coetzee ◽  
Butch KuKanich ◽  
Lorraine M. Sordillo ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Physiological State ◽  
Plasma Glucose Concentration ◽  
Utilization Rate ◽  
Peripheral Tissues ◽  
Tnf Α ◽  
Anti Inflammatory

Adapting to the lactating state requires metabolic adjustments in multiple tissues, especially in the dairy cow, which must meet glucose demands that can exceed 5 kg/day in the face of negligible gastrointestinal glucose absorption. These challenges are met through the process of homeorhesis, the alteration of metabolic setpoints to adapt to a shift in physiological state. To investigate the role of inflammation-associated pathways in these homeorhetic adaptations, we treated cows with the nonsteroidal anti-inflammatory drug sodium salicylate (SS) for the first 7 days of lactation. Administration of SS decreased liver TNF-α mRNA and marginally decreased plasma TNF-α concentration, but plasma eicosanoids and liver NF-κB activity were unaltered during treatment. Despite the mild impact on these inflammatory markers, SS clearly altered metabolic function. Plasma glucose concentration was decreased by SS, but this was not explained by a shift in hepatic gluconeogenic gene expression or by altered milk lactose secretion. Insulin concentrations decreased in SS-treated cows on day 7 compared with controls, which was consistent with the decline in plasma glucose concentration. The revised quantitative insulin sensitivity check index (RQUICKI) was then used to assess whether altered insulin sensitivity may have influenced glucose utilization rate with SS. The RQUICKI estimate of insulin sensitivity was significantly elevated by SS on day 7, coincident with the decline in plasma glucose concentration. Salicylate prevented postpartum insulin resistance, likely causing excessive glucose utilization in peripheral tissues and hypoglycemia. These results represent the first evidence that inflammation-associated pathways are involved in homeorhetic adaptations to lactation.

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