Glucose Kinetics: Measurement of Flux Rates

Abstract Objective Lactate has been shown to be preferentially metabolized in comparison to glucose after physiological stress, such as strenuous exercise. Derangements of lactate and glucose are common after out-of-hospital cardiac arrest (OHCA). Therefore, we hypothesized that lactate decreases faster than glucose after return-to-spontaneous-circulation (ROSC) after OHCA. Results We included 155 OHCA patients in our analysis. Within the first 8 h of presentation to the emergency department, 843 lactates and 1019 glucoses were available, respectively. Lactate decreased to 50% of its initial value within 1.5 h (95% CI [0.2–3.6 h]), while glucose halved within 5.6 h (95% CI [5.4–5.7 h]). Also, in the first 8 h after presentation lactate decreases more than glucose in relation to their initial values (lactate 72.6% vs glucose 52.1%). In patients with marked hyperlactatemia after OHCA, lactate decreased expediently while glucose recovered more slowly, whereas arterial pH recovered at a similar rapid rate as lactate. Hospital non-survivors (N = 82) had a slower recovery of lactate (P = 0.002) than survivors (N = 82). The preferential clearance of lactate underscores its role as a prime energy substrate, when available, during recovery from extreme stress.

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Effect of burn trauma on glucose turnover, oxidation, and recycling in guinea pigs.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1977.233.2.e80 ◽

1977 ◽

Vol 233 (2) ◽

pp. E80

Author(s):

R R Wolfe ◽

J F Burke

Keyword(s):

Clearance Rate ◽

Guinea Pigs ◽

Glucose Oxidation ◽

Burn Injury ◽

Constant Infusion ◽

Glucose Turnover ◽

Glucose Kinetics ◽

Burn Trauma ◽

Glucose Clearance ◽

Low Rate

The simultaneous primed-constant infusion of [6-3H]- and [U-14C]glucose was used to determine the effect of burn injury on glucose turnover, oxidation, and recycling in guinea pigs. Eleven burned animals survived more than 72 h (survivors), whereas five died between 60 and 72 h postburn. All of the controls (n = 9) survived more than 72 h. At 48 h postburn, glucose turnover in the burned survivors was elevated 40% above that in control animals. A greater portion of the burned survivors' turnover was due to recycling and less was directed towards oxidation. The nonsurvivors had both a significantly depressed rate of appearance of glucose and an increased glucose clearance rate. Consequently, they were profoundly hypoglycemic and had a low rate of glucose oxidation. The alterations in glucose kinetics and oxidation apparent after burn did not reflect an inability of burned animals to oxidize exogenously infused glucose, however, because of 2-h infusion of 55 mumol/kg-min of unlabeled glucose doubled glucose oxidation in the burned survivors and tripled it in the nonsurvivors.

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Five weeks of insulin-like growth factor-I treatment does not alter glucose kinetics or insulin sensitivity during a hyperglycemic clamp in older women

Metabolism ◽

10.1016/s0026-0495(03)00166-5 ◽

2003 ◽

Vol 52 (9) ◽

pp. 1182-1190 ◽

Cited By ~ 1

Author(s):

Barry Braun ◽

Anne L Friedlander ◽

Margaret Pollack ◽

Gail E Butterfield ◽

Robert Marcus ◽

...

Keyword(s):

Insulin Sensitivity ◽

Growth Factor ◽

Older Women ◽

Insulin Like Growth Factor ◽

Glucose Kinetics ◽

Factor I ◽

Hyperglycemic Clamp ◽

Growth Factor I

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Glucose Kinetics During Exercise in Late Pregnancy and Post-Par tum

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-200605001-01728 ◽

2006 ◽

Vol 38 (Supplement) ◽

pp. S189

Author(s):

Juul Achten ◽

Elizabeth Quinlan-Jones ◽

Mark D. Kilby ◽

Julie P. Greeves ◽

Asker E. Jeukendrup

Keyword(s):

Late Pregnancy ◽

Glucose Kinetics

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Kinetic analysis of thyroid hormone action on glucose metabolism in man

Acta Endocrinologica ◽

10.1530/eje.0.1320413 ◽

1995 ◽

Vol 132 (4) ◽

pp. 413-418 ◽

Cited By ~ 3

Author(s):

MJ Müller ◽

CA Reynard ◽

AG Burger ◽

G Toffolo ◽

C Cobelli ◽

...

Keyword(s):

Thyroid Hormone ◽

Glucose Metabolism ◽

Distribution Volume ◽

Hormone Action ◽

Glucose Kinetics ◽

Thyroid Hormone Action ◽

Thyroxine Treatment ◽

Glucose Clearance ◽

Endogenous Glucose ◽

Plasma Triiodothyronine

Müller MJ, Reynard CA, Burger AG, Toffolo G, Cobelli C, Ferrannini E. Kinetic analysis of thyroid hormone action on glucose metabolism in man. Eur J Endocrinol 1995;132:413–18. ISSN 0804–4643 Thyroid hormone action on insulin's effect on glucose kinetics was investigated with the use of a physiological three compartment model. In six healthy volunteers before and after 14 days of thyroxine treatment (300 μg/day), a bolus of [3-H3]glucose was injected and the time course of plasma radioactivity was followed closely for 150 min. Then a hyperinsulinemic (1 mU · min−1 · kg−1) and euglycemic clamp was started, and euglycemia was maintained for another 250 min. A second bolus of the tracer was then given at 240 min, and the plasma radioactivity was followed for 160 min. Insulin stimulated basal plasma glucose clearance fourfold (p < 0.001) and completely suppressed basal hepatic glucose production (p < 0.001). Concomitantly, the total distribution volume of glucose was increased by 19% (p < 0.05); this change was accompanied by about 50% expansion of the slowly exchanging glucose pool (putatively representing the insulin-dependent compartment). Thyroxine treatment increased plasma triiodothyronine by about 20% (0.1 > p > 0.05) but did not affect basal glucose turnover, insulin-stimulated plasma glucose clearance or the insulin-induced suppression of endogenous glucose output. However, thyroxine treatment blunted the insulin-induced increases in total distribution volume and the slowly exchanging pool of glucose (p = NS vs the basal state). We conclude that minor changes in plasma triiodothyronine (such as occur during overfeeding) do not interfere with the ability of insulin to stimulate the rate of disappearance of glucose or suppress endogenous glucose release; however, our data suggest that they induce finer changes in glucose kinetics, possibly reflecting acceleration or intracellular glucose degradation. Manfred J Müller, Institut für Humanernährung und Lebensmittelkunde, Christian-Albrechts-Universität zu Kiel, Düsternbrooker Weg 17, D-24105 Kiel, Germany

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A wearable system for multi-segment foot kinetics measurement

Journal of Biomechanics ◽

10.1016/j.jbiomech.2014.02.027 ◽

2014 ◽

Vol 47 (7) ◽

pp. 1704-1711 ◽

Cited By ~ 19

Author(s):

H. Rouhani ◽

J. Favre ◽

X. Crevoisier ◽

K. Aminian

Keyword(s):

Wearable System ◽

Kinetics Measurement

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Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.255.5.e629 ◽

1988 ◽

Vol 255 (5) ◽

pp. E629-E635 ◽

Cited By ~ 1

Author(s):

D. M. Hargrove ◽

G. J. Bagby ◽

C. H. Lang ◽

J. J. Spitzer

Keyword(s):

Plasma Insulin ◽

Lactate Concentration ◽

Insulin Concentration ◽

Adrenergic Blockade ◽

Plasma Lactate ◽

Glucose Kinetics ◽

Plasma Insulin Concentration ◽

Beta Adrenergic ◽

Plasma Lactate Concentration ◽

Adrenergic Antagonists

Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

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