TURNOVER OF PLASMA GLUCOSE IN ANESTHETIZED WARM- AND COLD-ACCLIMATED RATS EXPOSED TO COLD

1959 ◽  
Vol 37 (1) ◽  
pp. 175-181
Author(s):  
Florent Depocas

The turnover of plasma glucose has been measured in anesthetized warm- and cold-acclimated white rats by a method involving a single injection of a tracer amount of uniformly labelled C14-glucose at 30 °C, and measurement of the rate of fall of the plasma glucose specific activity in animals maintained at 30 °C or moved to an environment at 6 °C. Analysis of the data indicated a significant increase in the rate of disappearance of the labelled glucose when the warm-acclimated rats were transferred from 30° to 6 °C but no significant change when the cold-acclimated rats were similarly treated. The concentration of plasma glucose remained essentially constant throughout the observation period. These results may be taken to indicate that the cold-induced increase in metabolism of anesthetized white rats is associated with an increase in plasma glucose turnover in warm-acclimated animals only.

1959 ◽  
Vol 37 (2) ◽  
pp. 175-181 ◽  
Author(s):  
Florent Depocas

The turnover of plasma glucose has been measured in anesthetized warm- and cold-acclimated white rats by a method involving a single injection of a tracer amount of uniformly labelled C14-glucose at 30 °C, and measurement of the rate of fall of the plasma glucose specific activity in animals maintained at 30 °C or moved to an environment at 6 °C. Analysis of the data indicated a significant increase in the rate of disappearance of the labelled glucose when the warm-acclimated rats were transferred from 30° to 6 °C but no significant change when the cold-acclimated rats were similarly treated. The concentration of plasma glucose remained essentially constant throughout the observation period. These results may be taken to indicate that the cold-induced increase in metabolism of anesthetized white rats is associated with an increase in plasma glucose turnover in warm-acclimated animals only.


2004 ◽  
Vol 287 (3) ◽  
pp. E414-E423 ◽  
Author(s):  
Yuka Fujimoto ◽  
E. Patrick Donahue ◽  
Masakazu Shiota

Hepatic glucose fluxes and intracellular movement of glucokinase (GK) in response to increased plasma glucose and insulin were examined in 10-wk-old, 6-h-fasted, conscious Zucker diabetic fatty (ZDF) rats and lean littermates. Under basal conditions, plasma glucose (mmol/l) and glucose turnover rate (GTR; μmol·kg−1·min−1) were slightly higher in ZDF (8.4 ± 0.3 and 53 ± 7, respectively) than in lean rats (6.2 ± 0.2 and 45 ± 4, respectively), whereas plasma insulin (pmol/l) was higher in ZDF (1,800 ± 350) than in lean rats (150 ± 14). The ratio of hepatic uridine 5′-diphosphate-glucose 3H specific activity to plasma glucose 3H specific activity ([3H]UDP-G/[3H]G; %), total hepatic glucose output (μmol·kg−1·min−1), and hepatic glucose cycling (μmol·kg−1·min−1) were higher in ZDF (35 ± 5, 87 ± 16, and 33 ± 10, respectively) compared with lean rats (18 ± 3, 56 ± 6, and 11 ± 2, respectively). [3H]glucose incorporation into glycogen (μmol glucose/g liver) was similar in lean (1.0 ± 0.7) and ZDF (1.6 ± 0.8) rats. GK was predominantly located in the nucleus in both rats. With elevated plasma glucose and insulin, GTR (μmol·kg−1·min−1), [3H]UDP-G/[3H]G (%), and [3H]glucose incorporation into glycogen (μmol glucose/g liver) were markedly higher in lean (191 ± 22, 62 ± 3, and 5.0 ± 1.4, respectively) but similar in ZDF rats (100 ± 6, 37 ± 3, and 1.4 ± 0.4, respectively) compared with basal conditions. GK translocation from the nucleus to the cytoplasm occurred in lean but not in ZDF rats. The unresponsiveness of hepatic glucose flux to the rise in plasma glucose and insulin seen in prediabetic ZDF rats was associated with impaired GK translocation.


1996 ◽  
Vol 270 (4) ◽  
pp. E709-E717 ◽  
Author(s):  
J. A. Tayek ◽  
J. Katz

Eight normal controls and nine non-insulin-dependent diabetes mellitus diabetics were, after an overnight fast, infused for 3 h with [6-3H]- and with [U-13C]glucose with six 13C carbons at rates from 0.03 to 0.15 mg.kg-1.min-1. Plasma glucose and lactate were assayed by gas chromatography-mass spectroscopy. Several parameters of glucose metabolism were calculated from the mass isotopomer distribution. Glucose production (GP) determined with [6-3H]- and [U-13C]glucose agreed closely. GP was 1.9 +/- 0.16 (range 1.3-2.5) mg.kg-1.min-1 in controls and 2.8 +/- 0.29 (1.7-4.5) mg.kg-1.min-1 in diabetics (P < 0.05). The correlation in diabetes between plasma glucose and GP (r = 0.911, P < 0.01) was close. Recycling of carbon (8 vs 7%) dilution by unlabeled carbon (2- vs 2.3-fold), and dilution via the tricarboxylic acid cycle (1.5-fold) were similar in controls and diabetics. Gluconeogenesis was 0.90 +/- 0.08 (0.5-1.3) mg.kg-1.min-1 in controls and 1.30 +/- 0.13 (0.8-1.9) mg.kg-1.min-1 in diabetics (P < 0.05). Gluconeogenesis contributions to GP were 46.6 +/- 4.0% (26-61%) in the controls and 48.8 +/- 5.7% (32-83%) in diabetics. We show that, using [U-13C]glucose infusion of 2-5% of glucose turnover (0.03-0.10 mg.kg-1.min-1), a large number of parameters of glucose metabolism may be determined in humans.


1995 ◽  
Vol 269 (1) ◽  
pp. R64-R72 ◽  
Author(s):  
C. M. Bishop ◽  
P. J. Butler ◽  
S. Egginton ◽  
A. J. el Haj ◽  
G. W. Gabrielsen

Preflight development of the goslings was typified by rapid increases in the mitochondrial enzymes of the semimembranosus and heart ventricular muscles resulting in near-adult values by 3 wk of age. In contrast, aerobic capacity of the pectoralis muscle initially developed slowly but showed a rapid increase between 5 and 7 wk of age, in preparation for becoming airborne. Activities of glycolytic enzymes in the pectoralis muscle showed similar patterns of development as those found for the aerobic enzymes, except for hexokinase, which was low at all ages, indicating an adaptation for catabolism of both intracellular glycogen and plasma fatty acids in preference to plasma glucose. Muscle mass specific activity of citrate synthase in the pectoralis increased by only 33% from goslings during the first few days of flight, compared with premigratory geese. Activities of anaerobic glycolytic enzymes in the ventricles were low, but values for hexokinase, which is involved in the phosphorylation of plasma glucose, developed rapidly. Values for lactate dehydrogenase were also high, reflecting the capacity of the heart to catabolize plasma lactate. Substrate flux supplied by carnitine palmitoyltransferase and oxoglutarate dehydrogenase (OGD), in the pectoralis muscles of the premigratory geese, appears to have the smallest excess capacities to meet the requirements of sustained aerobic flight. The average maximum oxygen uptake for premigratory geese during flight, as indicated by values for OGD, is calculated to be 484 ml O2/min (or 208 ml O2.min-1.kg-1).


1992 ◽  
Vol 263 (1) ◽  
pp. E17-E22 ◽  
Author(s):  
H. Katz ◽  
M. Homan ◽  
P. Butler ◽  
R. Rizza

[3-3H]glucose is frequently used to measure glucose turnover in humans. If fructose 6-phosphate-fructose 1,6-diphosphate cycling (Fpc) is negligible in both liver and muscle, then [3-3H]- and [6-14C]glucose (corrected for Cori cycle activity) should provide equivalent measures of glucose turnover. In addition, if glycogenolysis is fully suppressed, then [14C]lactate specific activity should equal that of [6-14C]glucose from which it was derived, and oxidation of [6-14C]glucose, as measured by rate of generation of 14CO2, should equal total glucose oxidation (i.e., that derived from intra- and extracellular pools) as measured by indirect calorimetry. To address these questions, glucose turnover was measured simultaneously with [3-3H]- and [6-14C]glucose in the basal state and in presence of low (approximately 200 pM) and high (approximately 750 pM) insulin concentrations. Glucose turnover rates measured with [3-3H]- and [6-14C]glucose were equivalent at all insulin concentrations, indicating that Fpc had no detectable effect on measurement of glucose appearance. [14C]lactate specific activity was lower (P less than 0.01) than that of [6-14C]glucose in the basal state but not during either low- or high-dose insulin infusion, implying that all lactate was derived from extracellular glucose. On the other hand, glucose oxidation as measured by rate of generation of 14CO2 was lower (P less than 0.05) than glucose oxidation as measured by indirect calorimetry during both insulin infusions, implying either that suppression of glycogenolysis was not complete in all tissues or that one or both of these techniques do not accurately measure glucose oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 271 (1) ◽  
pp. R191-R199 ◽  
Author(s):  
M. Kjaer ◽  
S. F. Pollack ◽  
T. Mohr ◽  
H. Weiss ◽  
G. W. Gleim ◽  
...  

To examine the importance of blood-borne vs. neural mechanisms for hormonal responses and substrate mobilization during exercise, six spinal cord-injured tetraplegic (C5-T1) males (mean age: 35 yr, range: 24-55 yr) were recruited to perform involuntary, electrically induced cycling [functional electrical stimulation (FES)] to fatigue for 24.6 +/- 2.3 min (mean and SE), and heart rate rose from 67 +/- 7 (rest) to 107 +/- 5 (exercise) beats/min. Voluntary arm cranking in tetraplegics (ARM) and voluntary leg cycling in six matched, long-term immobilized (2-12 mo) males (Vol) served as control experiments. In FES, peripheral glucose uptake increased [12.4 +/- 1.1 (rest) to 19.5 +/- 4.3 (exercise) mumol.min-1.kg-1; P < 0.05], whereas hepatic glucose production did not change from basal values [12.4 +/- 1.4 (rest) vs. 13.0 +/- 3.4 (exercise) mumol.min-1.kg-1]. Accordingly, plasma glucose decreased [from 5.4 +/- 0.3 (rest) to 4.7 +/- 0.3 (exercise) mmol/l; P < 0.05]. Plasma glucose did not change in response to ARM or Vol. Plasma free fatty acids and beta-hydroxybutyrate decreased only in FES experiments (P < 0.05). During FES, increases in growth hormone (GH) and epinephrine and decreases in insulin concentrations were abolished. Although subnormal throughout the exercise period, norepinephrine concentrations increased during FES, and responses of heart rate, adrenocorticotropic hormone, beta-endorphin, renin, lactate, and potassium were marked. In conclusion, during exercise, activity in motor centers and afferent muscle nerves is important for normal responses of GH, catecholamines, insulin, glucose production, and lipolysis. Humoral feedback and spinal or simple autonomic nervous reflex mechanisms are not sufficient. However, such mechanisms are involved in redundant control of heart rate and neuroendocrine activity in exercise.


1984 ◽  
Vol 57 (6) ◽  
pp. 1754-1759 ◽  
Author(s):  
B. Issekutz

Dogs with indwelling catheters in the jugular vein and in the carotid artery ran on the treadmill (slope: 15%, speed: 133 m/min). Lactate turnover and glucose turnover were measured using [U-14C]lactate and [3-3H]glucose as tracers, according to the primed constant-rate infusion method. In addition, the participation of plasma glucose in lactate production (Ra-L) was measured with [U-14C]glucose. Propranolol was given either (A) before exercise (250 micrograms/kg, iv) or (B) in form of a primed infusion administered to the dog running at a steady rate. Measurements of plasma propranolol concentration showed that in type A experiments plasma propranolol fell in 45 min below the lower limit of the complete beta-blockade. In the first 15 min of work Ra-L rose rapidly; then it fell below that of the control (exercise) values. During steady exercise, the elevated Ra-L was decreased by propranolol infusion close to resting values. beta-Blockade doubled the response of glucose production, utilization, and metabolic clearance rate to exercise. In exercising dogs approximately 40-50% of Ra-L arises from plasma glucose. This value was increased by the blockade to 85-90%. It is concluded that glycogenolysis in the working muscle has a dual control: 1) an intracellular control operating at the beginning of exercise, and 2) a hormonal control involving epinephrine and the beta-adrenergic receptors.


Metabolism ◽  
1996 ◽  
Vol 45 (1) ◽  
pp. 82-91 ◽  
Author(s):  
Ole Hother-Nielsen ◽  
Jan Erik Henriksen ◽  
Jens Juul Holst ◽  
Henning Beck-Nielsen

1955 ◽  
Vol 33 (6) ◽  
pp. 926-939 ◽  
Author(s):  
Margaret J. Henderson ◽  
Gerald A. Wrenshall ◽  
Paul Odense

An attempt to answer the question as to whether insulin acts to lower blood glucose by increasing utilization, or by decreasing production, or by both, has been made using a new experimental approach. A trace dose of radioactive glucose was injected into each of six postabsorptive depancreatized dogs which had been deprived of exogenous insulin for 66 hr. Blood samples were collected before and after the intravenous injection of insulin, and plasma glucose concentration and specific activity were measured. From these data the simultaneous rates of appearance and disappearance of plasma glucose were calculated for a sequence of time intervals, both before and after insulin, by a method which did not assume dynamic equilibrium. Previous in vivo experiments using radioactive tracers to measure rates of production and utilization of glucose have been made in animals which were in steady states, either with or without insulin, and the effects of insulin were ascertained by comparison of the state with insulin and the state without insulin. The method described in this paper has made it possible to follow the effects of insulin while it is acting in one and the same animal. Insulin was found to cause an abrupt and marked increase in the rate of disappearance of glucose, and this increased rate became less with time, reaching the preinsulin level in about 90 min. Insulin caused a slower and much smaller decrease in the rate of appearance, but the decrease became greater with time during the three hour period of observation. Thus, it appeared that insulin acted in vivo both to increase the utilization of glucose and to decrease its production, but the effects differed in magnitude and in speed of response.


1992 ◽  
Vol 263 (6) ◽  
pp. R1241-R1247 ◽  
Author(s):  
B. S. Washburn ◽  
M. L. Bruss ◽  
E. H. Avery ◽  
R. A. Freedland

Reports of changes in carbohydrate metabolism during vitellogenesis in fish prompted an investigation of the effects of estrogen on glucose utilization in rainbow trout. Estrogen pellets were implanted in both female and male fish, and a third group of male fish was given a sham operation. After cannulation of the dorsal aorta, D-[1-3H]glucose and 2-deoxy-D-[U-14C]glucose were injected into the fish to observe whole animal and tissue glucose use. We found that estrogen does not affect glucose turnover rate or transit time but causes a decrease in plasma glucose concentration and size of the glucose mixing pool. Adipose tissue in female fish utilized glucose at a higher rate than sham fish. Ovarian tissue used more glucose per kilogram of body weight than the testes of the male fish. Regardless of treatment, brain had the highest rate of glucose consumption per gram of tissue, followed by gonads and red blood cells. Muscle and adipose tissue utilized only small amounts (< 1 nmol.g tissue-1.min-1) of glucose. We conclude that an increase in the rate of whole body glucose use is not responsible for the fall in plasma glucose caused by estrogen and seen during vitellogenesis.


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