Glucose turnover in 48-hour-fasted running rats

1987 ◽  
Vol 252 (3) ◽  
pp. R587-R593 ◽  
Author(s):  
B. Sonne ◽  
K. J. Mikines ◽  
H. Galbo
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glucose Turnover ◽  
Feedback Mechanisms ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Fasted Rats

In fed rats, hyperglycemia develops during exercise. This contrasts with the view based on studies of fasted human and dog that euglycemia is maintained in exercise and glucose production (Ra) controlled by feedback mechanisms. Forty-eight-hour-fasted rats (F) were compared to fed rats (C) and overnight food-restricted (FR) rats. [3-3H]- and [U-14C] glucose were infused and blood and tissue sampled. During running (21 m/min, 0% grade) Ra increased most in C and least in F and only in F did Ra not significantly exceed glucose disappearance. Plasma glucose increased more in C (3.3 mmol/l) than in FR (1.6 mmol/l) and only modestly (0.6 mmol/l) and transiently in F. Resting liver glycogen and exercise glycogenolysis were highest in C and similar in FR and F. Resting muscle glycogen and exercise glycogenolysis were highest in C and lowest in F. During running, lactate production and gluconeogenesis were higher in FR than in F. At least in rats, responses of production and plasma concentration of glucose to exercise depend on size of liver and muscle glycogen stores; glucose production matches increase in clearance better in fasted than in fed states. Probably glucose production is stimulated by “feedforward” mechanisms and “feedback” mechanisms are added if plasma glucose decreases.

Effects of Acute Exposure to Bleached Kraft Pulpmill Effluent on Carbohydrate Metabolism of Juvenile Coho Salmon (Oncorhynchus kisutch) During Rest and Exercise

1975 ◽  
Vol 32 (6) ◽  
pp. 753-760 ◽  
Author(s):  
D. J. McLeay ◽  
D. A. Brown
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Coho Salmon ◽  
Liver Glycogen ◽  
Plasma Lactate ◽  
Mean Values ◽  
Glucose Levels ◽  
Lactate Levels ◽  
Sugar Levels ◽  
Glycogen Stores

In the static study (no exercise), liver glycogen stores were unchanged during 12-h exposure to 0.8 of the 96-h LC50; longer exposures caused a progressive decrease to levels one fifth those of controls at 72 h. Plasma glucose levels in fish held in 0.8 LC50 effluent for 3–96 h were elevated; at 96 h, glucose had increased threefold. Mean values for plasma lactate were elevated significantly at 3, 6, 24, 72, and 96 h.In the exercise (swimming one body length per second)–rest study, muscle glycogen levels decreased 53–78% during exercise in water or effluent (0.7 LC50) for 4–12 h, and did not recover during 12-h rest in water. Muscle glycogen for fish exercised for 12 h in effluent and then rested for 4 or 12 h in effluent was lower compared to values for fish exercised in effluent and then rested in water. There was no difference in liver glycogen levels offish exercised in effluent or water for 4–12 h. Values of liver glycogen for fish exercised in effluent for 12 h and then rested for 4, 8, or 12 h in effluent decreased 60–70% compared to fish exercised in water for 12 h and then rested in water and by 55–65% from fish exercised in effluent for 12 h and rested in water for 4–12 h. Plasma glucose levels were elevated one- to fourfold during exercise in water or effluent. Fish resting in water for 4, 8, or 12 h following exercise in water had relatively stable glucose levels; whereas for fish exercised and then rested in effluent the glucose levels increased twofold during resting. Plasma lactate levels were elevated five- to sixfold during exercise in water or effluent for 4–12 h, declining to values 1–2 times those of stock fish within 4-h rest. Plasma lactate levels for fish exercised in effluent and then rested in effluent or water were continually higher than those for fish exercised and rested in water.It was concluded that measurement of carbohydrate metabolites, particularly blood sugar levels, in unexercised fish could prove useful as a rapid method for measuring toxicity of pulpmill effluents and other pollutants.

Glucose production, recycling, and gluconeogenesis in normals and diabetics: a mass isotopomer [U-13C]glucose study

1996 ◽  
Vol 270 (4) ◽  
pp. E709-E717 ◽  
Author(s):  
J. A. Tayek ◽  
J. Katz
Keyword(s):  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Tricarboxylic Acid Cycle ◽  
Glucose Production ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Glucose Turnover ◽  
Insulin Dependent ◽  
Gas Chromatography Mass Spectroscopy ◽  
Mass Isotopomer

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.

Regulation of glucose turnover and hormonal responses during electrical cycling in tetraplegic humans

1996 ◽  
Vol 271 (1) ◽  
pp. R191-R199 ◽  
Author(s):  
M. Kjaer ◽  
S. F. Pollack ◽  
T. Mohr ◽  
H. Weiss ◽  
G. W. Gleim ◽  
...  
Keyword(s):  
Heart Rate ◽  
Plasma Glucose ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Glucose Turnover ◽  
Hormonal Responses ◽  
Hepatic Glucose ◽  
Exercise Period ◽  
Exercise Activity ◽  
Beta Hydroxybutyrate

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.

Effect of beta-adrenergic blockade on lactate turnover in exercising dogs

1984 ◽  
Vol 57 (6) ◽  
pp. 1754-1759 ◽  
Author(s):  
B. Issekutz
Keyword(s):  
Plasma Glucose ◽  
Lactate Production ◽  
Hormonal Control ◽  
Glucose Turnover ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Metabolic Clearance ◽  
Beta Adrenergic ◽  
Indwelling Catheters ◽  
Lactate Turnover

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.

Effect of sequential infusions of glucagon and epinephrine on glucose turnover in the dog.

1978 ◽  
Vol 235 (3) ◽  
pp. E287 ◽  
Author(s):  
L Saccà ◽  
R Sherwin ◽  
P Felig
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Conscious Dogs ◽  
Glucose Turnover ◽  
Plasma Glucagon ◽  
Conscious Dog ◽  
Glucose Clearance ◽  
Glucose Output

Conscious dogs were infused with 1) glucagon (3 ng/kg.min) alone for 120 min followed by glucagon plus epinephrine (0.1 microgram/kg.min) for 60 min and 2) epinephrine alone (150 min) followed by epinephrine plus glucagon for 90 min. Glucagon alone caused a 10--15 mg/dl rise in plasma glucose and a 45% increase in glucose production that returned to baseline by 75--120 min. After addition of epinephrine, glucose production rose again by 80%. Infusion of epinephrine alone resulted in unchanged plasma glucagon levels, a 60--70 mg/dl rise in plasma glucose, and an 80--100% rise in glucose production that returned to baseline by 60--120 min. When glucagon was added, glucose output promptly rose again by 85%. When glucagon was infused alone, there was a rise in glucose uptake, whereas, with epinephrine, glucose uptake failed to rise and glucose clearance fell by 35--50%. We conclude that 1) hepatic refractoriness to persistent elevations of glucagon or epinephrine is specific for the hormone infused; 2) epinephrine stimulates glucose production in the conscious dog in the absence of a rise in plasma glucagon; 3) the hyperglycemic response to glucagon or epinephrine is determined in part by accompanying changes in glucose utilization.

Glucose carbon recycling and oxidation in human newborns

1986 ◽  
Vol 251 (1) ◽  
pp. E71-E77 ◽  
Author(s):  
S. C. Denne ◽  
S. C. Kalhan
Keyword(s):  
Plasma Glucose ◽  
Glucose Oxidation ◽  
Cerebral Metabolism ◽  
Glucose Production ◽  
Carbohydrate Oxidation ◽  
Glucose Turnover ◽  
Total Carbohydrate ◽  
True Rate ◽  
Glucose Carbon ◽  
Carbon Recycling

Total carbohydrate oxidation, plasma glucose oxidation, and glucose carbon recycling were measured in 11 fasting newborns using a constant infusion of D-[U-13C]glucose combined with respiratory calorimetry. The "true" rate of glucose appearance (Ra) was quantified from the enrichment of the nonrecycling tracer species (m + 6), while the "apparent" rate of glucose appearance was quantified from the enrichment of glucose C - 1. The plasma glucose concentration remained constant at approximately 50 mg/dl (2.8 mM) throughout the study. The true rate of glucose production was 5.02 +/- 0.41 mg X kg-1 X min-1, (means +/- SD). Glucose was oxidized at a rate of 2.67 +/- 0.34 mg X kg-1 X min-1 and represented 53% of the glucose turnover. Recycling of glucose carbon represented 36% of the glucose production rate, or 1.87 +/- 0.74 mg X kg-1 X min-1. The oxidation of plasma glucose provided 15.8 +/- 2.0 kcal X kg-1 X day-1, whereas total carbohydrate oxidation (measured by respiratory calorimetry) provided 19.9 +/- 6.6 kcal X kg X day. The data indicate that 1) recycling of glucose carbon accounts for about one-third of glucose production, demonstrating active gluconeogenesis in the fasting newborn; 2) the oxidation of plasma glucose represents only 80% of total carbohydrate oxidation, the remaining 20% possibly representing the local oxidation of tissue glycogen stores; and 3) as the measured rate of glucose oxidation will be insufficient to supply the entire calculated cerebral metabolic requirements, these data suggest that fuels in addition to glucose may be important for cerebral metabolism in the fasting human newborn.

Shivering thermogenesis and glucose uptake by muscles of normal or diabetic rats

1982 ◽  
Vol 242 (1) ◽  
pp. R109-R115 ◽  
Author(s):  
O. L. Smith ◽  
S. B. Davidson
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Serum Insulin ◽  
Liver Glycogen ◽  
Diabetic Rats ◽  
Glucose Levels ◽  
Severe Diabetes ◽  
Mild Diabetes ◽  
Fasted Rats ◽  
Shivering Thermogenesis

Acute cold exposure of normal rats (4 degrees C for 24 h) increased food intake, reduced plasma glucose and liver glycogen, caused a small increase in plasma free fatty acids, and lowered serum insulin concentration by 50%. In fasted rats, cold raised fatty acid levels twice as high as in fed. In mild diabetes (40 mg/kg streptozotocin iv) cold reduced glucose levels in blood and urine, but in severe diabetes (90 mg/kg) cold aggravated hyperglycemia and ketonuria. Changes in muscle glucose utilization were also studied, after evisceration (functional hepatectomy) of rats from each group. Uptake was calculated from the fall in plasma glucose concentration during the 4-h period after a load of 50% glucose iv. Cold normally increased uptake 67%, but it failed to do so in fasted rats. In diabetic rats, cold enhanced uptake, but only if the disease were mild or insulin controlled. Sensitivity of uptake to insulin was unaffected by cold. The results suggest that shivering thermogenesis, like exercise, can promote glucose uptake by skeletal muscle, if enough insulin is present to prevent excess mobilization of lipid substrates.

Effects of glucagon-like peptide-I on glucose turnover in rats

1996 ◽  
Vol 270 (6) ◽  
pp. E1015-E1021 ◽  
Author(s):  
G. Van Dijk ◽  
S. Lindskog ◽  
J. J. Holst ◽  
A. B. Steffens ◽  
B. Ahren
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glucose Turnover ◽  
Plasma Glucagon ◽  
Appearance Rate ◽  
Glucose Clearance ◽  
Peripheral Effect ◽  
Freely Moving ◽  
Glucagon Like Peptide ◽  
Fasted Rats

The influences of glucagon-like peptide-I-(7-36) amide (GLP-I; 15 mumol. kg-1.min-1) on glucose turnover were studied in freely moving Wistar rats. In fed rats, GLP-1 reduced plasma glucose (from 7.3 +/- 0.2 to 5.6 +/- 0.3 mmol/l; P = 0.017), increased plasma insulin (from 20 +/- 3 to 89 +/- 11 mU/l; P = 0.002), and reduced plasma glucagon (from 44 +/- 1 to 35 +/- 2 pg/ml; P = 0.009) and glucose appearance rate (Ra; from 3.9 +/- 0.2 to 1.7 +/- 0.7 micromol.min-1. 100 g-1 after 30 min; P = 0.049) without affecting glucose disappearance rate (Rd). The glucose clearance rate (MCR) was increased (P = 0.048). In 48-h-fasted rats, GLP-I reduced plasma glucose (from 5.0 +/- 0.2 to 4.4 +/- 0.3 mmol/l; P = 0.035) and increased plasma insulin (from 4 +/- 1 to 25 +/- 10 mU/l; P = 0.042) and plasma glucagon (from 43 +/- 3 to 61 +/- 7 pg/ml; P = 0.046). Ra and Rd were not significantly affected, although Ra was lower than Rd after 15-30 min (P = 0.005) and MCR was increased (P = 0.049). Thus GLP-I reduces Ra in fed rats and increases MCR in fed and fasted rats. The reduced Ra seems mediated by an increased insulin-to-glucagon ratio; the increased glucose clearance seems dependent on insulin and a peripheral effect of GLP-I.

Manipulation of dietary carbohydrate and muscle glycogen affects glucose uptake during exercise when fat oxidation is impaired by β-adrenergic blockade

2004 ◽  
Vol 287 (6) ◽  
pp. E1195-E1201 ◽  
Author(s):  
Theodore W. Zderic ◽  
Simon Schenk ◽  
Christopher J. Davidson ◽  
Lauri O. Byerley ◽  
Edward F. Coyle
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Fat Oxidation ◽  
Whole Body ◽  
Moderate Intensity ◽  
Glucose Turnover ◽  
Adrenergic Blockade ◽  
High Fat ◽  
Carbohydrate Diet

We have recently reported that, during moderate intensity exercise, low muscle glycogen concentration and utilization caused by a high-fat diet is associated with a marked increase in fat oxidation with no effect on plasma glucose uptake (Rd glucose). It is our hypothesis that this increase in fat oxidation compensates for low muscle glycogen, thus preventing an increase in Rd glucose. Therefore, the purpose of this study was to determine whether low muscle glycogen availability increases Rd glucose under conditions of impaired fat oxidation. Six cyclists exercised at 50% peak O2 consumption (V̇o2 peak) for 1 h after 2 days on either a high-fat (HF, 60% fat, 24% carbohydrate) or control (CON, 22% fat, 65% carbohydrate) diet to manipulate muscle glycogen to low and normal levels, respectively. Two hours before the start of exercise, subjects ingested 80 mg of propanolol (βB), a nonselective β-adrenergic receptor blocker, to impair fat oxidation during exercise. HF significantly decreased calculated muscle glycogen oxidation ( P < 0.05), and this decrease was partly compensated for by an increase in fat oxidation ( P < 0.05), accompanied by an increase in whole body lipolysis ( P < 0.05), despite the presence of βB. Although HF increased fat oxidation, plasma glucose appearance rate, Rd glucose, and glucose clearance rate were also significantly increased by 13, 15, and 26%, respectively (all P < 0.05). In conclusion, when lipolysis and fat oxidation are impaired, in this case by βB, fat oxidation cannot completely compensate for a reduction in muscle glycogen utilization, and consequently plasma glucose turnover increases. These findings suggest that there is a hierarchy of substrate compensation for reduced muscle glycogen availability after a high-fat, low-carbohydrate diet, with fat being the primary and plasma glucose the secondary compensatory substrate. This apparent hierarchy likely serves to protect against hypoglycemia when endogenous glucose availability is low.

Oxidation of an oral [13C]glucose load at rest and prolonged exercise in trained and sedentary subjects

1999 ◽  
Vol 86 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Y. Burelle ◽  
F. Péronnet ◽  
S. Charpentier ◽  
C. Lavoie ◽  
C. Hillaire-Marcel ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Glucose Oxidation ◽  
Prolonged Exercise ◽  
Glucose Load ◽  
Exogenous Glucose ◽  
Glycogen Stores ◽  
Male Subjects ◽  
Sedentary Subjects

The purpose of this study was to compare the oxidation of [13C]glucose (100 g) ingested at rest or during exercise in six trained (TS) and six sedentary (SS) male subjects. The oxidation of plasma glucose was also computed from the volume of13CO2and13C/12C in plasma glucose to compute the oxidation rate of glucose released from the liver and from glycogen stores in periphery (mainly muscle glycogen stores during exercise). At rest, oxidative disposal of both exogenous (8.3 ± 0.3 vs. 6.6 ± 0.8 g/h) and liver glucose (4.4 ± 0.5 vs. 2.6 ± 0.4 g/h) was higher in TS than in SS. This could contribute to the better glucose tolerance observed at rest in TS. During exercise, for the same absolute workload [140 ± 5 W: TS = 47 ± 2.5; SS = 68 ± 3 %maximal oxygen uptake (V˙o 2 max)], [13C]glucose oxidation was higher in TS than in SS (39.0 ± 2.6 vs. 33.6 ± 1.2 g/h), whereas both liver glucose (16.8 ± 2.4 vs. 24.0 ± 1.8 g/h) and muscle glycogen oxidation (36.0 ± 3.0 vs. 51.0 ± 5.4 g/h) were lower. For the same relative workload (68 ± 3% V˙o 2 max: TS = 3.13 ± 0.96; SS = 2.34 ± 0.60 l O2/min), exogenous glucose (44.4 ± 1.8 vs. 33.6 ± 1.2 g/h) and muscle glycogen oxidation (73.8 ± 7.2 vs. 51.0 ± 5.4 g/h) were higher in TS. However, despite a higher energy expenditure in TS, liver glucose oxidation was similar in both groups (22.2 ± 3.0 vs. 24.0 ± 1.8 g/h). Thus exogenous glucose oxidation was selectively favored in TS during exercise, reducing both liver glucose and muscle glycogen oxidation.

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