Glucose, glucagon, and insulin during adrenergic blockade in exercising sheep

1982 ◽  
Vol 52 (2) ◽  
pp. 315-319 ◽  
Author(s):  
R. P. Brockman ◽  
R. Halvorson
Keyword(s):  
Sympathetic Innervation ◽  
Glucagon Secretion ◽  
Glucose Turnover ◽  
Adrenergic Blockade ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Insulin And Glucagon Secretion ◽  
Propranolol Administration ◽  
Exercise Induced ◽  
Glucagon And Insulin

The interrelationships of glucagon and insulin with the sympathetic system on glucose turnover during exercise were examined in sheep. Six sheep were run for 45 min on a treadmill with and without alpha- and/or beta-adrenergic blockade. The exercise-induced increase in glucose appearance, as assessed by infusion of [2–3H]glucose, was reduced during the first 25 min of exercise by phentolamine administration. The metabolic clearance rate of glucose also was greater during exercise with phentolamine treatment than without. Phentolamine was associated with a rise in insulin concentrations and appeared to delay the exercise-induced rise in glucagon. Propranolol administration had no effect on glucose turnover and plasma glucagon and insulin. Nor did it have any effect on the changes in glucose, insulin, or glucagon induced by phentolamine administration. These observations are consistent with the alpha-adrenergic mediation of the sympathetic influences on insulin and glucagon secretion, which may account in part for the glucose adaptations to exercise in sheep. However, direct affects of circulating catecholamines on and increased stimulation of sympathetic innervation to the liver cannot be ruled out.

Effects of subbasal insulin infusion on resting and exercise-induced glucose turnover in depancreatized dogs

1993 ◽  
Vol 264 (3) ◽  
pp. E334-E341 ◽  
Author(s):  
Z. Q. Shi ◽  
A. Giacca ◽  
K. Yamatani ◽  
S. J. Fisher ◽  
H. L. Lickley ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Insulin Infusion ◽  
Glucose Turnover ◽  
Acid Oxidation ◽  
Minimal Amount ◽  
Adrenergic Blockade ◽  
Metabolic Clearance ◽  
Diabetic Dogs ◽  
Exercise Induced

beta-Adrenergic blockade suppressed lipolysis and normalized the exercise-induced increments in glucose uptake (GlcU) and metabolic clearance rate (MCR) in alloxan-diabetic dogs with residual insulin, but not in insulin-deprived depancreatized dogs even when combined with methylpalmoxirate (MP), which suppresses fatty acid oxidation. The effects of a minimal amount of insulin (as in the alloxan-diabetic dog), were studied in depancreatized, 24-h insulin-deprived dogs during rest and treadmill exercise (6 km/h, 10% slope) using a 1/4 basal insulin infusion (50 microU.kg-1.min-1, insulin, n = 6) alone, or with MP (20 mg.kg-1.day orally, 2.5 days, MP+insulin, n = 6). At rest, insulin decreased circulating fatty acids (31%) and Glc (13%) and increased GlcU and MCR (86 and 72%). Glc production was unaffected. MP plus insulin markedly suppressed hepatic fatty acid oxidation, decreased Glc (44%) and Glc production (50%), and markedly increased MCR (128%). The exercise-induced increments in MCR were markedly improved only by MP plus insulin but were still lower than in the propranolol-treated alloxan-diabetic dogs. Plasma Glc inversely correlated with the exercise-induced increase in MCR (r = -0.86). We conclude that 1) acute infusion of subbasal insulin improved GlcU in depancreatized dogs at rest but not during exercise; 2) inhibition of fatty acid oxidation combined with subbasal insulin improved the exercise-induced increase in MCR; and 3) the difference in GlcU and MCR between the MP plus insulin-treated depancreatized dogs and the beta-blockade-treated alloxan-diabetic dogs suggests a difference between acute and chronic effects of insulin.

Glucose-induced decrease in glucagon and pinephrine responses to exercise in man

1977 ◽  
Vol 42 (4) ◽  
pp. 525-530 ◽  
Author(s):  
H. Galbo ◽  
N. J. Christensen ◽  
J. J. Holst
Keyword(s):  
Prolonged Exercise ◽  
Glucagon Secretion ◽  
Glucose Infusion ◽  
Nonesterified Fatty Acid ◽  
Adrenergic Blockade ◽  
Plasma Glucagon ◽  
Beta Adrenergic ◽  
Propranolol Administration ◽  
Glycogen Utilization ◽  
Exercise Induced

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol or without drugs. After propranolol administration the increases during exercise in plasma glucagon and epinephrine concentrations as well as the decrease in plasma glucose concentrations were faster than in control experiments. When euglycemia was maintained by glucose infusion during beta-adrenergic blockade, glucagon and epinephrine responses to exercise, although not abolished, were markedly reduced. The diminution of the exercise-induced decline in glucose concentrations correlated significantly with the diminution of the glucagon as well as the epinephrine responses. Thus decreased glucose concentrations may significantly enhance the secretion of glucagon and epinephrine during prolonged exercise in man. Since the diminution of the glucagon response produced by glucose infusion was not accompanied by significant alterations in the levels of nonesterified fatty acid (NEFA) and glycerol, increased glucagon secretion does not seem to be a major determinant of lipolysis during exercise in man. During glucose infusion, glycogen utilization rates in muscle (n = 4) tended to decrease, whereas carbohydrate combustion rate and concentrations of norepinephrine, insulin, alanine, and lactate were unchanged.

Glucose and lactate kinetics after endotoxin administration in dogs.

1977 ◽  
Vol 232 (2) ◽  
pp. E180 ◽  
Author(s):  
R R Wolfe ◽  
D Elahi ◽  
J J Spitzer
Keyword(s):  
Lactate Concentration ◽  
Constant Infusion ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Plasma Lactate ◽  
Metabolic Clearance Rate ◽  
Metabolic Substrate ◽  
E Coli ◽  
Lactate Kinetics ◽  
Plasma Lactate Concentration

We studied the effects of E. coli endotoxin on the glucose and lactate kinetics in dogs by means of the primed constant infusion of [6(-3)H] glucose and Na-L-(+)-[U-14C] lactate. The infusion of endotoxin induced a transient hyperglycemic level, followed by a steady fall in plasma glucose to hypoglycemic levels. The rate of appearance (Ra) and the rate of disappearance (Rd) of glucose were both significantly elevated (P less than .05) for 150 min after endotoxin, after which neither differed from the preinfusion value. The metabolic clearance rate of glucose was significantly elevated at all times 30 min postendotoxin. By 30 min postendotoxin, Ra and Rd of lactate, plasma lactate concentration, and the percent of glucose turnover originating from lactate were significantly elevated and remained so for the duration of the experiment. We concluded that after endotoxin hypoglycemia developed because of an enhanced peripheral uptake of glucose and a failure of the liver to maintain an increased Ra of glucose. We also concluded that lactate became an important precursor for gluconeogenesis and an important metabolic substrate.

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.

Glucagon and insulin metabolism in a portal-hypertensive rat model

1987 ◽  
Vol 253 (2) ◽  
pp. G110-G115 ◽  
Author(s):  
E. Sikuler ◽  
J. Polio ◽  
R. J. Groszmann ◽  
R. Hendler
Keyword(s):  
Portal Vein ◽  
Rat Model ◽  
Clearance Rate ◽  
Portal Blood Flow ◽  
Portal System ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Insulin Metabolism ◽  
Portosystemic Shunting ◽  
Glucagon And Insulin

The role that portosystemic shunting plays in inducing the alterations of glucagon and insulin metabolism, which are observed in chronic liver disease, was studied in a rat model of prehepatic portal hypertension induced by portal vein constriction. Net splanchnic output of the hormones into the portal circulation was calculated from the difference between portal and systemic concentrations multiplied by portal plasma flow. Metabolic clearance rate was calculated as the ratio between output and systemic concentration. Portal blood flow was measured by the radioactive microsphere technique. Glucagon output in the portal vein-ligated rats was higher than in the sham-operated controls (5.9 +/- 1.5 vs. 2.0 +/- 0.2 ng/min, P less than 0.05). The metabolic clearance rate of glucagon was not significantly different between the two groups. Insulin output was not significantly different between the two groups; however, the metabolic clearance rate of insulin in the portal vein-ligated rats was reduced in comparison with the sham-operated group (9.5 +/- 1.5 vs. 18.4 +/- 3.3 ml/min, P less than 0.05). Our results indicate that portosystemic shunting per se is sufficient to cause an increased splanchnic output of glucagon into the portal system and a decreased metabolic clearance of insulin.

Glucose uptake during centrally induced stress is insulin independent and enhanced by adrenergic blockade

1999 ◽  
Vol 87 (2) ◽  
pp. 722-731 ◽  
Author(s):  
Michael C. Lekas ◽  
Simon J. Fisher ◽  
Ban El-Bahrani ◽  
Mayliza van Delangeryt ◽  
Mladen Vranic ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Marked Rise ◽  
Induced Stress ◽  
Adrenergic Activation

Glucose utilization increases markedly in the normal dog during stress induced by the intracerebroventricular (ICV) injection of carbachol. To determine the extent to which insulin, glucagon, and selective (α/β)-adrenergic activation mediate the increment in glucose metabolic clearance rate (MCR) and glucose production (Ra), we used five groups of normal mongrel dogs: 1) pancreatic clamp (PC; n = 7) with peripheral somatostatin (0.8 μg ⋅ kg−1⋅ min−1) and intraportal replacement of insulin (1,482 ± 84 pmol ⋅ kg−1⋅ min−1) and glucagon (0.65 ng ⋅ kg−1⋅ min−1) infusions; 2) PC plus combined α (phentolamine)- and β (propranolol)-blockade (7 and 5 μg ⋅ kg−1⋅ min−1, respectively; α+β; n = 5); 3) PC plus α-blockade (α; n = 6); 4) PC plus β-blockade (β; n = 5); and 5) a carbachol control group without PC (Con; n = 10). During ICV carbachol stress (0–120 min), catecholamines, ACTH, and cortisol increased in all groups. Baseline insulin and glucagon levels were maintained in all groups except Con, where glucagon rose 33%, and α, where insulin increased slightly but significantly. Stress increased ( P < 0.05) plasma glucose in Con, PC, and α but decreased it in β and α+β. The MCR increment was greater ( P < 0.05) in β and α+β than in Con, PC, and α. Raincreased ( P < 0.05) in all groups but was attenuated in α+β. Stress-induced lipolysis was abolished in β ( P < 0.05). The marked rise in lactate in Con, PC, and α was abolished in α+β and β. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by β-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that Rais augmented by glucagon and α- and β-catecholamine effects.

Effect of somatostatin on plasma glucagon and insulin, and glucose turnover in exercising sheep

1979 ◽  
Vol 47 (2) ◽  
pp. 273-278 ◽  
Author(s):  
R. P. Brockman
Keyword(s):  
Insulin Secretion ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Strenuous Exercise ◽  
Glucose Turnover ◽  
Moderate Exercise ◽  
Plasma Glucagon ◽  
Hepatic Glucose ◽  
Exercise Induced ◽  
Glucagon And Insulin

To examine the roles of glucagon and insulin in exercise, four sheep were run on a treadmill with and without simultaneous infusion of somatostatin (SRIF), a peptide that suppresses glucagon and insulin secretion. SRIF infusion suppressed the exercise-induced rise in plasma glucagon during both moderate (5--5.5 km/h) and strenuous exercise (7.0 km/h). In addition, SRIF prevented the rise insulin concentrations during moderate exercise. During strenuous exercise, insulin concentrations were depressed in both groups. The infusion of SRIF was associated with a reduction in exercise-induced glucose production, as determined by infusion of [6–3H]glucose, during the first 15 min of both moderate and strenuous exercise compared to controls. Beyond 15 min glucose production was not significantly altered by SRIF infusions. These data are consistent with glucagon having an immediate, but only transient, stimulatory effect on the exercise-induced hepatic glucose production.

Effect of adrenal denervation on the glucose, insulin, and glucagon responses to exercise in sheep

1982 ◽  
Vol 60 (12) ◽  
pp. 1459-1463 ◽  
Author(s):  
Ronald P. Brockman
Keyword(s):  
Insulin Secretion ◽  
Adrenal Gland ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Hormonal Stimulation ◽  
Hormonal Responses ◽  
Exercise Induced ◽  
The Right ◽  
Induced Changes ◽  
Stimulation Of

Previous studies suggest that adrenal catecholamines mediate, in part, the glucose and pancreatic hormonal responses to exercise in sheep. This was examined in sheep whose adrenals were denervated to prevent stress-induced changes in catecholamine secretion. The innervation to the right adrenal gland was severed and the left adrenal was removed. Adrenal denervation was associated with a reduction in exercise-induced hyperglycemia and impairment, as measured by [2-3H]glucose, of the increase in glucose appearance during the first 10 min of exercise and increased metabolic clearance rate of glucose after 20 min of exercise. Insulin concentrations were significantly higher during exercise after adrenal denervation than in the controls. Adrenal denervation did not alter the rise in glucagon due to exercise. These effects are consistent with adrenomedullary hormonal stimulation of hepatic and muscular glycogenolysis, either directly or indirectly through the regulation of insulin secretion during exercise in sheep.

scholarly journals A possible mechanism for the anti-ketogenic action of alanine in the rat

1980 ◽  
Vol 190 (2) ◽  
pp. 323-332 ◽  
Author(s):  
Romano Nosadini ◽  
Harish Datta ◽  
Alan Hodson ◽  
K. George M. M. Alberti
Keyword(s):  
Ketone Body ◽  
Ketone Bodies ◽  
Regulatory System ◽  
Glucagon Secretion ◽  
Diabetic Rats ◽  
Metabolic Clearance ◽  
Endogenous Insulin ◽  
Feedback Cycle ◽  
Insulin And Glucagon Secretion ◽  
Acetoacetate Infusion

1. The anti-ketogenic effect of alanine has been studied in normal starved and diabetic rats by infusing l-alanine for 90min in the presence of somatostatin (10μg/kg body wt. per h) to suppress endogenous insulin and glucagon secretion. 2. Infusion of alanine at 3mmol/kg body wt. per h caused a 70±11% decrease in [3-hydroxybutyrate] and a 58±9% decrease in [acetoacetate] in 48h-starved rats. [Glucose] and [lactate] increased, but [non-esterified fatty acid], [glycerol] and [3-hydroxybutyrate]/[acetoacetate] were unchanged. 3. Infusion of alanine at 1mmol/kg body wt. per h caused similar decreases in [ketone body] (3-hydroxybutyrate plus acetoacetate) in 24h-starved normal and diabetic rats, but no change in other blood metabolites. 4. Alanine [3mmol/kg body wt. per h] caused a 72±9% decrease in the rate of production of ketone bodies and a 57±8% decrease in disappearance rate as assessed by [3-14C]acetoacetate infusion. Metabolic clearance was unchanged, indicating that the primary effect of alanine was inhibition of hepatic ketogenesis. 5. Aspartate infusion at 6mmol/kg body wt. per h had similar effects on blood ketone-body concentrations in 48h-starved rats. 6. Alanine (3mmol/kg body wt. per h) caused marked increases in hepatic glutamate, aspartate, malate, lactate and citrate, phosphoenolpyruvate, 2-phosphoglycerate and glucose concentrations and highly significant decreases in [3-hydroxybutyrate] and [acetoacetate]. Calculated [oxaloacetate] was increased 75%. 7. Similar changes in hepatic [malate], [aspartate] and [ketone bodies] were found after infusion of 6mmol of aspartate/kg body wt. per h. 8. It is suggested that the anti-ketogenic effect of alanine is secondary to an increase in hepatic oxaloacetate and hence citrate formation with decreased availability of acetyl-CoA for ketogenesis. The reciprocal negative-feedback cycle of alanine and ketone bodies forms an important non-hormonal regulatory system.

Assessment of Glucose Turnover in Normal Man with the Use of a Non-Radioactive Isotopically Labelled Preparation, [6,6-2H]Glucose, as Tracer

1982 ◽  
Vol 63 (5) ◽  
pp. 437-440 ◽  
Author(s):  
J. W. Haigh ◽  
D. G. Johnston ◽  
A. J. McCulloch ◽  
M. F. Laker ◽  
J. Welby ◽  
...  
Keyword(s):  
Gas Chromatography Mass Spectrometry ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Intravenous Bolus ◽  
Metabolic Clearance Rate ◽  
Glucose Kinetics ◽  
Radioactive Label ◽  
Normal Man ◽  
The Mean ◽  
Male Subjects

1. Glucose kinetics were assessed in seven normal adult male subjects by an intravenous bolus technique with the use of a non-radioactive isotopically labelled preparation, [6,6-2H]glucose, as tracer. Tracer enrichment in plasma was assessed by gas chromatography-mass spectrometry. For comparison five subjects also received a simultaneous intravenous bolus of [6-3H]glucose and kinetics were assessed by conventional means. 2. Administration of [6,6-2H]glucose did not alter circulating glucose or insulin concentrations. 3. Glucose turnover, assessed by the use of [6,6-2H]glucose, was 11·4 (±0·9) μmol min−1 kg−1 and 11·6 (±0·5) μmol min−1 kg−1 with [6-3H]glucose. The mean metabolic clearance rate of glucose was 2·3 (±0·3) ml min−1 kg−1 with both isotopically labelled tracers. Estimates of mean residence time, glucose pool and glucose space were also similar by each technique. 4. [6,6-2H]Glucose is therefore an effective tracer and allows investigation of glucose kinetics without administration of a radioactive label.

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