The Effect of Exercise on Glucagon Secretion*

Böttger, I.; Schlein, Edward; Faloona, Gerald R.; Knöchel, James P.; Unger, Roger H

doi:10.1210/jcem-35-1-117

Cited by 85 publications

(22 citation statements)

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“…The failure of IRG to increase in response to infusions of arginine in insulininfused depancreatized dogs (22) and the altered relationship between plasma levels of glucose and IRG (7) had suggested that the regulation of the release of extrapancreatic glucagon differs from that of pancreatic glucagon. This is corroborated in the present experiments: as reported previously serum IRG rose during exercise in intact animals (6,28,29), but not in the depancreatized dogs. These dissimilar IRG responses to exercise may be due to differences in the innervation and/or anatomical distribution of the glucagon-producing cells.…”

Section: Depancreatizedsupporting

confidence: 94%

The essentiality of insulin and the role of glucagon in regulating glucose utilization and production during strenuous exercise in dogs.

et al. 1976

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A B S T R A C T In order to elucidate the role of insulin and glucagon during strenuous exercise (100 m/min, slope 10-12°), we have determined the rates of production (Ra), utilization (Rd), and metabolic clearance (M) of glucose in normal dogs before pancreatectomy and 2 wk after total pancreatectomy (a) when they were being maintained on constant intraportal basal insulin infusion, (245 uU/kg-min)

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Section: Depancreatizedsupporting

confidence: 94%

The essentiality of insulin and the role of glucagon in regulating glucose utilization and production during strenuous exercise in dogs.

et al. 1976

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“…In dog, glucagon increases gradually with the onset of exercise (in these studies glucagon doubled after 90 min). In man, glucagon only increases in strenuous or prolonged exercise (5,6). With ST infusion during exercise, cortisol and epinephrine levels were both higher than during normoglycemic exercise (Fig.…”

Section: Discussionmentioning

confidence: 92%

“…To maintain euglycemia, hepatic glucose production (Ra)' must increase to match peripheral glucose uptake. Increased sympathetic drive (4), an increase in glucagon (5,6) and circulating catecholamines (6,7), and a decrease in insulin (2,7) are all characteristic responses to exercise. All of these hormonal and neural changes are known to increase Ra (8).…”

Section: Introductionmentioning

confidence: 99%

Interactions between glucagon and other counterregulatory hormones during normoglycemic and hypoglycemic exercise in dogs.

Wasserman¹,

Lickley²,

Vranić³

1984

J. Clin. Invest.

103

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A bstract. Somatostatin (ST)-induced glucagon suppression results in hypoglycemia during rest and exercise. To further delineate the role of glucagon and interactions between glucagon and the catecholamines during exercise, we compensated for the counterregulatory responses to hypoglycemia with glucose replacement. Five dogs were run (100 m/min, 120) during exercise alone, exercise plus ST infusion (0.5 gg/kg-min), or exercise plus ST plus glucose replacement (3.5 mg/kgmin) to maintain euglycemia. During exercise alone there was a maximum increase in immunoreactive glucagon (IRG), epinephrine (E), norepinephrine (NE), FFA, and lactate (L) of 306±147 pg/ml, 360±80 pg/ml, 443±140 pg/ml, 541±173 geq/liter, and 6.3±0.7 mg/dl, respectively. Immunoreactive insulin (IRI) decreased by 10.2±4 ttU/ml and cortisol (C) increased only slightly (2.1±0.3 ug/dl). The rates of glucose production (Ra) and glucose uptake (Rd) rose markedly by 6.6±2.2 mg/ kg-min and 6.2±1.5 mg/kg-min. In contrast, when ST was given during exercise, IRG fell transiently by 130±20 pg/ml, Ra rose by only 3.6±0.5 mg/kg-min, and plasma glucose decreased by 29±6 mg/dl. The decrease in IRI was no different than with exercise alone (10.2±2.0 ,U/ ml). As plasma glucose fell, C, FFA, and L rose excessively to peaks of 5.4±1.3 ig/dl, 1,166±182 geq/liter and 15.5±7.0 mg/dl. The peak increment in E (765±287 pg/ml) coincided with the nadir in plasma glucose and was four times greater than during normoglycemic exercise. Hypoglycemia did not affect the rise in NE. The increase in Rd was attenuated and reached a peak of only 3.7±0.8 mg/kg-min. During glucose replacement, IRG decreased by 109±30 pg/ml and the IRI response did not differ from the response to normal exercise. Ra rose minimally by 1.5±0.3 mg/kg-min. The changes in E, C, Rd, and L were restored to normal, whereas the FFA response remained excessive. In all protocols increments in Ra were directly correlated to the IRG/IRI molar ratio while no correlation could be demonstrated between epinephrine or norepinephrine and Ra. In conclusion, (a) glucagon controlled -70% of the increase of Ra during exercise. This became evident when counterregulatory responses to hypoglycemia (E and C) were obviated by glucose replacement; (b) increments in Ra were strongly correlated to the IRG/IRI molar ratio but not to the plasma catecholamine concentration; (c) the main role of E in hypoglycemia was to limit glucose uptake by the muscle; (d) with glucagon suppression, glucose production was deficient but a further decline of glucose was prevented through the peripheral effects of E; (e) the hypoglycemic stimulus for E secretion was facilitated by exercise; and (f) we hypothesize that an important role of glucagon during exercise could be to spare muscle glycogen by stimulating glucose production by the liver.

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“…Situations of heightened sympathetic activity are, in general, "stress" situations in which an increased supply of oxidative fuel in the form of endogenous glucose would be advantageous. Indeed, in exercise an increased secretion of glucagon has been demonstrated (26,(35)(36)(37), and it is well known that the secretion of insulin is diminished. The cause of such altered secretion has not heretofore been demonstrated, but in exercise a role for hyperalaninemia is possible in man (38,39) 'Wollheim, C. B., E. B. Marliss, B. Blondel, and L. Orci.…”

Section: Methodsmentioning

confidence: 99%

Glucagon Release Induced by Pancreatic Nerve Stimulation in the Dog

Marliss¹,

Girardier²,

Seydoux³

et al. 1973

J. Clin. Invest.

130

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A B S T R A C T A direct neural role in the regulation of immunoreactive glucagon (IRG) secretion has been investigated during stimulation of mixed autonomic nerves to the pancreas in anesthetized dogs. The responses were evaluated by measurement of blood flow and hormone concentration in the venous effluent from the stimulated region of pancreas.Electrical stimulation of the distal end of the discrete bundles of nerve fibers isolated along the superior pancreaticoduodenal artery was invariably followed by an increase in IRG output. With 10-min periods of nerve stimulation, the integrated response showed that the higher the control glucagon output, the greater was the increment. Atropinization did not influence the response to stimulation. That the preparation behaved in physiologic fashion was confirmed by a fall in IRG output, and a rise in immunoreactive insulin (IRI) output, during hyperglycemia induced by intravenous glucose (0.1 g/kg). The kinetics of this glucose effect on IRG showed characteristics opposite to those of nerve stimulation: the lower the control output, the less the decrement. Furthermore, during the control steady state, blood glucose concentration was tightly correlated with the IRI/

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The Effect of Exercise on Glucagon Secretion*

Cited by 85 publications

References 0 publications

The essentiality of insulin and the role of glucagon in regulating glucose utilization and production during strenuous exercise in dogs.

The essentiality of insulin and the role of glucagon in regulating glucose utilization and production during strenuous exercise in dogs.

Interactions between glucagon and other counterregulatory hormones during normoglycemic and hypoglycemic exercise in dogs.

Glucagon Release Induced by Pancreatic Nerve Stimulation in the Dog

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