Plasma Glucagon Levels in Exercising Man

Self Cite

703

184

A B S T R A C T Arterial concentrations and substrate exchange across the leg and splanchnic vascular beds were determined for glucose, lactate, pyruvate, glycerol, individual acidic and neutral amino acids, and free fatty acids (FFA) in six subjects at rest and during 4 h of exercise at approximately 30% of maximal oxygen uptake. FFA turnover and regional exchange were evaluated using "C-labeled oleic acid.The arterial glucose concentration was constant for the first 40 min of exercise, but fell progressively thereafter to levels 30% below basal. The arterial insulin level decreased continuously, while the arterial glucagon concentration had risen fivefold after 4 h of exercise. Uptake of glucose and FFA by the legs was markedly augmented during exercise, the increase in FFA uptake being a consequence of augmented arterial levels rather than increased fractional extraction. As exercise was continued beyond 40 min, the relative contribution of FFA to total oxygen metabolism rose progressively to 62%. In contrast, the contribution from glucose fell from 40% to 30% between 90 and 240 min. Leg output of alanine increased as exercise progressed.Splanchnic glucose production, which rose 100% above basal levels and remained so throughout exercise,

Section: Discussionsupporting

confidence: 87%

Substrate Turnover during Prolonged Exercise in Man

Ahlborg¹,

Felig²,

Hagenfeldt³

et al. 1974

Self Cite

703

184

“…In addition, many states characterized by catecholamine excess are associated with hyperglucagonemia (9, [15][16][17][18][19][20]; nevertheless, a cause-effect relationship between sympathetic nervous system discharge or epinephrine release from the adrenal, and stimulation of glucagon secretion, especially in man, has not been identified. During hypoglycemia there is stimulation of glucagon secretion (9), increased sympathetic neural outflow, and increased adrenal medullary secretion with resultant increases in plasma and urinary epinephrine and norepinephrine levels (21,22).…”

Section: Discussionmentioning

confidence: 99%

Glucagon response to hypoglycemia in sympathectomized man.

Palmer¹,

Henry²,

Benson³

et al. 1976

109

A B S T R A C T Hypoglycemia stimulates immunoreactive glucagon (IRG) secretion and increases the activity of the sympathetic nervous system. To ascertain if the augmented alpha cell activity evoked by glucopenia is mediated by the adrenergic nervous system, the glucagon response to insulin-induced hypoglycemia of five subj ects with neurologically complete cervical transections resulting from trauma, thereby disrupting their hypothalamic sympathetic outflow, was compared to six healthy volunteers. In addition to clinical neurological evaluation, completeness of sympathectomy was verified by failure to raise plasma norepinephrine levels during hypoglycemia compared to the two-to threefold increase observed in controls. Total IRG response (IRG area above basal 0-90 min) and peak IRG levels achieved were the same in the quadriplegics and the controls. Although the glucagon rise tended to be slower, and the peak levels attained occurred later in the quadriplegic patients than in the controls, this response was appropriate for their sugar decline, which was slower and reached the nadir later than in the control subjects.These observations that the glucagon release during insulin-induced hypoglycemia is normal in subjects whose hypothalamic sympathetic outflow has been interrupted provide strong evidence that the sympathetic nervous system does not mediate the glucagon response to hypoglycemia. INTRODUCTIONIn addition to the control of insulin and glucagon secretion by circulating levels of substrates such as amino

“…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

128

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/