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Hyperglucagonemia during insulin deficiency accelerates protein catabolism

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:5032864
; ; ;  [1]
  1. Univ. of Rochester School of Medicine and Dentistry, NY (USA) Clinical Research Centre, Harrow (England) Cornell Univ. Medical College, New York, NY (USA)
Hyperglucagonemia coexists with insulin deficiency or insulin resistance in many conditions where urinary nitrogen excretion is increased, but the precise role of glucagon in these conditions is controversial. The purpose of this study was to evaluate the effect of hyperglucagonemia on protein metabolism in insulin-deficient subjects. The authors used the stable isotope of an essential amino acid (L-(1-{sup 13}C)leucine) as a tracer of in vivo protein metabolism. A combined deficiency of insulin and glucagon was induced by intravenous infusion of somatostatin. Hyperglucagonemia and hypoinsulinemia were induced by infusions of somatostatin and glucagon. When somatostatin alone was infused leucine flux increased, indicating a 6-17% increase in proteolysis. When somatostatin and glucagon were infused, leucine flux increased, indicating a 12-32% increase in proteolysis. The increase in leucine flux during the infusion of somatostatin and glucagon was higher than the increase during infusion of somatostatin alone. Somatostatin alone did not change leucine oxidation, whereas the somatostatin plus glucagon increased leucine oxidation 100%. They conclude that hyperglucagonemia accelerated proteolysis and leucine oxidation in insulin-deficient humans.
OSTI ID:
5032864
Journal Information:
American Journal of Physiology; (USA), Journal Name: American Journal of Physiology; (USA) Vol. 253:2; ISSN 0002-9513; ISSN AJPHA
Country of Publication:
United States
Language:
English