Glucagon and the insulin: glucagon ratio in severe trauma

C. A. Lindsey, G. R. Faloona, Roger H Unger

Research output: Chapter in Book/Report/Conference proceedingChapter

4 Citations (Scopus)

Abstract

Most patients with severe traumatic shock exhibit hyperglucagonemia, usually without a commensurate increase in insulin, within the first few hours after injury. Hyperglucagonemia was not observed in three patients during major surgery unaccompanied by hypotension. Hyperglucagonemia can be produced in dogs by inducing hypovolemic shock through exsanguination. Exsanguination hyperglucagonemia can be significantly reduced by beta adrenergic blockage with propranolol but not by alpha adrenergic blockade with phentolamine. It is concluded that hyperglucagonemia and lowering of the insulin glucagon ratio are part of the endocrine response to injury and are at least partially mediated via beta adrenergic stimulation. It has been reported by Marco, Valverde and co workers and more recently by Wise et al. that corticosteroids also known to be elevated in trauma, increase basal and stimulated glucagon secretion and could, therefore, contribute to the hyperglucagonemia in these studies. The presence of a reduced insulin glucagon ratio results in increased hepatic glucose production and thus contributes to the elevation of plasma glucose levels that accompany shock. The hyperglycemia of shock may well constitute an important and appropriate survival response by helping to maintain glucose delivery to the brain in the face of a declining cerebral blood flow. However, if inappropriately long continued, the low insulin glucagon ratio would promote increased use of amino acids for new glucose production at the expense of protein synthesis and thus contribute to or perhaps mediate the catabolic state associated with injury and other stressful illness.

Original languageEnglish (US)
Title of host publicationTransactions of the Association of American Physicians
Pages264-271
Number of pages8
VolumeNo. 86
StatePublished - 1973

Fingerprint

Glucagon
Adrenergic Agents
Insulin
Exsanguination
Glucose
Shock
Wounds and Injuries
Cerebrovascular Circulation
Traumatic Shock
Phentolamine
Propranolol
Hyperglycemia
Hypotension
Adrenal Cortex Hormones
Dogs
Amino Acids
Survival
Liver
Brain
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Lindsey, C. A., Faloona, G. R., & Unger, R. H. (1973). Glucagon and the insulin: glucagon ratio in severe trauma. In Transactions of the Association of American Physicians (Vol. No. 86, pp. 264-271)

Glucagon and the insulin : glucagon ratio in severe trauma. / Lindsey, C. A.; Faloona, G. R.; Unger, Roger H.

Transactions of the Association of American Physicians. Vol. No. 86 1973. p. 264-271.

Research output: Chapter in Book/Report/Conference proceedingChapter

Lindsey, CA, Faloona, GR & Unger, RH 1973, Glucagon and the insulin: glucagon ratio in severe trauma. in Transactions of the Association of American Physicians. vol. No. 86, pp. 264-271.
Lindsey CA, Faloona GR, Unger RH. Glucagon and the insulin: glucagon ratio in severe trauma. In Transactions of the Association of American Physicians. Vol. No. 86. 1973. p. 264-271
Lindsey, C. A. ; Faloona, G. R. ; Unger, Roger H. / Glucagon and the insulin : glucagon ratio in severe trauma. Transactions of the Association of American Physicians. Vol. No. 86 1973. pp. 264-271
@inbook{db73bff73a174c5f842cc25d9b98cf99,
title = "Glucagon and the insulin: glucagon ratio in severe trauma",
abstract = "Most patients with severe traumatic shock exhibit hyperglucagonemia, usually without a commensurate increase in insulin, within the first few hours after injury. Hyperglucagonemia was not observed in three patients during major surgery unaccompanied by hypotension. Hyperglucagonemia can be produced in dogs by inducing hypovolemic shock through exsanguination. Exsanguination hyperglucagonemia can be significantly reduced by beta adrenergic blockage with propranolol but not by alpha adrenergic blockade with phentolamine. It is concluded that hyperglucagonemia and lowering of the insulin glucagon ratio are part of the endocrine response to injury and are at least partially mediated via beta adrenergic stimulation. It has been reported by Marco, Valverde and co workers and more recently by Wise et al. that corticosteroids also known to be elevated in trauma, increase basal and stimulated glucagon secretion and could, therefore, contribute to the hyperglucagonemia in these studies. The presence of a reduced insulin glucagon ratio results in increased hepatic glucose production and thus contributes to the elevation of plasma glucose levels that accompany shock. The hyperglycemia of shock may well constitute an important and appropriate survival response by helping to maintain glucose delivery to the brain in the face of a declining cerebral blood flow. However, if inappropriately long continued, the low insulin glucagon ratio would promote increased use of amino acids for new glucose production at the expense of protein synthesis and thus contribute to or perhaps mediate the catabolic state associated with injury and other stressful illness.",
author = "Lindsey, {C. A.} and Faloona, {G. R.} and Unger, {Roger H}",
year = "1973",
language = "English (US)",
volume = "No. 86",
pages = "264--271",
booktitle = "Transactions of the Association of American Physicians",

}

TY - CHAP

T1 - Glucagon and the insulin

T2 - glucagon ratio in severe trauma

AU - Lindsey, C. A.

AU - Faloona, G. R.

AU - Unger, Roger H

PY - 1973

Y1 - 1973

N2 - Most patients with severe traumatic shock exhibit hyperglucagonemia, usually without a commensurate increase in insulin, within the first few hours after injury. Hyperglucagonemia was not observed in three patients during major surgery unaccompanied by hypotension. Hyperglucagonemia can be produced in dogs by inducing hypovolemic shock through exsanguination. Exsanguination hyperglucagonemia can be significantly reduced by beta adrenergic blockage with propranolol but not by alpha adrenergic blockade with phentolamine. It is concluded that hyperglucagonemia and lowering of the insulin glucagon ratio are part of the endocrine response to injury and are at least partially mediated via beta adrenergic stimulation. It has been reported by Marco, Valverde and co workers and more recently by Wise et al. that corticosteroids also known to be elevated in trauma, increase basal and stimulated glucagon secretion and could, therefore, contribute to the hyperglucagonemia in these studies. The presence of a reduced insulin glucagon ratio results in increased hepatic glucose production and thus contributes to the elevation of plasma glucose levels that accompany shock. The hyperglycemia of shock may well constitute an important and appropriate survival response by helping to maintain glucose delivery to the brain in the face of a declining cerebral blood flow. However, if inappropriately long continued, the low insulin glucagon ratio would promote increased use of amino acids for new glucose production at the expense of protein synthesis and thus contribute to or perhaps mediate the catabolic state associated with injury and other stressful illness.

AB - Most patients with severe traumatic shock exhibit hyperglucagonemia, usually without a commensurate increase in insulin, within the first few hours after injury. Hyperglucagonemia was not observed in three patients during major surgery unaccompanied by hypotension. Hyperglucagonemia can be produced in dogs by inducing hypovolemic shock through exsanguination. Exsanguination hyperglucagonemia can be significantly reduced by beta adrenergic blockage with propranolol but not by alpha adrenergic blockade with phentolamine. It is concluded that hyperglucagonemia and lowering of the insulin glucagon ratio are part of the endocrine response to injury and are at least partially mediated via beta adrenergic stimulation. It has been reported by Marco, Valverde and co workers and more recently by Wise et al. that corticosteroids also known to be elevated in trauma, increase basal and stimulated glucagon secretion and could, therefore, contribute to the hyperglucagonemia in these studies. The presence of a reduced insulin glucagon ratio results in increased hepatic glucose production and thus contributes to the elevation of plasma glucose levels that accompany shock. The hyperglycemia of shock may well constitute an important and appropriate survival response by helping to maintain glucose delivery to the brain in the face of a declining cerebral blood flow. However, if inappropriately long continued, the low insulin glucagon ratio would promote increased use of amino acids for new glucose production at the expense of protein synthesis and thus contribute to or perhaps mediate the catabolic state associated with injury and other stressful illness.

UR - http://www.scopus.com/inward/record.url?scp=0015698056&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0015698056&partnerID=8YFLogxK

M3 - Chapter

C2 - 4151060

AN - SCOPUS:0015698056

VL - No. 86

SP - 264

EP - 271

BT - Transactions of the Association of American Physicians

ER -