Hyperglucagonæmia After Burns

Wilmore, Douglas W.; Moylan, Joseph A.; Pruitt, Basil A.; Lindsey, C. A.; Faloona, Gerald R.; Unger, Roger H

doi:10.1016/s0140-6736(74)92290-9

Cited by 154 publications

(31 citation statements)

References 15 publications

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“…Hyperglucagonemia occurs in a variety of catabolic conditions. These include trauma, burns, sepsis, cirrhosis, glucagonoma, the postoperative state, and poorly controlled type I diabetes (1)(2)(3)(4)(5). In patients with glucagonoma, in which glucose metabolism is only minimally disturbed, there is marked muscle wasting, skin atrophy, and hypoaminocidemia (6).…”

Section: Introductionmentioning

confidence: 99%

“…After isotope boluses had been administered and continuous infusion of l - [1][2][3][4][5][6][7][8][9][10][11][12][13] C]leucine at a rate of 7.5 mol/kg/h had begun, an infusion of normal saline at a rate of 1.5 ml/kg/h was initiated for the first 2 h of each study. After 2 h of each study, one of the following five infusion protocols was begun and continued for 4 h until completion of the study.…”

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confidence: 99%

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Evidence for a catabolic role of glucagon during an amino acid load.

Charlton¹,

Adey²,

Nair³

1996

J. Clin. Invest.

107

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Despite the strong association between protein catabolic conditions and hyperglucagonemia, and enhanced glucagon secretion by amino acids (AA), glucagon's effects on protein metabolism remain less clear than on glucose metabolism. To clearly define glucagon's catabolic effect on protein metabolism during AA load, we studied the effects of glucagon on circulating AA and protein dynamics in six healthy subjects. Five protocols were performed in each subject using somatostatin to inhibit the secretion of insulin, glucagon, and growth hormone (GH) and selectively replacing these hormones in different protocols. Total AA concentration was the highest when glucagon, insulin, and GH were low. Selective increase of glucagon levels prevented this increment in AA. Addition of high levels of insulin and GH to high glucagon had no effect on total AA levels, although branched chain AA levels declined. Glucagon mostly decreased glucogenic AA and enhanced glucose production. Endogenous leucine flux, reflecting proteolysis, decreased while leucine oxidation increased in protocols where AA were infused and these changes were unaffected by the hormones. Nonoxidative leucine flux reflecting protein synthesis was stimulated by AA, but high glucagon attenuated this effect. Addition of GH and insulin partially reversed the inhibitory effect of glucagon on protein synthesis. We conclude that glucagon is the pivotal hormone in amino acid disposal during an AA load and, by reducing the availability of AA, glucagon inhibits protein synthesis stimulated by AA. These data provide further support for a catabolic role of glucagon at physiological concentrations. ( J. Clin. Invest. 1996. 98:90-99.)

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

Evidence for a catabolic role of glucagon during an amino acid load.

Charlton¹,

Adey²,

Nair³

1996

J. Clin. Invest.

107

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“…Circulating glucagon concentrations were found to be elevated in burn patients, 34 and infusions of glucagon elevated the metabolic rate in normal subjects. 3336 In a series of studies, my associates and I observed glucagon and other circulating hormones under fasting supine conditions in 20 surviving patients with large burns (total burn size, TBS, 18 to 82% of body surface area) and correlated hormonal levels with the resting metabolic rate measured weekly between postburn day 3 and 26.…”

Section: Glucagon and Cortisolmentioning

confidence: 97%

Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Vaughan¹

1990

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The previous chapters have described many alterations in secreted hormones and metabolic processes that occur for weeks to months after major burn injury. Interpretation of these alterations can be bewildering; however, many of the findings can be simplified and/or unified to a certain extent if they are viewed as part of an overall alteration in central nervous system (CNS) function characterized by modified control settings. The Neuroendocrine Reflex ArcEarly work with acute surgical trauma provided the conceptual framework of the neuroendocrine reflex arc. 12 In this framework, a signal from an injured area is transmitted by an afferent limb to the brain, which integrates the formation and orchestrates a neural and hormonal output as the efferent limb.Hume and Egdahl 3 studied dogs anesthetized with ether or Nembutal and with a catheter in an adrenal vein. Upon application of a scald burn, the corticosteroid (CS) secretion rate rose promptly within minutes. This response was blocked by prior section of the medulla oblongata, the spinal cord, or the peripheral nerve innervating the area of the lesion. Subcutaneous injection of ACTH in the denervated burned area provoked a CS response, indicating that if a burn toxin were present and capable of stimulating this acute response humorally, it would likely have been detected. Thus, the acute CS response to a burn did not result from pain per se, which was blocked by the anesthesia, nor from systemic absorption of a humoral toxin from the burned area, but from afferent neural information signaling the presence of an injury. In some experiments, crude measurements of circulating ACTH indicated that the CS response was associated with a surge in endogenous ACTH release. Lesions of the anterior hypothalamus blocked the CS and ACTH responses to operative trauma. These and the cord section experiments indicated that the adrenocortical response was via brain control of ACTH secretion, not via innervation of the adrenals. Nevertheless, activation of the adrenal medullae through the neural route was indicated by observation of elevated catecholamine (CA) secretion rates in the adrenal vein after injury.

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“…Alterations in the concentrations and activities of plasma glucagon and insulin levels in burn injury patients may be responsible for mediating the changes in glucose metabolism (9)(10)(11)(12). There is general agreement that the elevated plasma glucagon is to some extent responsible for the increased rate of glucose production (9,10,12), whereas the role of insulin as a regulator of hepatic glucose output and as a stimulator of glucose uptake by peripheral tissues may be diminished (4,9,13).…”

Section: Introductionmentioning

confidence: 99%

“…There is general agreement that the elevated plasma glucagon is to some extent responsible for the increased rate of glucose production (9,10,12), whereas the role of insulin as a regulator of hepatic glucose output and as a stimulator of glucose uptake by peripheral tissues may be diminished (4,9,13). Ifthis is true, then lowering glucagon to a lower level should normalize glucose metabolism in burn patients, even if insulin is simultaneously lowered.…”

Section: Introductionmentioning

confidence: 99%

Role of insulin and glucagon in the response of glucose and alanine kinetics in burn-injured patients.

Jahoor¹,

Herndon²,

Wolfe³

1986

J. Clin. Invest.

114

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We investigated the roles of insulin and glucagon as mediators of changes in glucose and alanine kinetics during the hypermetabolic response to injury in 10 burn patients by infusing somatostatin with and without insulin replacement. Glucose and alanine kinetics were measured by primed-constant infusions of 6,6-d2-glucose and 13-3Cialanine.The basal rate of glucose production and alanine flux were significantly elevated in all patients. Lowering both hormones simultaneously caused an insignificant reduction in glucose production, but plasma glucose rose significantly (P < 0.01), because of reduced clearance. Alanine flux and total plasma amino nitrogen increased sign icantly (P < 0.05) above basal.Selectively lowering glucagon concentration decreased glucose production (P < 0.05), and exogenous glucose was infused to maintain euglycemia. Alanine flux and total plasma amino nitrogen remained unchanged.In severely burned patients (a) hyperglucagonemia stimulates increased glucose production, (b) basal insulin suppression glucose production, stimulates basal glucose clearance, and is important for regulation of plasma amino acid concentrations, and (c) the selective lowering of glucagon while maintaining basal insulin constant normalized glucose kinetics.

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Hyperglucagonæmia After Burns

Cited by 154 publications

References 15 publications

Evidence for a catabolic role of glucagon during an amino acid load.

Evidence for a catabolic role of glucagon during an amino acid load.

Neuroendocrine and Sympathoadrenal Response to Thermal Trauma

Role of insulin and glucagon in the response of glucose and alanine kinetics in burn-injured patients.

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