Hostname: page-component-78c5997874-xbtfd Total loading time: 0 Render date: 2024-11-13T05:58:34.414Z Has data issue: false hasContentIssue false
  • English
  • Français

Part 1 Substrate metabolism in the metabolic response to injury

Published online by Cambridge University Press:  28 February 2007

J. A. Romijn
J. A. Romijn
Affiliation:
Leiden University Medical Center, Department of Endocrinology, C4-R, PO Box 9600, 2300 RC Leiden, The Netherlands
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

In healthy subjects the metabolic response to starvation invokes regulatory mechanisms aimed at conservation of protein mass. This response is characterized by a decrease in energy expenditure and a progressive decrease in urinary N excretion. Many non-endocrine diseases induce anorexia and a decrease in food intake. However, in contrast to the metabolic reaction to starvation in healthy subjects, anorectic patients with serious diseases have increased energy expenditure and protein catabolism, associated with profound neuroendocrine alterations. These neuroendocrine changes are induced by two mechanisms. First, afferent nerves inform the central nervous system of tissue injury which results in neuroendocrine activation. Second, tissue injury stimulates the production of inflammatory mediators, which in turn results in neuroendocrine and metabolic effects. Although these metabolic changes enable the organism to survive short-lasting diseases by using endogenous substrates, in protracted serious diseases these changes will result in loss of functioning protein mass and may endanger survival. Moreover, tissue injury alters the metabolic responses to nutrition, reflected in the persistence of catabolism as long as serious tissue injury remains.

Keywords

MetabolismDiseaseNeuroendocrine changesCytokines
Type
Clinical Nutrition and Metabolism Group Symposium on ‘Nutrition in the severely-injured patient’
Information
Proceedings of the Nutrition Society , Volume 59 , Issue 3 , August 2000 , pp. 447 - 449
Copyright
Copyright © The Nutrition Society 2000

References

Bessey, PQ, Watters, JM, Aoki, TT & Wilmore, DW (1984) Combined hormonal infusion simulates the metabolic response to injury. Annals of Surgery 200, 264–281.CrossRefGoogle ScholarPubMed
Bloom, SR & Edwards, AV (1975) The release of pancreatic glucagon and inhibition of insulin in response to stimulation of sympathetic innervation. Journal of Physiology 253, 157–173.CrossRefGoogle ScholarPubMed
Dempsey, DT, Guenter, P & Mullen, JL (1985) Energy expenditure in acute trauma to the head with and without barbiturate therapy. Surgery, Gynecology and Obstetrics 160, 128–134.Google Scholar
Gardner, DF, Kaplan, MM, Stanley, CA & Utiger, RD (1979) Effect of tri-iodothyronine replacement on the metabolic and pituitary responses to starvation. New England Journal of Medicine 300, 579–584.CrossRefGoogle ScholarPubMed
George, JM, Reier, CE, Ianese, RR & Rower, JM (1974) Morphine anesthesia blocks cortisol and growth hormone response to surgical stress in humans. Journal of Clinical Endocrinology and Metabolism 38, 736–741.CrossRefGoogle ScholarPubMed
Grunfeld, C, Zhao, C, Fuller, J, Polock, A, Moser, A, Friedman, J & Feingold, K (1996) Endotoxin and cytokines induce expression of leptin, the ob gene product in hamsters. Journal of Clinical Investigation 97, 2152–2157.CrossRefGoogle ScholarPubMed
Moeniralam, HS, Endert, E, Ackermans, MT, van Lanschot, JJB, Sauerwein, HP & Romijn, JA (1998) Sufentanil alters the inflammatory, endocrine and metabolic responses to endotoxin in dogs. American Journal of Physiology 275, E440-E447.Google ScholarPubMed
Sauerwein, HP & Romijn, JA (1991) Cytokines: role in human metabolism. In Update in Intensive Care and Emergency Medicine 1991, pp. 254–261 [Vincent, JL, editor]. Berlin: Springer Verlag.Google Scholar
Sauerwein, HP & Romijn, JA (1995) Adult macronutrient requirements. In Artificial Nutritional Support in Clinical Practice, pp. 137–149 [Payne-James, J, Grimble, G and Silk, D, editors]. London: Edward Arnold.Google Scholar
Stouthard, JML, Romijn, JA, van der Poll, T, Endert, E, Klein, S, Bakker, PJM, Veenhof, CHN & Sauerwein, HP (1995) Endocrine and metabolic effects of interleukin-6 in humans. American Journal of Physiology 268, E813–E819.Google ScholarPubMed
van der, Poll T, Romijn, JA, Endert, E, Borm, JJ, Buller, HR & Sauerwein, HP (1991) Tumor necrosis factor mimics the metabolic response to acute infection in healthy humans. American Journal of Physiology 261, E457-E465.Google Scholar
Warren, RS, Donner, DB, Starnes, HF & Brennan, M (1987) Modulation of endogenous hormone action by recombinant human tumor necrosis factor. Proceedings of the National Academy of Sciences USA 84, 8619–8622.CrossRefGoogle ScholarPubMed
Wolfe, RR, Herndon, D, Jahoor, F, Miyoshi, H & Wolfe, M (1987) Effect of severe burn injury on substrate cycling by glucose and fatty acids. New England Journal of Medicine 317, 403–408.CrossRefGoogle ScholarPubMed
Youngstrom, TG & Bartness, TJ (1995) Catecholaminergic innervation of white adipose tissue in Siberian hamsters. American Journal of Physiology 265, R744–R751.Google Scholar