Hostname: page-component-78c5997874-t5tsf Total loading time: 0 Render date: 2024-11-13T04:50:45.320Z Has data issue: false hasContentIssue false
  • English
  • Français

Carbohydrate and lipid metabolism at rest and under physical and metabolic load in normal pigs and those with the genetic mutation for malignant hyperthermia

Published online by Cambridge University Press:  02 September 2010

W. Otten  and
H. M. Eichinger
W. Otten
Affiliation:
Research Institute for Biology of Farm Animals, 18196 Dummerstorf, Germany
H. M. Eichinger
Affiliation:
Institute for Animal Breeding, Technical University of Munich, 85354 Freising-Weihenstephan, Germany
Get access

Abstract

The plasma concentrations of glucose, insulin, lactate, cortisol and free fatty acids were investigated in normal pigs and those with the homozygous and heterozygous genetic mutation for malignant hyperthermia (MH). Blood samples were obtained during a 24-h resting period, a glucose tolerance test and during a treadmill test with submaximal physical load conditions. The homozygous MH positive animals elicited the highest glucose concentrations and the homozygous MH negative animals the lowest at each sampling time during the 24-h period (P < 0·01). During the glucose tolerance test, the most pronounced post-prandial increase and the highest plasma concentrations of glucose were found for the homozygous MH positive animals (P < 0·01), which was associated with a late release of insulin. Increasing work loads during the treadmill test run resulted in an increase of plasma cortisol concentrations in all animals (P < 0·01), with the more pronounced increase for the homozygous and heterozygous MH positive animals. Plasma free fatty acid concentrations during the treadmill test differed between the genotypes (P < 0·05). A pronounced increase was found for the homozygous and heterozygous MH positive animals, whereas the MH negative animals provided very constant free fatty acid values, at a low level, independent of the work load. These results indicate that the genetic mutation for MH in pigs affects the metabolic pathways of the energy metabolism, resulting in higher plasma glucose concentrations at rest and higher lipolytic activities under physical load conditions.

Keywords

fatty acidsglucosehydrocortisonehyperthermiainsulinpigs
Type
Research Article
Information
Animal Science , Volume 62 , Issue 3 , June 1996 , pp. 581 - 590
Copyright
Copyright © British Society of Animal Science 1996

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Adam, H., Olthoff, D., Adam, H., Rüstow, B., Kunze, D., Lengerken, G. van and Schwalbe, M. 1987. Veränderungen des Membranphospholipidgehaltes subzellulärer Strukturen des Skelettmuskels bei Halothan-induzierter Maligner Hyperthermie des Hausschweins. Anaestliesiologie und Reaniwation 12:201–206.Google Scholar
Blum, J. W. and Eichinger, H. M. 1988. Epinephrine and Norepinephrine related to cardiorespiratory and metabolic changes in calves during physical exercise. Hormone and Metabolic Research 20:738–742.CrossRefGoogle ScholarPubMed
Campbell, I. T., Ellis, F. R., Evans, R. T. and Mortimer, M. G. 1983. Studies of body temperature, blood lactate, cortisol and free fatty acid levels during exercise in human subjects susceptible to malignant hyperpyrexia. Ada Anaesthesiologica Scandinavica 27:349–355.CrossRefGoogle ScholarPubMed
Carrier, L., Villaz, M. and Dupont, Y. 1991. Abnormal rapid Ca2' release from sarcoplasmatic reticulum of malignant hyperthermia susceptible pigs. Biodiimica et Biophysica Acta 1064:175–183.CrossRefGoogle Scholar
Chambers, J. and Hall, R. R. 1987. Porcine malignant hyperthermia. Compendium on Continuing Education for Practicing Veterinarian 9:F317–F320.Google Scholar
Ellis, F. R., Drake, J. D., Halsall, P. J., Hay, E. and Campbell, I. T. 1982. Increased glycolysis of muscle in unstressed patients susceptible to malignant hyperpyrexia. British Journal of Anaesthesia 54:1132–1133.Google Scholar
Fill, M., Coronado, R., Mickelson, J. R., Vilven, J., Ma, J., Jacobsen, B. A. and Louis, C. F. 1990. Abnormal ryanodine receptor channels in malignant hyperthermia. Biophysical Journal 50:471–476.CrossRefGoogle Scholar
Foster, P. S. 1990. Malignant hyperpyrexia. International journal of Biochemistry 22:1217–1222.CrossRefGoogle ScholarPubMed
Gronert, G. A. 1980. Malignant hyperthermia. Anesthesiology 53:395–423.CrossRefGoogle ScholarPubMed
Gronert, G. A., Mott, J. and Lee, J. 1988. Aetiology of Malignant Hyperthermia. British journal of Anaesthesia 60:253–267.CrossRefGoogle ScholarPubMed
Harrison, G. G. 1989. Malignant Hyperthermia. In General Anaesthesia (ed. Nunn, J. F., Ulting, J. E. and Brown, B. R.), pp.655–667. Butterworths, London.Google Scholar
Hartman, S., Otten, W. and Eichinger, H. M. 1991. Stress testing effects on blood lipid concentrations and organic lipid composition of different genotypes of swine. Proceedings of the 37th International Congress on Meat and Technology, Kuhnbach, Vol. 1: pp.373–376. Congress Secretariat of ICOMST, Helsinki, Finland.Google Scholar
Heffron, J. J. A. 1988. Malignant hyperthermia: biochemical aspects of the acute episode. Britisli journal of Anaesthesia 60:274–278.CrossRefGoogle ScholarPubMed
Heinze, P. H. and Mitchell, G. 1989. Stress resistant and stress susceptible landrace pigs: comparison of blood variables after exposure to halothane or exercise on a treadmill. Veterinary Record 124:163–168.CrossRefGoogle ScholarPubMed
Hohorst, H. J. 1962. L(+)-Lactat, Bestimmung mit Lactat-Dehydrogenase und DPN. In Methoden der enzymatischen Analyse (ed. Bergmeyer, H. U.), Verlag Chemie, Weinheim/ Bergstraβe, Germany.Google Scholar
Iaizzo, P. A., Seewald, M. J., Olsen, R., Wedel, D. J., Chapman, D. E., Berggren, M., Eichinger, H. M. and Powis, G. 1991. Enhanced mobilization of intracellular Ca2+induced by halothane in hepatocytes isolated from swine susceptible to malignant hyperthermia. Anesthesiology 74:531–538.Google ScholarPubMed
Iaizzo, P. A. and Wedel, D. J. 1994. Response to succinylcholine in porcine malignant hyperthermia. Anesthesia and Analgesia 79:143–151.CrossRefGoogle ScholarPubMed
Louis, C. F., Gallant, E. M., Remple, E. and Mickelson, J. R. 1990. Malignant hyperthermia and porcine stress syndrome: a tale of two species. Pig News and Information 11:341–343.Google Scholar
Mitchell, G. and Heffron, J. J. A. 1982. Porcines stress syndromes. Advances in Food Research 28:167–230.CrossRefGoogle ScholarPubMed
Murphy, M. G. 1990. Dietary fatty acids and membrane protein function. journal of Nutritional Biochemistry 1:68–79.CrossRefGoogle ScholarPubMed
Niebroj-Dobosz, I., Kwiatkowski, H. and Mayzner-Zawadzka, E. 1984. Experimental porcine malignant hyperthermia: macromolecular characterization of muscle plasma membranes. Medical Biology 62:250–254.Google ScholarPubMed
Otten, W., Berrer, A., Bergerhoff, T., Goldberg, M. and Eichinger, H. M. 1995. Effects of a dietary magnesium fumarate supplementation on blood metabolites and meat quality in swine. Magnesium Bulletin 17:91–95.Google Scholar
Seewald, M. J., Eichinger, H. M. and Iaizzo, P. A. 1991. Malignant hyperthermia: an altered phospholipid and fatty acid composition in muscle membranes. Ada Anaesthesiologica Scandinavica 35:380–386.CrossRefGoogle ScholarPubMed
Statistical Analysis Systems Institute. 1989. SAS/STAT user's guide, version 6, fourth edition, volume 2. SAS Institute, Inc., Cary, NC.Google Scholar
Wedel, D. J., Gammel, S. A., Milde, J. H. and Iaizzo, P. A. 1993. Delayed onset of malignant hyperthermia induced by isoflurane and desflurane compared with halothane in susceptible swine. Anesthesiology 78:1138–1144.CrossRefGoogle ScholarPubMed
Wolf-Schwerin, C. and Kallweit, E. 1991. Belastungsreaktionen und Leistungmerkmale von definierten Halothangenotypen der Deutschen Landrasse. Zuchtungskunde 6:51–64.Google Scholar