Basic Research in Cardiology

, Volume 79, Issue 3, pp 307–312 | Cite as

Glycolysis and glucose oxidation in the rat heart under nonrecirculating perfusion conditions

  • P. Rösen
  • M. Adrian
  • J. Feuerstein
  • H. Reinauer
Original Contributions


Isolated rat hearts were perfused according to Langendorff and as a working heart preparation with glucose as the only exogenous substrate under nonrecirculating conditions to avoid accumulation of heart metabolites and, thereby, changes in the composition of the perfusion medium. In the absence of insulin or at low work, oxidation of endogenous substrates as glycogen is of importance for myocardial energy metabolism. Accordingly, about 1/3 of the glucose oxidized by the heart was derived from myocardial glycogen. Lipolysis of endogenous triglycerides and oxidation of the fatty acids produced were, however, low in normal rat hearts. By contrast, in the presence of insulin or at high work load endogenous substrates play a minor role for energy provision. About 80% of the total oxygen consumption could be attributed to the oxidation of exogenous glucose. Furthermore, insulin exerted its major effect in accelerating glucose uptake and glycolysis, but had little influence on PDH-activity. Insulin increased lipolysis in control hearts, however, changes in the endogenous triglycerides were less than valves calculated from the rate of lipolysis. Thus, glycerol release can be taken as a measure for lipolysis, but not as a measure for fatty acid oxidation, since the produced fatty acids were partly reesterified to glycerides. On the basis of the metabolic data obtained, the oxygen and energy balance was calculated. We conclude that a sufficient energy provision is only warranted if the rat heart is perfused either in the presence of insulin or at higher-more physiological-work load.

Key words

perfused rat heart insulin action glucose metabolism lipolysis energy metabolism oxygen consumption 


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  1. 1.
    Opie LH, Tansey MJ, Kennelly BM (1979) S Afr med J 56:207–211PubMedGoogle Scholar
  2. 2.
    Opie LH (1968) Am Heart J 76:685–698PubMedGoogle Scholar
  3. 3.
    Denton DM, Randle PJ (1976) Biochem J 104:426–433Google Scholar
  4. 4.
    Neely JR, Denton DM, England PJ, Randle PJ (1972) Biochem J 128:147–159PubMedGoogle Scholar
  5. 5.
    Neely JR, Morgan HE (1974) Ann Rev Physiol 36:413–459CrossRefGoogle Scholar
  6. 6.
    Neely JR, Rovetto MJ, Oram JF (1972) Progr Cardiovasc Dis 15:289–329CrossRefGoogle Scholar
  7. 7.
    Langendorff O (1895) Pflügers Arch 61:291–332CrossRefGoogle Scholar
  8. 8.
    Müller-Ruchholz ER, Lochner W (1971) J Mol Cell Cardiol 3:15–29CrossRefPubMedGoogle Scholar
  9. 9.
    Rösen P, Adrian M, Herzfeld D, Feuerstein J, Müller W, Reinauer H (1981) Diabète et Métabolisme 6:205–211Google Scholar
  10. 10.
    Krebs HA, Henseleit K (1932) Z Physiol Chem 210:33–66Google Scholar
  11. 11.
    Bergmeyer HU (1947) Methoden der enzymatischen Analyse. Verlag Chemie, WeinheimGoogle Scholar
  12. 12.
    Rösen P, Budde Th, Reinauer H (1981) J Mol Cell Cardiol 13:539–550CrossRefPubMedGoogle Scholar
  13. 13.
    Mowbray J, Ottaway JH (1973) Eur J Biochem 36:362–368CrossRefPubMedGoogle Scholar
  14. 14.
    Peuhkurinen KJ, Hassinen IE (1982) Biochem J 202:67–76PubMedGoogle Scholar
  15. 15.
    Wieland O, Syster M (1957) Biochem Z 329:320–331PubMedGoogle Scholar
  16. 16.
    Robinson J, Newsholme EA, (1967) Biochem J 104:2c-4cPubMedGoogle Scholar
  17. 17.
    Williamson JR, Krebs HA (1961) Biochem J 80:540–547PubMedGoogle Scholar
  18. 18.
    Neely JR, Bowman RH, Morgan HE (1969) Am J Physiol 216:804–811PubMedGoogle Scholar
  19. 19.
    Morgan HE, Neely JR, Wood RE, Liebecq C, Liebermeister H, Park CR (1965) 24:1040–1045Google Scholar
  20. 20.
    Taegtmeyer H, Hems R, Krebs HA (1980) Biochem J 186:701–711PubMedGoogle Scholar

Copyright information

© Dr. Dietrich Steinkopff Verlag 1984

Authors and Affiliations

  • P. Rösen
    • 1
  • M. Adrian
    • 1
  • J. Feuerstein
    • 1
  • H. Reinauer
    • 1
  1. 1.Dept. of BiochemistryDiabetesforschungsinstitut an der UniversitätDüsseldorfGermany

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