Hostname: page-component-8448b6f56d-xtgtn Total loading time: 0 Render date: 2024-04-25T00:05:32.504Z Has data issue: false hasContentIssue false
  • English
  • Français

The Concentration of Adenosinetriphosphate (ATP) Citrate and Calcium in Blood During Insulin Shock Therapy

Published online by Cambridge University Press:  08 February 2018

H. Weil-Malherbe
H. Weil-Malherbe*
Affiliation:
Runwell Hospital, Wickford, Essex
Get access Rights & Permissions [Opens in a new window]

Extract

Concentration changes of blood constituents other than glucose occurring during hypoglycaemia, and particularly during insulin shock therapy, have been studied by several authors (e.g., Harris, Blalock and Horwitz, 1938; Katzenelbogen et al., 1939) though not always with concordant results. One of the most constant features of insulin hypoglycaemia is a decrease in the level of inorganic phosphate during the phase of blood-sugar fall and a gradual return to normal after the blood-sugar curve has reached its lowest value. This fact which was described soon after the discovery of insulin (see Cori (1931) for a review of the older literature) is generally attributed to the increased phosphate esterification consequent upon the enhancement of glucose utilisation and is in harmony with the current concept that the function of insulin is primarily that of a promotor of glucose phosphorylation.

Type
Part I.—Original Articles
Information
Journal of Mental Science , Volume 96 , Issue 402 , January 1950 , pp. 226 - 234
Copyright
Copyright © Royal College of Psychiatrists, 1950 

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

Accornero, F., and Bini, L. (1937), Schweiz. Arch. Neurol. Psychiat., 39, Suppl., 145.Google Scholar
Alwall, N. (1945), Acta Med. Sc and., 122, 448.Google Scholar
Bailey, K. (1942), Biochem. J., 36, 121.Google Scholar
Beiglböck, W., and Dussik, Th. (1937), Schweiz. Arch. Neurol. Psychiat., 39, Suppl., 38.Google Scholar
Berenblum, I., and Chain, E. (1938), Biochem. J., 32, 295.Google Scholar
Cori, C. F. (1931), Physiol. Rev., 11, 143.CrossRefGoogle Scholar
Delay, J., Soulairac, A., and Jouannais, S. (1945), Compt. rend. soc. biol., 139, 460.Google Scholar
Fiske, C. H., and Subbarow, Y. (1925), J. biol. Chem., 66, 375.CrossRefGoogle Scholar
Georgi, F. (1936), Schweiz. med. Wochschr., 17, 935.Google Scholar
Goranson, E. S., Hamilton, J. E., and Haist, R. E. (1948), J. biol. Chem., 174, 1.Google Scholar
Harris, M. N., Blalock, J. R., and Horwitz, W. A. (1938), Arch. Neurol. Psychiat., 40, 116.Google Scholar
Hevesy, G. (1947), Advances in Enzymology, 7, 111, New York.Google Scholar
Kaplan, N. O., and Greenberg, D. M. (1944), J. biol. Chem., 156, 553.Google Scholar
Katzenelbogen, S., Harms, H. E., Willmans, R., Barkoff, S., Brody, M., and Hayman, M. (1939), Am. J. Psychiat., 95, 793.Google Scholar
Kerr, S. E., and Daoud, L. (1935), J. biol. Chem., 109, 301.Google Scholar
Natelson, S., Pincus, J. B., and Lugovoy, J. K. (1948), J. clin. Invest., 27, 446.Google Scholar
Nelson, N. (1944), J. biol. Chem., 153, 375.Google Scholar
Olsen, N. S., and Klein, J. R. (1947), Arch. Biochem., 13, 343.Google Scholar
Sacks, J. (1945), Am. J. Physiol., 143, 157.Google Scholar
Wang, C. C. (1935), J. biol. Chem., 111, 443.Google Scholar
Weil-Malherbe, H., and Bone, A. D. (1949), Biochem. J., 45, 377.Google Scholar
Submit a response

eLetters

No eLetters have been published for this article.