This paper is only available as a PDF. To read, Please Download here.
Abstract
The relationship between changes in glucose tolerance and in mitochondrial phosphorylative
activity was studied after massive liver resection. In rabbits twenty-four hours after
hepatectomy, when the phosphorylative activity in the mitochondria of the remnant
liver was enhanced maximally, the blood glucose level did not increase significantly
after glucose administration. Fortyeight hours after hepatectomy, when the phosphorylative
activity decreased to a submaximal level, the blood glucose level increased gradually
but without a return toward normal. About six weeks after partial hepatectomy, mitochondrial
function returned gradually to normal levels and the glucose tolerance test results
returned to within normal limits. Considering the previous report that an enhancement
of mitochondrial phosphorylative activity is required for a later increase in nuclear
DNA synthesis, it was suggested that the plateau pattern, with hypoglycemia, and the
gradual increase, with a prolonged return toward normal, in the glucose tolerance
test are indicative of marked enhancement of mitochondrial phosphorylative activity
preceding an increase in nuclear DNA synthesis. The changes in the glucose tolerance
test results in hepatectomized rabbits also were observed in rats and in man; however,
they were more rapid in rats and slower in man. From these results it was suggested
that the glucose tolerance test is very useful in the evaluation of the stage of regeneration
in the liver remnant after massive liver resection.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to The American Journal of SurgeryAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Role of insulin as a portal factor in maintaining the viability of the liver.Ann Surg. 1974; 180: 716
- Role of portal blood on the enhancement of liver mitochondrial metabolism.Am J Sura. 1972; 124: 16
- Energy requirement in regenerating and atrophic process of the liver in man and mammals.Surg Gynecol Obstet. 1974; 139: 234
- Hepatic cellular responses to liver cancer: abnormalities in metabolism of mitochondria isolated from human liver involved with carcinoma.Ann Surg. 1974; 179: 79
- Clinical application of cytochrome a(+a3) assay of mitochondria from liver specimens. an aid in determining metabolic tolerance of liver remnant for hepatic resection.Ann Surg. 1974; 180: 868
- Insulin as the primary factor governing changes in mitochondrial metabolism leading to liver regeneration and atrophy.Am J Surg. 1974; 127: 669
- Experimental pathology of the liver; restoration of liver of white rat following partial surgical removal.Arch Path. 1931; 12: 186
- Rapid specific method for determination of aldosaccharide in body fluids.Nature. 1959; 183: 108
- Human liver mitochondria.Clin Chim Acta. 1972; 38: 385
- Effect of ligation of portal vein on liver mitochondrial metabolism.J Biochem. 1971; 70: 755
- Protein measurement with folin phenol reagent.J Biol Chem. 1951; 193: 265
- Quantitative aspects on the control of oxygen utilization.in: Ciba Foundation Symposium on Regulation Cell Metabolism. Little, Brown, Boston1959: 91
- Adenosine nucleotide metabolism in regenerative, atrophic and necrotizing process of the liver.Gastroenterology. 1974; 67: 1225
Article info
Footnotes
☆This work was supported by grants from the Scientific Research Fund of the Ministry of Education, the Japanese Association for Study of Metabolism and Disease, and Miura Scientific Research Fund.
Identification
Copyright
© 1975 Published by Elsevier Inc.