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[Cancer Research 48, 602-608, February 1, 1988]
© 1988 American Association for Cancer Research

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Energy Substrate Utilization in Freshly Isolated Morris Hepatoma 7777 Cells1

Julie A. Mares-Perlman2 and Earl Shrago

Departments of Nutritional Sciences and Medicine, University of Wisconsin, Madison, Wisconsin 53706

Freshly isolated Morris Hepatoma 7777 cells were prepared for a study of the utilization of palmitate and ß-hydroxybutyrate as metabolic fuels compared to other major energy substrates (glucose and glutamine). These cells were capable of oxidizing both [U-14C]palmitate and ß-[3-14C]hydroxybutyrate although the rates accounted for only 10 ± 3 (SD) and 9 ± 4% of total oxygen consumed, respectively; n = 4. Incorporation of [U-14C]glutamine and [U-14C]glucose carbon into 14CO2 made up for 38 ± 13 and 9 ± 2% of oxygen consumed by these cells, respectively. The conversion of glucose carbon into lactate was estimated to supply 26 ± 6% of ATP. Thus, glutamine oxidation and lactate formation from glucose were the major contributors to estimated ATP needs. Conversion of these substrates into lipids was also studied and compared with oxidized products. Incorporation of glucose, glutamine, and ß-hydroxybutyrate into nonsaponifiable lipids and fatty acids was only 6.0 ± 2.9, 0.8 ± 0.2 and 17.7 ± 6.65% (n = 3) of their respective rates of CO2 formation. This suggests that in freshly isolated Morris Hepatoma 7777 cells, citrate export from the mitochondria for cholesterogenesis and lipogenesis is a minor fate of substrate carbon entering the mitochondria for oxidation.

1 Supported by NIH Grants 5 P30 DDK/CA26659, GM-14033, and T32 CA09451.

2 To whom requests for reprints should be addressed, at Department of Nutritional Sciences, University of Wisconsin, 1415 Linden Drive, Madison, WI 53706.

Received 7/14/87. Revised 10/12/87. Accepted 11/ 2/87.




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L. D. Shewchuk, V. E. Baracos, and C. J. Field
Dietary L-Glutamine Supplementation Reduces the Growth of the Morris Hepatoma 7777 in Exercise-Trained and Sedentary Rats
J. Nutr., January 1, 1997; 127(1): 158 - 166.
[Abstract] [Full Text]




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Copyright © 1988 by the American Association for Cancer Research.