Energy substrate utilization in freshly isolated Morris Hepatoma 7777 cells

• Published in: Cancer research (Chicago, Ill.) Vol. 48; no. 3; pp. 602 - 608
• Main Authors: MARES-PERLMAN, J. A, SHRAGO, E
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 01.02.1988
• Subjects: Adenine Nucleotides - metabolism; Amino Acids - metabolism; Animal tumors. Experimental tumors; Animals; Biological and medical sciences; Cell Separation - methods; Energy Metabolism; Experimental digestive system and abdominal tumors; Glucose - metabolism; Glutamine - metabolism; Glycolysis; Hydroxybutyrates - metabolism; Liver Neoplasms, Experimental - metabolism; Medical sciences; Oxygen Consumption; Palmitates - metabolism; Rats; Tumors; Uridine - metabolism; Morris hepatoma; Rat; Rodentia; Lipids; Biosynthesis; Glucose; Experimental study; Metabolism; Cholesterol; Butyrate; Vertebrata; Mammalia; Energy; Digestive diseases; Experimental tumor; Tumor cell
• ISSN: 0008-5472; 1538-7445

Freshly isolated Morris Hepatoma 7777 cells were prepared for a study of the utilization of palmitate and beta-hydroxybutyrate as metabolic fuels compared to other major energy substrates (glucose and glutamine). These cells were capable of oxidizing both [U-14C]palmitate and beta-[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 beta-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.