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Hepatic Glycerol Metabolism in Tumorous Rats: A ¹³¹C Nuclear Magnetic Resonance Study¹

Department of Surgery, Cook County Hospital, and Department of Surgery, Hektoen Institute for Medical Research, Chicago, Illinois 60612

Cancer cachexia contributes to the demise of a significant number of cancer patients, and severe loss of adipose tissue is a prominent component of this syndrome. One of the products of fat catabolism is glycerol, and its turnover is elevated in the cancerous state. Since glycerol is also one of the most important gluconeogenic substrates, its role in the augmented and abnormal gluconeogenesis of cancer hosts needs to be defined. In the present study, we examined hepatic glycerol metabolism in livers of Fischer 344 rats bearing s.c. nonmetastatic adenocarcinoma R3230AC. Five weeks after tumor inoculation, the liver was removed and perfused with 5 mM [2-¹³C]glycerol while ¹³C nuclear magnetic resonance spectroscopy was performed. In the livers of tumorous rats, we found: (a) lipogenesis from glycerol was augmented; (b) the rate of hepatic glycerol uptake was unchanged; (c) glucose production from glycerol was not altered; and (d) conversion of glycerol 3-phosphate to dihydroxyacetone phosphate remains the rate-limiting step. Therefore, it appears that, in cancer hosts, diminished glycerol clearance is not due to reduction in hepatic glycerol uptake or metabolism, and the abnormal gluconeogenesis involves the pathway prior to the entry of glycerol. The exaggerated lipolysis is probably used for the pathological hepatomegaly, and the availability of the cytosolic hydrogen acceptor remains the rate-limiting factor for glycerol metabolism.

¹ This work was supported by American Institute for Cancer Research Grant 88B58 and National Cancer Institute Grant CA50710.

² To whom requests for reprints should be addressed, at Room 6428, Main Building, Cook County Hospital, 1835 West Harrison Street, Chicago, IL 60612.

Received 8/ 9/94. Accepted 12/14/94.