This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Noguchi, Y. Articles by Brennan, M. F. Search for Related Content PubMed PubMed Citation Articles by Noguchi, Y. Articles by Brennan, M. F.

Tumor-induced Alterations in Tissue Lipoprotein Lipase Activity and mRNA Levels¹

Surgical Metabolism Laboratory, Memorial Sloan-Kettering Cancer Center [Y. N., N. A. V., R. N. Y., M. F. B.], and Laboratory of Human Behavior and Metabolism, The Rockefeller University [S. K. F.], New York, New York 10021

To elucidate the mechanisms of hypertriglyceridemia observed in the tumor-bearing rat, tissue lipoprotein lipase (LPL) activity and LPL mRNA levels were examined in the fed and fasted states at different degrees of tumor burden and after tumor removal.

LPL activity in the epididymal fat pad and cardiac muscle in the 24-h-fasted rats was significantly decreased with increasing tumor burden (r = -0.53, P < 0.05 and r = -0.72, P < 0.01, respectively). Tumor removal completely reversed these changes. In contrast, no change in LPL activity was detected in the fed state since food intake stimulated LPL activity to the same extent in both tumor-bearing (TBR) and control rats. LPL activity in the diaphragm and skeletal muscle was only marginally altered in TBR, as compared to controls.

LPL mRNA from the epididymal fat pad and cardiac muscle migrated to the same site on agarose gel and hybridized to a LPL-specific complementary DNA probe. The decline in LPL activity in epididymal fat pad observed in TBR was associated with a decrease in LPL mRNA levels. In contrast, there was no significant difference in LPL mRNA levels in cardiac muscle between the two groups despite significantly suppressed enzyme activity in tumor bearers.

This study provides evidence that hypertriglyceridemia in TBR is due in part to tumor-dependent suppression of adipose and cardiac LPL activity in the fasted state, which is stimulated by the presence of tumor. Unlike cardiac LPL, the tumor-induced changes in adipose LPL activity are regulated at the mRNA level in this tumor model.

¹ This work was supported by USPHS Grants CA 38858 (M. F. B.) and AM-34141 (N. A. V.) and by the Surgical Metabolism Fund.

² To whom requests for reprints should be addressed, at Surgical Metabolism Laboratory, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021.

Received 2/ 8/90. Accepted 11/20/90.