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Loss of Regulation of Lipid Metabolism in Morris Hepatomas: A Potential Role for Cytoplasmic Binding Proteins

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Book cover Morris Hepatomas

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 92))

Abstract

It is well established that fatty acid and cholesterol synthesis are not inhibited in Morris hepatomas during the fasting state in contradistinction to normal liver. The constitutive enzymes of these pathways in hepatomas appear to be normal. We observed that the tumor content of the feedback inhibitor of lipo-genesis, long chain fatty acyl CoA and its cytoplasmic binding protein, Z protein, were both low and did not increase significantly during fasting. We proposed that the basic defect could be defective net production of Z protein. Preliminary data suggest that there is also a decrease in cholesterol affinity for its cytosolic binding protein in Morris hepatomas. This raises the intriguing possibility that the common denominator for these metabolic defects in hepatomas resides in the abnormal metabolism of a family of cytosolic binding proteins.

Scholar of the Medical Research Council of Canada, to whom requests for reprints should be addressed: c/o Division of Gastroenterology, Royal Victoria Hospital, 687 Pine Avenue, W., Montreal, Quebec H3A 1A1.

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Author information

Authors and Affiliations

  1. Department of Medicine, Royal Victoria Hospital and McGill University Clinic, Montreal, Quebec, Canada

    S. Mishkin & M. L. Halperin

  2. Department of Medicine, University of Toronto, Toronto, Ontario, Canada

    S. Mishkin & M. L. Halperin

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  1. S. Mishkin
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  2. M. L. Halperin
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Editors and Affiliations

  1. Department of Biochemistry and Howard Cancer Research Center, Howard University Medical School, Washington, D.C., USA

    Harold P. Morris  & Wayne E. Criss  & 

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Mishkin, S., Halperin, M.L. (1978). Loss of Regulation of Lipid Metabolism in Morris Hepatomas: A Potential Role for Cytoplasmic Binding Proteins. In: Morris, H.P., Criss, W.E. (eds) Morris Hepatomas. Advances in Experimental Medicine and Biology, vol 92. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-8852-8_23

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  • DOI: https://doi.org/10.1007/978-1-4615-8852-8_23

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