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Role of Dietary Sphingolipids and Inhibitors of Sphingolipid Metabolism in Cancer and Other Diseases¹

Alfred H. Merrill, Jr.², Eva-Maria Schmelz, Elaine Wang, Joseph J. Schroeder, Dirck L. Dillehay^* and Ronald T. Riley

Departments of Biochemistry ^* Pathology, Center for Nutrition and Health Sciences and Division of Animal Resources, Emory University School of Medicine, Atlanta, GA 30322-3050 Toxicology and Mycotoxins Research Unit, USDA-ARS, P. O. Box 5677, Athens, GA 30613.

Sphingolipids are found in all eukaryotic and some prokaryotic organisms and participate in the regulation of cell growth, differentiation, and diverse cell functions including cell-cell communication, cell-substratum interactions and intracellular signal transduction. Nonetheless, the field of nutrition has given scant attention to these compounds so that little is known about the following fundamental questions: What is the fate of sphingolipids that are consumed in food? Does consumption of dietary sphingolipids affect the behavior of cells in the gastrointestinal tract or other organs? How do other factors in the diet affect sphingolipid metabolism? Several recent findings underscore the importance of these questions, for examples: 1) Sphingolipids are digested throughout the GI tract to ceramide and sphingosine, which are highly bioactive compounds that affect cellular regulatory pathways; 2) addition of sphingomyelin to a standard AIN diet (which is essentially devoid of sphingolipids) reduces the appearance of aberrant colonic crypts, and perhaps the number of tumors, in mice treated with a colon carcinogen; and 3) an enzyme of sphingolipid metabolism has been discovered to be the target of a class of toxic and carcinogenic mycotoxins called fumonisins. Given these recent findings, it is possible that some of the confusion that has arisen regarding the relationships between dietary fat and disease might be due to the lack of consideration of the sphingolipids that are also present.

KEY WORDS: • sphingolipids • ceramide • mycotoxins • cancer

¹ Presented as part of the symposium "Nutritional Modulation of Lipid-Mediated Signal Transduction Systems" given at Experimental Biology 94 meeting, Anaheim, CA, April 26, 1994. This symposium was sponsored by the American Institute of Nutrition and supported by a grant from the Mead Johnson Corporation. Guest editor for this symposium was Alfred H. Merrill, Jr., Emory University School of Medicine, Atlanta, GA.

² To whom correspondence should be addressed: Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322-3050.

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