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Abstract
Carnitine is known for its essential role in intermediary metabolism. In vitro studies suggest that its antioxidant and anti-inflammatory properties are potentially beneficial toward cancer prevention. This study tested effects of carnitine on the development of colon cancer in vivo using 2 murine models: azoxymethane (AOM) treatment as a model of carcinogen-induced colon cancer and a genetically induced model using Apc Min/+ mice. AOM and Apc Min/+ mice divided into dietary groups varying in lipid content, with or without carnitine supplementation (0.08%). AOM-exposed mice on a high butterfat diet had significantly increased aberrant crypts (ACF) (9.3 ± 0.88 vs. 6.3 ± 0.65), and macroscopic tumors (3.8 ± 0.95 vs. 2.0 ± 0.25) compared to mice on a control diet. In AOM mice fed the high butterfat diet, carnitine supplementation inhibited ACF (4.9 ± 0.7 vs. 9.3 ± 0.88, P < 0.001), crypt multiciplicity (1.6 ± 0.08 vs. 1.92 ± 0.1, P < 0.01) and tumors (1.5 ± 0.38 vs. 3.8 ± 0.95, P < 0.001). Carnitine supplementation resulted in significantly increased tissue carnitine and acylcarnitine levels. Carnitine inhibited the development of precancerous lesions and macroscopic colonic tumors in AOM-treated mice. However, carnitine did not exert protective effects on intestinal tumors in Apc Min/+ mice.
ACKNOWLEDGMENTS
This study was supported by a research operating grant from the Dairy Farmers of Canada. Support in the form of a graduate student award was provided by the Sainte Justine Hospital Foundation (Marie-Josée Roy), and by a Tier 1 Canada Research Chair (Ernest G. Seidman). This work constitutes a part of Marie-Josée Roy's M.Sc. thesis submitted to the Department of Nutrition at the University of Montreal.