Butter fat may protect against colon carcinogenesis through decreased cell proliferation mediated by changes in prostaglandin production.
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Certain poryunsaturated fate appear to be more promeuve of experimentally-induced colon carcinogenesis than saturated fats. This suggests that butter fat, high in saturated fatty acids, might be protective. We hypothesized that butter fat would decrease the linoleic acid and arachidonic acid content of mucosal phospholipids, as well as prostaglandin production, with a resultant decrease in cell proliferation (a predictor of later tumor development) Ninety male Sprague Dawley rats were fed one of 3 fats (butter, corn oil and palm oil) at 3 levels (5, 7.5, and 15% by weight), for 4 weeks in a 3 3 factorial design. In vivo cell proliferation was measured immunohistochemically using incorporation of bromodeoxyuridine into DNA. The fatty acid composition of mucosal phospholipids was measured by gas chromatography after separation of phospholipids by thin-layer chromatography. Endogenous prostaglandin Ej (PGEj) and prostacyclin synthetic capacity were determined by radioirnmunoassay. Results: Butter fat resulted in a lower labeling index (P<0.0001) and proliferative zone (P<0.0018) than either palm oil or com oil in both the proximal and distal colon. The linoleic acid content of mucosal phospholipids was lower in butter fat fed animals than in those fed corn oil or palm oil (P<0.0001). Butter fat also resulted in a lower amount of arachidonic acid in mucosal phospholipids in the proximal colon (P<0.0003), and lower levels of PGE, (P<0.04) at this same site. Collectively, these data suggest that butter fat may be protective against experimentally-induced colon carcinogenesis by decreasing precursors for PG synthesis thus decreasing synthesis of PGE, and decreasing cell proliferation. Supported by the Norwegian Dairies Association.
