Abstract
We speculated that a diet with a high glycemic index (GI) or a diet with a low nutrient density (nutrient-to-calorie ratio) would enhance colon carcinogenesis, presumably via increased insulin resistance. Forty-eight Sprague-Dawley (SD) rats received an azoxymethane injection (20 mg/kg) and were randomized into five groups given an AIN-76 diet containing 1) 65% starch by weight, 2) 65% glucose (GI = 100), 3) 65% fructose (GI = 23), 4) 82% starch, or 5) 39% oil and 39% sucrose. The nutrient density of Diets 4 and 5 was one-half that of Diets 1-3. Promotion was assessed by the multiplicity (number of crypts) of aberrant crypt foci (ACF), an early marker of colon carcinogenesis. Insulin resistance was estimated by the FIRI index (blood insulin x blood glucose), by plasma triglycerides, and by visceral fat. To confirm the results in another rat strain, the experiment was duplicated in 48 Fischer (F344) rats. Results show that 1) the ACF multiplicity was not different in glucose- and fructose-fed rats (p > 0.7): diets with contrasting GI had the same effect on ACF growth; 2) diets of low nutrient density increased visceral fat (p < 0.05) but reduced the ACF size in F344 rats (p < 0.001, no reduction in SD rats); and 3) indirect insulin resistance markers (FIRI index, blood triglycerides, and visceral fat) did not correlate with ACF multiplicity. These results do not support the hypothesis that diets with a high GI or low nutrient density or diets that increase some indirect insulin resistance markers can promote colon carcinogenesis in F344 or SD rats.