title: Dietary fat, fiber, and carcinogen alter fecal diacylglycerol composition and mass.
abstract: Fecal diacylglycerols (DAGs) are known activators of protein kinase C (PKC), which in turn modulates colonic epithelial cell growth programs and, therefore, could play a role in the malignant transformation process. However, the effects of physiological modifiers such as diet and carcinogen on fecal DAG mass and composition have not been reported. We therefore designed a 2 x 2 x 2 factorial study (2 fats: corn oil and fish oil; 2 fibers: pectin and cellulose; with and without carcinogen). Rats were provided with diets for 5 weeks. Three weeks after the second injection of azoxymethane, feces were collected from 10 rats/treatment (n = 80 total) and analyzed for DAG mass and fatty acyl composition by combined TLC and gas chromatography. Dietary fat had a significant effect on the mol% fatty acyl composition of fecal DAG. Greater amounts of long chain n-3 polyunsaturated fatty acids (20:5n-3, 22:5n-3, and 22:6n-3) were detected in fecal DAG of fish oil-fed animals relative to corn oil (P < 0.001). In contrast, corn oil resulted in a higher mol % of 18:2n-6 relative to fish oil (P < 0.016). The most salient effect of fiber was on total production (nmol/day) of DAG, which was 2.5 times higher with cellulose than pectin supplementation. In addition, there was an effect of fiber on both mol % and concentration of 22:6n-3, with cellulose producing higher amounts relative to pectin (P < 0.04). A significant interaction between fat and fiber was observed with nmols of 17:0 excreted in 24 h, with fish oil/cellulose producing 94.2 nmol as compared to 3.5 seen with corn oil/pectin (P < 0.02). There was a significant interaction between fat and carcinogen on all of the DAG n-3 fatty acids, which were elevated with carcinogen/fish oil treatment. These data show that fat, fiber, and carcinogen can modulate the fatty acyl composition and mass of fecal DAG. Since the production of fecal DAG, an activator of PKC, may alter colonic mucosal cell proliferation, our data offer insight into a mechanism by which diet may modify the risk of colon cancer development.
authors.affiliation: Faculty of Nutrition, Molecular and Cell Biology Group, Texas A&M University, College Station 77843-2471, USA.
authors.forename: J S
authors.initials: JS
authors.lastname: Pickering
authors.forename: J R
authors.initials: JR
authors.lastname: Lupton
authors.forename: R S
authors.initials: RS
authors.lastname: Chapkin
mesh_terms: D000818:Animals; D001391:Azo Compounds / Q000494:pharmacology*; D002273:Carcinogens / Q000494:pharmacology*; D003110:Colonic Neoplasms / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism; D004041:Dietary Fats / Q000494:pharmacology*; D004043:Dietary Fiber / Q000627:therapeutic use*; D004075:Diglycerides / Q000145:classification / Q000378:metabolism*; D004195:Disease Models, Animal; D005243:Feces / Q000737:chemistry*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C011439:1,2-diacylglycerol; D001391:Azo Compounds; D002273:Carcinogens; D004041:Dietary Fats; D004043:Dietary Fiber; D004075:Diglycerides; C001825:azomethane