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The study was a microarray (Applied Biosystems, AB) on cecal cells from rats to see effects of resistant starch (RS) on expression of the whole genome: control (CC, 3.6 kcal/g), energy control (EC, 3.2 kcal/g), and RS (3.2 kcal/g, high amylose cornstarch). Male Sprague Dawley (8 wk) rats (RS, n=10; CC and EC, n=9) fed 4 wk. A gene's expression was "present" if signal/noise ≥3. Gene lists were done in R Scripts (t-tests), CC-EC, CC-RS, EC-RS. Lists were >10,000 genes. Differences (p<0.05; <0.01) were: CC-EC, 630; 158; CC-RS, 3193; 1769; EC-RS, 2641; 1301 genes. The Protein Analysis through Evolutionary Relationships of AB was used to determine the number of pathways (CC-EC, 18; CC-RS, 23; EC-RS, 17) affected greater than by random chance (p<0.05); and genes not known in a pathway (CC-EC, 515; CC-RS, 2711; EC-RS, 2266). A large number of hormone genes were affected (CC-EC, 18; CC-RS, 34; EC-RS, 26). Spotfire® was used for clustering analyses. Genes that were up-regulated (down-regulated) by RS were down-regulated (up-regulated) by CC and EC. Cells obtained from the cecum would be a heterogeneous mix therefore, gene expression for RS should result in signaling from the gut to the rest of the body via endocrine, neural, and immune mechanisms. These effects by RS may lead to a healthier phenotype, and decreased risk for chronic diseases such as heart disease, diabetes, and cancer. [ABSTRACT FROM AUTHOR]

This study examined the effects of resistant starch in a high fat diet (28% fat) on body weight, abdominal fat, cecal weight and pH, serum gut peptide YY (PYY) and gene expression for PYY and proglucagon in male Sprague Dawley rats. Three groups of rats (8wk) were fed one of these diets for ten wks: energy control (EC; 3.7 kcal/g), resistant starch (RS; 3.7 kcal/g) and fiber control (FC; 2.9 kcal/g). Results were significant when p≤ 0.05. The consumption of RS resulted in significant increases in cecal weight (full and empty), serum PYY, gene expression for PYY and proglucagon in cecum, and significant decrease in cecal pH compared to the other groups. However the disemboweled body weight and abdominal fat for RS were not lower compared to the EC. In previous studies, we observed that RS in a low fat diet (18% of fat), produced similar gut signaling, as in current study, but reduced disemboweled body weight and abdominal fat compared to EC. Mechanism for the contradictory results needs further study. Since high fat diets have been shown to alter brain response to other satiety signals (leptin), a high fat diet might affect neuronal response to PYY and GLP-1 signaling from the gut caused by dietary RS. [ABSTRACT FROM AUTHOR]