Date of Award:

2013

Document Type:

Thesis

Degree Name:

Master of Science (MS)

Department:

Animal, Dairy, and Veterinary Sciences

Advisor/Chair:

Abby D Benninghoff

Abstract

The typical Western dietary pattern is characterized by the consumption of energy-dense, nutrient-poor foods and has been linked to increased risk of colorectal cancer (CRC). Our research group previously developed the total Western diet (TWD) that emulates typical human dietary intakes of macro- (carbohydrates, proteins, and fats) and micronutrients (vitamins and minerals) on an energy density basis for rodents. In the present study, we sought to determine the impact of TWD on biomarkers of metabolic syndrome and obesity in comparison to a commercial 45% fat diet used for models of diet-induced obesity (DIO diet) and the standard basal AIN93G diet, which is optimized for rodent health. Also, we included 2 additional test diets to evaluate the contribution of the micronutrient (vitamin- and mineral-modified diet, [VMM]) or macronutrient (macro-modified diet [MM]) contents of the TWD in development of cancer, obesity, and glucose intolerance. A chemical carcinogenesis model of inflammation-associated colon cancer was employed to evaluate impact of diets on colon cancer in mice. As expected, mice consuming the DIO diet acquired an obesity/metabolic syndrome phenotype typified by increased food energy intake, greater rate of body weight gain, increased proportion of body composition as fat mass, higher fasting glucose, impaired glucose tolerance, and higher circulating levels of leptin. However, consumption of TWD did not alter any of these classic biomarkers of metabolic health, as these mice adjusted food intake so that energy consumption was similar to that for mice fed AIN93G. A different pattern was observed for colon carcinogenesis. Consumption of the TWD or VMM diet markedly increased colon tumor multiplicity and size compared to the AIN93G control, whereas consumption of the DIO or MM diets did not enhance colon tumorigenesis. Collectively, these observations point to a critical role of dietary micronutrients in colon carcinogenesis, and that this promoting effect is likely unrelated to the metabolic syndrome phenotype induced by a high fat diet. Moreover, our observations emphasize the need to take into account the micronutrient content of rodent basal diets when modeling typical U.S. nutrition in pre-clinical animal experiments in order to improve the translation of these studies to human nutrition and dietary intervention programs.

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