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Obesity rates have been climbing steadily for the past hundred years, and in conjunction so have the rates of many metabolic disease. The reasons for this are both complex and multifaceted. Homecooked meals have been replaced by many highly processed foods, while lifestyles have become more sedentary. Throughout this time, as obesity rates have grown, the consumption of fructose has increased in parallel. In addition to the correlation between fructose consumption and obesity it has been linked to the development of multiple metabolic diseases, including hypertension, NAFLD, diabetes, and cancer. While great strides have been made to begin to understand these associations, more work is required to mechanistically link fructose-induced metabolism to the development of metabolic disease. More specifically, evidence is lacking for how fructose catabolism is altered after the continued ingestion of a high-fructose diet for long periods of time, and these specific changes to metabolic pathways are hypothesized to drive the development of many of these metabolic diseases which continue to plague society. In the following chapters we strove to answer some of these questions through investigating the effects of long-term high-fructose feeding in FVB/N mice. Overall, these mice were resistant to the development of fructose-driven obesity and glucose intolerance, while still showing evidence of metabolic disturbance in peripheral tissues. Furthermore, while short-term high-fructose feeding in these mice led to an increase in fructolytic and adipogenic genes, as expected, long-term high-fructose feeding caused these same metabolic pathways to no longer be elevated. These data provide evidence for a fructolytic pathway which cannot be maintained after excessive and prolonged high-fructose feeding.




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