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There has long been a link tied between obesity and such pathological conditions as nonalcoholic fatty liver disease and type two diabetes. Studies have shown that feeding rats a diet high in fat results in hepatic steatosis and steatohepatitis. Using a novel short term diet of six weeks with male

There has long been a link tied between obesity and such pathological conditions as nonalcoholic fatty liver disease and type two diabetes. Studies have shown that feeding rats a diet high in fat results in hepatic steatosis and steatohepatitis. Using a novel short term diet of six weeks with male adolescent Sprague-Dawley rats, our laboratory sought to investigate the early effects of high fat intake on the liver. Prior findings in our laboratory found that a high fat diet (HFD) leads to nonalcoholic fatty liver disease as well as other symptoms of metabolic syndrome. This study hypothesized that rats fed a 60% HFD for 6 weeks, unlike a high sucrose or standard chow diet, would have an elevated expression of pro-inflammatory cytokines associated with steatohepatitis. TNF-α, TLR4 and XBP1 were chosen for their link to hepatic inflammation. The results of this study found that contrary to the hypothesis, the high fat diet did not induce significant changes in the expression of any inflammatory marker in comparison to a high sucrose or control chow diet.
ContributorsCalhoun, Matthew (Author) / Sweazea, Karen (Thesis director) / Deviche, Pierre (Reviewer) / Barrett, The Honors College (Contributor)
Created2015-05
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Adaptive thermogenesis is an innate mechanism that assists the body in controlling its core temperature that can be stimulated in two ways: cold and diet. When adaptive thermogenesis is stimulated through diet, the metabolic rate of the body should increase and the metabolic efficiency of the body should decrease. This

Adaptive thermogenesis is an innate mechanism that assists the body in controlling its core temperature that can be stimulated in two ways: cold and diet. When adaptive thermogenesis is stimulated through diet, the metabolic rate of the body should increase and the metabolic efficiency of the body should decrease. This activation should, theoretically, help to control weight gain. A protocol was developed to study four male Sprague-Dawley rats throughout a fourteen week period through the measurement of brown adipose tissue blood flow and brown adipose tissue, back, and abdomen temperatures to determine if diet induced thermogenesis existed and could be activated through norepinephrine. The sedative used to obtain blood flow measurements, ketamine, was discovered to induce a thermal response prior to the norepinephrine injection by mimicking the norepinephrine response in the sympathetic nervous system. This discovery altered the original protocol to exclude an injection of norepinephrine, as this injection would have no further thermal effect. It was found that ketamine sedation excited diet induced thermogenesis in periods of youth, low fat diet, and early high fat diet. The thermogenic capacity was found to be at a peak of 2.1 degrees Celsius during this time period. The data also suggested that the activation of diet induced thermogenesis decreased as the period of high fat diet increased, and by week 4 of the high fat diet, almost all evidence of diet induced thermogenesis was suppressed. This indicated that diet induced thermogenesis is time and diet dependent. Further investigation will need to be made to determine if prolonged high fat diet or age suppress diet induced thermogenesis.
ContributorsJayo, Heather Lynn (Author) / Caplan, Michael (Thesis director) / Herman, Richard (Committee member) / Chemical Engineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12