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Epidemiological studies have identified obesity as a risk factor for numerous chronic diseases such as adult onset diabetes, hypertension, and hypercholesterolemia. In both humans and laboratory animals, high-fat diets have been shown to cause obesity. Increases in dietary fat lead to increased energy consumption and, consequently, significant increases in body

Epidemiological studies have identified obesity as a risk factor for numerous chronic diseases such as adult onset diabetes, hypertension, and hypercholesterolemia. In both humans and laboratory animals, high-fat diets have been shown to cause obesity. Increases in dietary fat lead to increased energy consumption and, consequently, significant increases in body fat content. CD36 has been implicated in fat perception, preference, and increased consumption, but it is yet to be tested using a behavior paradigm. To study the effect of CD36 on fat taste transmission and fat consumption, four CD36 knockout (experimental) mice and four Black 6 wildtype (control) mice underwent 20 days of fat preference and perception testing. Both groups of mice were exposed to foods with progressively increasing fat content (10%, 12.5%, 15% 17.5%, 20%, 45%) in order to assess the effect of CD36 on fat preference. Afterward, the mice were subjected to an aversive conditioning protocol designed to test the effect of CD36 on fat taste perception; development of a conditioned taste aversion was indicative of ability to taste fat. Especially, knockout mice exhibited diminished preference for and reduced consumption of fat during preference testing and were unable to identify fat taste as the conditioned stimulus during aversive conditioning. A repeated measures ANOVA with Bonferroni correction revealed a significant main effect of group on fat consumption, energy intake, and weight. Linear regression revealed CD36 status to account for a majority of observed variance in fat consumption across both phases of the experiment. These results implicate CD36 in fat taste perception and preference and add to the growing body of evidence suggesting fat as a primary taste.
ContributorsJasbi, Paniz (Author) / Johnston, Carol (Thesis advisor) / Lespron, Christy (Committee member) / Wadhera, Devina (Committee member) / Arizona State University (Publisher)
Created2018
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The effects of iron and chromium blood concentrations have been linked to blood glucose control in diabetics. It is suggested that iron causes oxidative stress in the beta cells of the pancreas and adipocytes creating insulin insufficiency and resistance. Chromium is believed to increase the action of insulin

The effects of iron and chromium blood concentrations have been linked to blood glucose control in diabetics. It is suggested that iron causes oxidative stress in the beta cells of the pancreas and adipocytes creating insulin insufficiency and resistance. Chromium is believed to increase the action of insulin through its biologically active molecule chromodulin. Both of these mechanisms are not clear. This 20 week case study tests the feasibility of combining iron depletion therapy followed by chromium supplementation to improve insulin sensitivity. This single case study followed a protocol of two blood donations separated by eight weeks followed by chromium supplementation of 250 µg of chromium picolinate once a day four weeks after the second blood donation. Fasting blood draws were taken at baseline, post blood draws and pre and post chromium supplementation. Results were not promising for the first hypothesis of lowering HbA1c, but the results were promising for the second hypothesis of improving insulin sensitivity by lowering the HOMA score.
ContributorsJarrett, Nia (Author) / Johnston, Carol (Thesis advisor) / Lespron, Christy (Committee member) / Mayol-Kreiser, Sandra (Committee member) / Arizona State University (Publisher)
Created2015