Date of Graduation

5-2018

Document Type

Thesis

Degree Name

Bachelor of Science in Human Environmental Sciences

Degree Level

Undergraduate

Department

Human Nutrition and Hospitality Innovation

Advisor/Mentor

Kim, Jae Kyeom

Committee Member/Reader

Hill, Laura Leigh

Committee Member/Second Reader

Trudo, Sabrina

Committee Member/Third Reader

Bailey, Mechelle

Abstract

Obesity prevalence in the United States continues to increase and is associated with health consequences such as type 2 diabetes, hypertension, atherosclerosis, and hyperlipidemia. Among many contributing factors to obesity, fructose may be one of the major reasons as it disrupts the antioxidant system thereby resulting in an accumulation of reactive oxidative species and leading to obese conditions. The enzyme, isocitrate dehydrogenase 2 (IDH2), reduces nicotinamide adenine dinucleotide phosphate from the TCA Cycle, hence might be implicated with not only energy metabolism but also cellular redox homeostasis. Therefore, the hypothesis was that IDH2 deficiency in mice would exacerbate hepatic lipid metabolism in response to fructose intervention. The study consisted of a total of 24 IDH2 knockout female mice and their background strain (C57BL/6N) mice; the animals were assigned to either fructose or control diet group. After intervention of fructose over six weeks (34%; v/v), tissue weight, liver expression of lipogenesis gene (SREBP-1, SCD1, FAS, and DGAT2), and liver expressions of lipolysis genes (AMPK, SIRT1, and PPARɑ) were measured. There was a significant increase in visceral fat, while the body mass remained the same. Further, there was a trend of increase in expression of lipogenesis genes, whereas no change was shown in lipolysis gene expression in IDH2 mice fed fructose. In conclusion, even though changes in visceral fat mass were statistically significant in IDH2 deficient mice, hepatic lipid metabolism did not support the phenotypes in this study. Additional studies with larger sample size are warranted to find a potential link between IDH2 and increase in visceral fat accumulation.

Keywords

IDH2; Obesity; fructose; NAFLD

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