Date of Award

1-1-2012

Document Type

Campus Access Thesis

Department

Biomedical Science

First Advisor

Angela Murphy

Abstract

Obesity is a chronic low-grade inflammatory disease that can lead to a variety of health complications including coronary heart disease, type 2 diabetes, hypertension, degenerative diseases and a wide array of cancers. For this reason, dietary supplements with anti-inflammatory properties have been the focal point of many recent studies on diet-induced obesity. Quercetin, a polyphenolic compound found in many fruits and vegetables, is of interest due to its low toxicity and its wide range of bioactivity. While multiple studies have revealed the anti-inflammatory capabilities of quercetin in different mouse models, quercetin's effects on metabolic and inflammatory biomarkers in a high fat diet induced obesity model have not yet been well established. We examined the effects of three different doses (0.02%, 0.2% & 2%) of quercetin on obesity markers, macrophage populations, and inflammatory mediators in a mouse model of high fat diet induced obesity. Our high fat diet treatment was 16 weeks and based on the American Standard Diet that contains approximately 40% of calories from fat (12% saturated, 28% unsaturated). The results show that the 0.02% and 2% doses of quercetin reduced total body weight, fat mass, and mesenteric fat weight, while all three quercetin doses reduced the mRNA gene expression of the macrophage marker EMR1 as well as the pro-inflammatory M1 macrophage marker CD11c in the epididymal adipose tissue. This was consistent with a general decrease in the gene expression of inflammatory mediators (MCP-1, TNF-á, and TLR-4). This data confirm the ability of quercetin to reduce metabolic and inflammatory biomarkers in a high fat diet induced obesity model. These findings may lead to the development of a safe and effective dose of a natural dietary supplement that has protective anti-inflammatory effects against the visceral adipose tissue inflammation associated with obesity.

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