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Advisory Committee Chair

Franklin R Amthor

Advisory Committee Members

Karen L Gamble

Document Type

Thesis

Date of Award

2014

Degree Name by School

Master of Arts (MA) College of Arts and Sciences

Abstract

Circadian rhythms are the daily biological changes present within most organisms that occur in a predictable, approximately 24 hour pattern, even in the absence of external stimuli. These rhythms occur both at a global and cellular level, and although the molecular mechanics are highly conserved, their functions may vary depending on the tissues in which they are expressed. These functions include various aspects of metabolic processes such as satiety signaling and cellular proliferation. In order to explore the specific functions of circadian rhythms within adipocytes, a mouse model with Clock disruption driven by the fatty acid-binding protein 2 (aP2) promoter was created. aP2 has been shown to be expressed in adipocytes as well as macrophages, and clock disruption was verified in adipocytes. This model showcased a phenotype including increased total weight, body fat percentage, and surprisingly, a large increase in early and unexpected death. Since clock disruption likely has occurred within macrophages, immune disruption was identified as a potential cause for these unexpected deaths. To investigate, an immune challenge was presented to both transgenic and wild-type mice, and several behavioral and physiological variables were recorded. Unfortunately, no significant differences were apparent between genotypes. At this point, the cause of higher rates of deaths among the adipocyte and macrophage specific circadian disruption mouse models remains unknown.

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