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Approximately 70% of Americans are overweight or obese and studies have shown that poverty-dense American counties are the most prone to obesity (Levine, 2011). Along with diet, the endogenous circadian rhythms have been found to be an important piece of human metabolic health. Circadian disruption in humans, such as jet-lag and shift work, have been linked to metabolic problems such as Type 2 Diabetes Mellitus and Metabolic Syndrome. Since circadian disruption affects many demographics including shift workers and routine business travelers it is imperative to understand the biological mechanism behind the relationship between circadian disruption and weight gain. One potential connection between circadian function and eating behaviors is the Neuropeptide Y (NPY)/Peptide YY (PYY) system which causes satiety after food intake. This study conducted three experiments (i) in a 12:12 light dark cycle (LD) were assigned to four temporal sac groups (ZT 0, ZT 6, ZT 12, or ZT 18) (ii) in a LD mice were assigned to four temporal injection groups (ZT 0, ZT 6, ZT 12, or ZT 18) and paired with either a PYY3-36 or vehicle (control) (iii) mice were exposed to LD or constant light (LL) paired with either a PYY3-36 or vehicle (control) injection during the onset of their active period, ZT 12. In the first experiment, it was found that PYY3-36 is regulated cyclically. In the second experiment, PYY3-36 reduced food intake, being most effective during the beginning of the night. PYY3-36injections were also found to be effective in inhibiting food intake regardless of the light cycle. This suggests that photic cues are not essential for PYY3-36 active period efficacy.



Thesis Comittee

Dr. Joseph Seggio, Thesis Advisor

Dr. Kenneth Adams, Committee Member

Dr. Heather Marella, Committee Member

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Original document was submitted as an Honors Program requirement. Copyright is held by the author.

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