Date of Graduation

12-2015

Document Type

Thesis

Degree Name

Master of Science in Poultry Science (MS)

Degree Level

Graduate

Department

Poultry Science

Advisor/Mentor

Dridi, Sami

Committee Member

Bottje, Walter G.

Second Committee Member

Coon, Craig N.

Third Committee Member

Anthony, Nicholas B.

Fourth Committee Member

Wideman, Robert F. Jr.

Fifth Committee Member

Baum, Jamie I.

Sixth Committee Member

Cline, Mark

Keywords

Biological sciences; Autophagy; Chicken; Expression; Genes; Leptin; Regulates

Abstract

Autophagy or cellular self-digestion, a lysosomal degradation pathway that is conserved from yeast to human, plays a key role in recycling cellular constituents, including damaged organelles. It also plays a pivotal role in the adaptation of cells to a plethora of distinct stressors including starvation. Autophagy has been extensively studied in mammals and yeast, but little is known in avian species. Thus, the major objective of the present study was to determine the effects of leptin on autophagy-related genes in chicken hypothalamus, muscle and liver. Leptin is an adipocytokine that is mostly produced by white adipose cells in mammals (as fat storage increases), mediating sensing mechanism for fat deposition, signaling the brain via leptin receptor-mediated signal transduction to inhibit feed intake and increase energy expenditure. In the present study, recombinant chicken leptin (625 pmol, 10 µL) diluted in artificial cerebrospinal fluid was injected intracerebroventricularly (ICV) in one week-old Hubbard x Cobb 500 chicks (n=10) and feed intake was recorded at 30, 60 and 180 min after injection. At the end of the experiment, hypothalamii, muscle, and liver were collected for gene expression and protein level analysis. Leptin significantly reduce feed intake after 30 min compared to the control group. ICV administration of both chicken and ovine leptin significantly down-regulated genes (mRNA and protein levels) in hypothalamic and muscle tissues. In the muscle, leptin upregulates the expression of AMPKβ1 and AMPKϒ1, and downregulates the expression of mTOR, upstream regulator of autophagy pathway. Expectedly, there were upregulations of leptin receptors, ObR (P

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