Date of Graduation

8-2018

Document Type

Thesis

Degree Name

Master of Science in Poultry Science (MS)

Degree Level

Graduate

Department

Poultry Science

Advisor/Mentor

Sami Dridi

Committee Member

Walter Bottje

Second Committee Member

Samuel Rochell

Third Committee Member

Jason Apple

Fourth Committee Member

Sun-Ok Lee

Keywords

Chicken, Heat Stress, Lipid Metabolism, Liver, Noni, Quercetin

Abstract

Heat stress (HS) has been reported to alter fat deposition in broilers, however the underlying molecular mechanisms are not well-defined; therefore, the objectives of the current study were to: (1) determine the effects of acute (2 h) and chronic (3 wk) HS on the expression of key molecular signatures involved in hepatic lipogenic and lipolytic programs; and (2) assess if diet supplementation with dried Noni medicinal plant (0.2% of the diet) modulates these effects. Broilers (n=480 males, 1 d) were randomly assigned to 12 environmental chambers, subjected to two environmental conditions (HS at 35°C vs. thermoneutral condition [TN] at 24°C) and fed two diets (control vs. Noni) in a 2 × 2 factorial design. Feed intake and body weights were recorded, and blood and liver samples were collected at 2 h and 3 wk post-heat exposure. HS depressed feed intake, reduced body weight, and up-regulated the hepatic expression of heat shock protein HSP60, HSP70, HSP90, as well as key lipogenic proteins fatty acid synthase (FASN), acetyl co-A carboxylase alpha (ACCα), and ATP citrate lyase (ACLY). HS down-regulated the hepatic expression of lipoprotein lipase (LPL) and hepatic triacylglycerol lipase (LIPC), but up-regulated adipose triglyceride lipase (ATGL). Although it did not affect growth performance, Noni supplementation regulated the hepatic expression of lipogenic proteins in a time- and gene-specific manner. Prior to HS, Noni increased ACLY and FASN in acute and chronic experimental conditions, respectively. During acute HS, Noni increased ACCα, but reduced FASN and ACLY expression. Under chronic HS, Noni up-regulated ACCα and FASN but it down-regulated ACLY. In cells, HS exposure to 45°C for 2 hours down-regulated ACCα, FASN, and ACLY compared to TN exposure at 37°C. Treatment with quercetin, one bioactive ingredient in Noni, up-regulated the expression of ACCα, FASN, and ACLY under TN conditions, but it appeared to down-regulate ACCα and increase ACLY levels under HS exposure. In conclusion, our findings indicate that HS induces hepatic lipogenesis in chickens and this effect is probably mediated via HSPs. The modulation of hepatic heat-shock protein HSP expression suggests that Noni might be involved in modulating the stress response in chicken liver.

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