Effect of Morinda citrifolia (Noni)-enriched diet on hepatic heat shock protein and lipid metabolism-related genes in heat stressed broiler chickens

Authors: FLEES, JOSHUA - UNIVERSITY OF ARKANSAS; RAJAEL-SHARLFABADL, HOSSELIN - UNIVERSITY OF ARKANSAS; GREENE, ELIZABETH - UNIVERSITY OF ARKANSAS; BEER, LESLEIGH - UNIVERSITY OF ARKANSAS; HARGIS, BILLY - UNIVERSITY OF ARKANSAS; ELLESTAD, LAURA - UNIVERSITY OF MARYLAND; PORTER, TOM - UNIVERSITY OF MARYLAND; Donoghue, Ann - Annie; DRIDI, SAMI - UNIVERSITY OF ARKANSAS

Submitted to: Frontiers in Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/30/2017
Publication Date: 11/27/2017
Citation: Flees, J., Rajael-Sharlfabadl, H., Greene, E., Beer, L., Hargis, B.M., Ellestad, L., Porter, T., Donoghue, A.M., Dridi, S. 2017. Effect of Morinda citrifolia (Noni)-enriched diet on hepatic heat shock protein and lipid metabolism-related genes in heat stressed broiler chickens. Frontiers in Physiology. 8:919. https://doi.org/10.3389/fphys.2017.00919.
DOI: https://doi.org/10.3389/fphys.2017.00919

Interpretive Summary: Driven by economic demands and consumer preference for low fat and high protein sources, commercial broiler chickens have been intensively selected for high growth rate and high breast yield. Poultry meat and egg production has seen the largest increase during past decades and supports the livelihoods and food security of billions of people worldwide. However, this spectacular progress is also accompanied by several undesirable changes including hyperphagia, metabolic disorders, and hypersensitivity to high environmental temperature due to high metabolic activity and lack of sweat glands. Heat stress (HS) is detrimental to poultry production from its strong adverse effects on feed intake, growth, meat yield, welfare, and mortality. Drinking Morinda citrifolia (Noni) juice has been shown to enhance hepatic antioxidant capacity, improve lipid homeostasis and protect the liver from environmental and chemical stressors. This medicinal plant has been widely used in human nutrition and health. However, the effect of Noni on chicken liver metabolism under control and HS conditions is not known. Chicken liver is the main site for de novo fatty acid synthesis (lipogenesis) and also a site for fat storage, and as there is a subtle balance between hepatic lipogenesis and lipolysis. The present studies were conducted to determine the effects of Noni-enriched diet on growth performance, circulating metabolite and hormone levels as well as on the expression of hepatic lipogenesis- and lipolysis-related genes in broiler chickens exposed to acute and chronic HS. Our findings indicate that HS induces hepatic lipogenesis in chickens and this effect is probably mediated via heat shock proteins (HSPs). The modulation of hepatic HSP expression suggest that Noni might be involved in modulating the stress response in chicken liver.

Technical Abstract: Heat stress (HS) has been reported to alter fat deposition in broilers, however the underlying molecular mechanisms are not well-defined. The objectives of the current study were, therefore: (1) to determine the effects of acute (2 h) and chronic (3 weeks) HS on the expression of key molecular signatures involved in hepatic lipogenic and lipolytic programs, and (2) to assess if diet supplementation with dried Noni medicinal plant (0.2% of the diet) modulates these effects. Broilers (480 males, 1 d) were randomly assigned to 12 environmental chambers, subjected to two environmental conditions (heat stress, HS, 35°C vs. thermoneutral condition, TN, 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 weeks 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, ACCa and ATP citrate lyase, ACLY). HS down regulated the hepatic expression of lipoprotein lipase (LPL) and hepatic triacylglycerol lipase (LIPC), but up-regulated 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 the acute and chronic experimental conditions, respectively. During acute HS, Noni increased ACCa, but reduced FASN and ACLY expression. Under chronic HS, Noni up regulated ACCa and FASN but it down regulated ACLY. In vitro studies, using chicken hepatocyte cell lines, showed that HS down-regulated the expression of ACCa, FASN, and ACLY. Treatment with quercetin, one bioactive ingredient in Noni, up-regulated the expression of ACCa, FASN, and ACLY under TN conditions, but it appeared to down-regulate ACCa 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 HSP expression suggest also that Noni might be involved in modulating the stress response in chicken liver.