Lipid metabolism in avian species places unique demands on the liver in comparison to most mammals. The avian liver synthesizes the vast majority of fatty acids that provide energy and support cell membrane synthesis throughout the bird. Egg production intensifies demands to the liver as hepatic lipids are needed to create the yolk. The enzymatic reactions that underlie de novo lipogenesis are energetically demanding and require a precise balance of vitamins and cofactors to proceed efficiently. External stressors such as overnutrition or nutrient deficiency can disrupt this balance and compromise the liver’s ability to support metabolic needs. Heat stress is an increasingly prevalent environmental factor that impairs lipid metabolism in the avian liver. The effects of heat stress-induced oxidative stress on hepatic lipid metabolism are of particular concern in modern commercial chickens due to the threat to global poultry production. Chickens are highly vulnerable to heat stress because of their limited capacity to dissipate heat, high metabolic activity, high internal body temperature, and narrow zone of thermal tolerance. Modern lines of both broiler (meat-type) and layer (egg-type) chickens are especially sensitive to heat stress because of the high rates of mitochondrial metabolism. While this oxidative metabolism supports growth and egg production, it also yields oxidative stress that can damage mitochondria, cellular membranes and proteins, making the birds more vulnerable to other stressors in the environment. Studies to date indicate that oxidative and heat stress interact to disrupt hepatic lipid metabolism and compromise performance and well-being in both broilers and layers. The purpose of this review is to summarize the impact of heat stress-induced oxidative stress on lipid metabolism in the avian liver. Recent advances that shed light on molecular mechanisms and potential nutritional/managerial strategies to counteract the negative effects of heat stress-induced oxidative stress to the avian liver are also integrated.

High environmental temperature has strong adverse effects on poultry production, welfare, and sustainability and, thereby, constitutes one of the most challenging stressors. Although colossal information has been published on the effects of heat stress on poultry productivity and gut health, the fundamemntal mechanisms associated with heat stress responses and intestinal barrier function are still not well defined. The aim of the present study was, therefore, to determine the effects of acute (2 h) heat stress on growth performance, gut integrity, and intestinal expression of heat shock and tight junction proteins in slow- (broilers of the 1950's, ACRB), moderate- (broilers of 1990's, 95RAN), rapid-(modern broilers, MRB) growing birds, and their ancestor wild jungle fowl (JF). Heat stress exposure significantly increased the core body temperature of 95RAN and MRB chickens by ~0.5–1°C, but not that of JF and ACRB compared to their counterparts maintained at thermoneutral conditions. Heat stress also depressed feed intake and increased serum fluorescein isothiocyanate-dextran (FITC-D) levels (P < 0.05) in modern broilers (95RAN and MRB) but not in JF and ACRB, indicating potential leaky gut syndrome. Molecular analyses showed that heat stress exposure significantly up regulated the duodenal expression of occludin (OCLN) and lipocalin (LCN2) in ACRB, zonula occludens (ZO-2), villin1 (VIL1), and calprotectin (CALPR) in 95 RAN, and only CALPR in MRB compared to their TN counterparts. In the jejunum however, heat stress down regulated the expression of PALS1-associated tight junction protein (PATJ) in ACRB, 95RAN, and MRB, and that of cadherin1 (CDH1) in MRB. In the ileum, heat stress significantly down regulated the expression of OCLN in 95 RAN, ZO-1 in MRB, gap junction protein alpha1 (GJA1) in JF, and VIL1 in ACRB compared to their TN counterparts. In summary, this is the first report, to our knowledge, showing that tight junction protein expression is environmental-, genotype-, and intestinal segment-dependent and identifying molecular signatures, such as CDH1, CALPR, and ZO-1, potentially involved in leaky gut syndrome-induced by heat stress in MRB.

Due to the important functions of arginine in poultry, it should be questioned whether the currently adopted dietary Arg:Lys ratios are sufficient to meet the modern broiler requirement in arginine. The present study aimed, therefore, to evaluate the effects of the dietary supplementation of L-arginine in a commercial broiler diet on productive performance, breast meat quality attributes, incidence and severity of breast muscle myopathies and foot pad dermatitis (FPD), and plasma and muscle metabolomics profile in fast-growing broilers. A total of 1,170 1-day-old Ross 308 male chicks was divided into two experimental groups of 9 replicates each fed either a commercial basal diet (CON, digestible Arg:Lys ratio of 1.05, 1.05, 1.06 and 1.07 in each feeding phase, respectively) or the same basal diet supplemented on-top with crystalline L-arginine (ARG, digestible Arg:Lys ratio of 1.15, 1.15, 1.16 and 1.17, respectively). Productive parameters were determined at the end of each feeding phase (12, 22, 33, 43 d). At slaughter (43 d), incidence and severity of FPD and breast myopathies were assessed, while plasma and breast muscle samples were collected and analyzed by proton nuclear magnetic resonance-spectroscopy. The dietary supplementation of arginine significantly reduced cumulative feed conversion ratio compared to the control diet at 12 d (1.352 vs. 1.401, P < 0.05), 22 d (1.398 vs. 1.420; P < 0.01) and 33 d (1.494 vs. 1.524; P < 0.05), and also tended to improve it in the overall period of trial (1.646 vs. 1.675; P = 0.09). Body weight was significantly increased in ARG compared to CON group at 33 d (1,884 vs. 1,829 g; P < 0.05). No significant effect was observed on meat quality attributes, breast myopathies and FPD occurrence. ARG birds showed significantly higher plasma concentration of arginine and leucine, and lower of acetoacetate, glutamate, adenosine and proline. Arginine and acetate concentrations were higher, whereas acetone and inosine levels were lower in the breast of ARG birds (P < 0.05). Taken together, these data showed that increased digestible Arg:Lys ratio had positive effects on feed efficiency in broiler chickens probably via modulation of metabolites that play key roles in energy and protein metabolism.

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, ACCα 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 ACCα, but reduced FASN and ACLY expression. Under chronic HS, Noni up regulated ACCα and FASN but it down regulated ACLY. In vitro studies, using chicken hepatocyte cell lines, showed that HS down-regulated the expression of ACCα, FASN, and ACLY. 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 HSP expression suggest also that Noni might be involved in modulating the stress response in chicken liver.

Background: In recent years, there has been a growing body of evidence indicating that replacing cholecalciferol (vitamin D3) with 25-hydroxycholecalc

The poultry industry is continuously facing substantial and different challenges such as the increasing cost of feed ingredients, the European Union’s ban of antibiotic as growth promoters, the antimicrobial resistance and the high incidence of muscle myopathies and breast meat abnormalities. In the last decade, there has been an extraordinary development of many genomic techniques able to describe global variation of genes, proteins and metabolites expression level. Proper application of these cutting-edge omics technologies (mainly transcriptomics, proteomics and metabolomics) paves the possibility to understand much useful information about the biological processes and pathways behind different complex traits of chickens. The current review aimed to highlight some important knowledge achieved through the application of omics technologies and proteo-genomics data in the field of feed efficiency, nutrition, meat quality and disease resistance in broiler chickens.