Effects of chronic heat exposure on growth performance, intestinal epithelial histology, appetite-related hormones and genes expression in broilers. He Xiaofang,Lu Zhuang,Ma Bingbing,Zhang Lin,Li Jiaolong,Jiang Yun,Zhou Guanghong,Gao Feng Journal of the science of food and agriculture BACKGROUND:Heat stress often occurs in the modern poultry industry, which impairs growth performance, particularly via reducing appetite. This study was aimed to investigate the mechanism of attenuating appetite by chronic heat exposure in broilers. A total of 144 broilers (28 days old) were allocated to normal control (NC, 22 °C), heat stress (32 °C), and pair-fed (22 °C) groups. RESULTS:Chronic heat exposure significantly increased cloacal temperatures and respiration rates, decreased the average daily feed intake and average daily gain, increased feed-to-gain ratio compared with the NC group, and elevated the concentrations of ghrelin and cholecystokinin (CCK) both in serum and intestine, as well as peptide YY and somatostatin in intestine on 35- or 42-day-old broilers. Moreover, heat exposure decreased villi height (VH) and the ratio of VH to crypt depth (CD), while it increased CD in the jejunum on 35- and 42 day-olds, increased (P < 0.05) the concentrations of valine and isoleucine in plasma on 42 days, and upregulated (P < 0.05) the expression of taste receptor type 1 members 1 and 3 (T1R1 and T1R3), CCK, and ghrelin in the intestine on 35- or 42-day-old broilers. CONCLUSION:Chronic heat exposure impairs the performance, intestinal morphology and appetite, which may be correlated with the increased secretion or gene expression of appetite-related hormones and genes, and the higher expression of nutrient-sensing receptors (T1R1 and T1R3) in broilers. © 2018 Society of Chemical Industry. 10.1002/jsfa.8971

Experimental Cyclic Heat Stress on Intestinal Permeability, Bone Mineralization, Leukocyte Proportions and Meat Quality in Broiler Chickens. Animals : an open access journal from MDPI The goal of this research was to assess cyclic heat stress on gut permeability, bone mineralization, and meat quality in chickens. Two separate trials were directed. 320 day-of-hatch Cobb 500 male chicks were randomly assigned to four thermoneutral (TN) and four cyclic heat stress (HS) chambers with two pens each, providing eight replicates per treatment in each trial (n = 20 chicks/replicate). Environmental conditions in the TN group were established to simulate commercial production settings. Heat stress chickens were exposed to cyclic HS at 35 °C for 12 h/day from days 7−42. Performance parameters, intestinal permeability, bone parameters, meat quality, and leukocyte proportions were estimated. There was a significant (p < 0.05) reduction in body weight (BW), BW gain, and feed intake, but the feed conversion ratio increased in chickens under cyclic HS. Moreover, HS chickens had a significantly higher gut permeability, monocyte and basophil levels, but less bone mineralization than TN chickens. Nevertheless, the TN group had significant increases in breast yield, woody breast, and white striping in breast fillets compared to HS. These results present an alternative model to our previously published continuous HS model to better reflect commercial conditions to evaluate commercially available nutraceuticals or products with claims of reducing the severity of heat stress. 10.3390/ani12101273

Blockage of protease-activated receptor 1 ameliorates heat-stress induced intestinal high permeability and bacterial translocation. Xu Qiu-lin,Guo Xiao-hua,Liu Jing-xian,Chen Bin,Liu Zhi-feng,Su Lei Cell biology international Accumulated evidences indicate intestinal lesions play an important role in the pathogenesis of heatstroke. However, the underlying mechanisms by which heat stress causes intestinal barrier dysfunction and bacterial translocation remain unclear. In this study, we investigated the role of protease-activated receptor 1 (PAR1) in heat stress-induced intestinal hyper-permeability and bacterial translocation. Intestinal permeability in heat stressed mouse was evaluated by determining plasma endotoxin concentration and urinal lactulose/mannitol (L/M) ratio with gastric administration of L/M solution. Venous blood, liver, spleen and mesenteric lymph node tissues were collected for bacterial load test. Real time PCR was used to determine ileum PAR1 mRNA expression. In vitro study, permeability was assessed by determining trans-epithelial electrical resistance (TEER) in human intestinal Caco-2 cell line. RWJ-58259, a selective antagonist of PAR1, was used both in vivo and in vitro studies. The results showed that heat stress could increase ileum PAR1 mRNA level, urinal L/M ratio, plasma endotoxin concentration and bacterial load in the blood, spleen and mesenteric lymph nodes. Blocking PAR1 with RWJ-58259 (10 mg/kg) pretreatment could significantly reduce heat stress-induced above changes, but have no role to PAR1 mRNA level. In Caco-2 cells, heat stress-induced high permeability could also be reduced by RWJ-58259 (5-20 µmol/L). In summary, our results demonstrated that PAR1 signaling pathway may play an important role in the heat stress-induced elevation of intestinal permeability, bacterial translocation and the occurrence of endotoxemia. 10.1002/cbin.10408

Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens. Nanto-Hara Fumika,Kikusato Motoi,Ohwada Shyuichi,Toyomizu Masaaki The journal of poultry science A study using pair-feeding technique was conducted to determine whether heat exposure directly or indirectly (via reduced feed intake) increases intestinal mucosal damage and permeability to endotoxin in broiler chickens. Male broiler chickens (Ross 308), 27-d-old, were subjected to one of the three treatments (=8): 1) thermo-neutral conditions (24°C) with feed intake, 2) heat stress conditions (33°C) with feed intake, or 3) pair-feeding under thermo-neutral conditions, with the feed intake identical to that of heat-stressed chickens. Using these groups, two experiments were performed to evaluate temporal changes in the intestinal morphology in response to each treatment. In experiment 1, chickens were sacrificed after 24 h of exposure to the treatment conditions, while in experiment 2, chickens were sacrificed after 12 or 72 h of exposure to the treatment conditions. In experiment 1, exposure to heat stress conditions for 24 h significantly decreased both the villus height to crypt depth ratio and number of proliferating cell nuclear antigen (PCNA)-positive cells in the duodenum and increased the plasma endotoxin concentration. These findings were not observed in pair-fed chickens. In experiment 2, intestinal integrity and function were unaffected by 12 h of heat stress. On the other hand, chickens exposed to heat stress for 72 h exhibited significantly damaged intestinal morphology in the duodenum as well as increased plasma endotoxin concentration; these negative effects were not observed in pair-fed chickens. These findings suggest that the intestinal morphology and permeability changes observed in chickens that are heat-stressed for 24-72 h are due to the heat stress conditions and not due to reduced feed intake. 10.2141/jpsa.0190004