The use of dried olive pomace as complementary energy sources in poultry feed is still limited due to its low protein and high fiber contents. Bioconversion of olive pomace through solid-state fermentation with or without exogenous enzymes is considered as a trial for improving its nutritional value. This study aimed to evaluate the effects of fermented olive pomace with or without enzymatic treatment on the growth, modulations of genes encoding digestive enzymes and glucose transporters, meat oxidative stability, and economic efficiency of broiler chickens. A total of 1400 day-old broiler chicks (Ross 308) were randomly allocated to seven dietary treatments with 10 replicates of 20 birds/replicate. Treatments included control (basal corn–soybean diet) and other six treatments in which basal diet was replaced by three levels (7.5, 15, and 30%) of fermented olive pomace (FOPI) or enzymatically fermented olive pomace (FOPII) for 42 days. The highest body weight gain was observed in groups fed 7.5 and 15% FOPII (increased by 6.6 and 12.5%, respectively, when compared with the control group). Also, feeding on 7.5 and 15% FOPII yielded a better feed conversion ratio and improved the digestibility of crude protein, fat, and crude fiber. The expression of the SGLT-1 gene was upregulated in groups fed FOPI and FOPII when compared with the control group. Moreover, the expression of the GLUT2 gene was elevated in groups fed 7.5 and 15% FOPII. By increasing the levels of FOPI and FOPII in diets, the expression of genes encoding pancreatic AMY2A, PNLIP, and CCK was upregulated (p < 0.05) when compared with the control. Fat percentage and cholesterol content in breast meat were significantly reduced (p < 0.05) by nearly 13.7 and 16.7% in groups fed FOPI and FOPII at the levels of 15 and 30%. Total phenolic and flavonoid contents in breast meat were significantly increased in groups fed 15 and 30% FOPI and FOPII when compared with the control group and even after a long period of frozen storage. After 180 days of frozen storage, the inclusion of high levels of FOP significantly increased (p < 0.05) the levels of glutathione peroxide and total superoxide dismutase and meat ability to scavenge free radical 1,1-diphenyl-2-picrylhydrazyl. Furthermore, the highest net profit and profitability ratio and the lowest cost feed/kg body gain were achieved in groups fed 7.5 and 15% of FOPII, respectively. The results of this study indicated that dietary inclusion of 15% FOPII could enhance the growth performance and economic efficiency of broiler chickens. Moreover, a higher inclusion level of FOPI or FOPII could enhance the quality and increase the oxidative stability of frozen meat and extend the storage time.

Aim: The present study was designed to explore the effects of hydrogen sulfide (H 2 S) on Ca 2+ homeostasis in rat pancreatic acini. Results: Sodium hydrosulfide (NaHS; an H 2 S donor) induced a biphasic increase in the in- ] i increase was markedly inhibited in the presence of NG-monomethyl L-arginine or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), and diaminofluorescein-2/diaminofluorescein-2 triazole (DAF-2/DAF-2T) fluorometry demonstrated that nitric oxide (NO) was also produced by H 2 S in a dose-dependent manner with an EC 50 of 64.8 lM, indicating that NO was involved in the H 2 S effect. The H 2 S-induced [Ca 2+ ] i increase was inhibited by pretreatment with U73122, xestospongin C, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, KT5823, and GP2A, indicating that phospholipase C (PLC), the inositol 1,4,5-trisphosphate (IP 3 ) receptor, soluble guanylate cyclase (sGC), protein kinase G (PKG), and G q -protein play roles as intermediate components in the H 2 S-triggered intracellular signaling. Innovation: To our knowledge, our study is the first one highlighting the effect of H 2 S on intracellular Ca 2+ dynamics in pancreatic acinar cells. Moreover, a novel cascade was presumed to function via the synergistic interaction between H 2 S and NO. Conclusion: We conclude that H 2 S affects [Ca 2+ ] i homeostasis that is mediated by H 2 S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-G q -protein-PLC-IP 3 pathway to induce Ca 2+ release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca 2+ homeostasis. Antioxid. Redox Signal. 20, 747-758.

The use of natural plant extracts in poultry feed could improve their productivity as well as the oxidative stability of stored derived meat. The roles of cornelian cherry extract (CCE) in growth, cecal microbes, and meat antioxidative markers of broiler chickens were evaluated. A total of 500 Ross 308 broiler chicks were fed diets supplemented with CCE (0, 50, 100, 200, 400 mg/kg of diet) for 38 days. The highest levels of weight gain and feed utilization were observed in a group fed 200 mg/kg of CCE. Maximum upregulation of glucose transporters—1 and 2 and sodium-dependent glucose transporter genes—were found in the group fed 200 mg/kg of CCE. Lactobacilli and Bifidobacterium colonization increased as the CCE levels increased. The greatest upregulation of antioxidant genes (glutathione peroxidase, catalase, and superoxide dismutase) in breast meat was observed in groups fed CCE (200 and 400 mg/kg). Dietary CCE significantly delayed the lipid oxidation of breast meat compared with that of the control group. The total phenolic content, 2,2-Diphenyl-1-Picrihydrzyl (DPPH) radical scavenging activity and reducing power in meat improved with higher levels of CCE. Dietary CCE improved the growth, performance of broilers, and meat antioxidant stability after 90 days of storage.

Carbon monoxide (CO) is known as an essential gaseous messenger that regulates a wide array of physiological and pathological processes, similar to nitric oxide (NO) and hydrogen sulfide. The aim of the present study was to elucidate the potential role of CO in Ca(2+) homeostasis and to explore the underlying mechanisms in pancreatic acinar cells. The exogenous application of a CO-releasing molecule dose-dependently increased intracellular Ca(2+) concentration ([Ca(2+)]i). A heme oxygenase (HO) inducer increased [Ca(2+)]i in a concentration-dependent manner, and the increase was diminished by an HO inhibitor. The CO-induced [Ca(2+)]i increase persisted in the absence of extracellular Ca(2+), indicating that Ca(2+) release is the initial source for the increase. The inhibition of G protein, phospholipase C (PLC), and inositol 1,4,5-trisphosphate (IP3) receptor diminished the CO-induced [Ca(2+)]i increase. CO upregulated endothelial nitric oxide synthase (eNOS) expression and stimulated NO production, and NOS inhibitor, calmodulin inhibitor, or the absence of extracellular Ca(2+) eliminated the latter response. Blocking the phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) pathway abolished CO-induced NO production. Pretreatment with an NOS inhibitor, NO scavenger, or soluble guanylate cyclase inhibitor, did not affect the CO-induced [Ca(2+)]i increase, indicating that NO, soluble guanylate cyclase, and cyclic guanosine 5'-monophosphate are not involved in the CO-induced [Ca(2+)]i increase. CO inhibited the secretory responses to CCK-octapeptide or carbachol. We conclude that CO acts as a regulator not only for [Ca(2+)]i homeostasis via a PLC-IP3-IP3 receptor cascade but also for NO production via the calmodulin and PI3K-Akt/PKB pathway, and both CO and NO interact. Moreover, CO may provide potential therapy to ameliorate acute pancreatitis by inhibiting amylase secretion.

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This study investigated the influence of circadian misalignment on the male reproductive system. Adult Sprague-Dawley male rats were exposed to prolonged light (20 h light : 4 h dark) or prolonged darkness (4 h light : 20 h dark) for 12 consecutive weeks. The somatic index of seminal vesicles and prostates increased due to prolonged light exposure. Sperm count and motility were enhanced solely by prolonged light exposure, whereas the percentage of sperm abnormalities was reduced by both prolonged light and darkness. The serum levels of reproductive hormones (follicle-stimulating hormone, luteinizing hormone, testosterone, and prolactin) were elevated, and the estradiol level was reduced by long-term light and dark exposure. Testicular total antioxidant capacity and antioxidant enzyme activities were improved, and lipid peroxidation was inhibited following chronic exposure to light or dark. Chronic light exposure increased, but chronic darkness decreased, testicular nitric oxide production. The mRNA expression of the hypothalamic and testicular clock genes including PER1-2, CRY1-2, BMAL1, CLOCK, and Rev-Erbα was altered by circadian disruption. Prolonged light exposure decreased the levels of thyroid hormones and suppressed the mRNA expression of adiponectin receptors 1 and 2. The immunohistochemical expression of proliferating cell nuclear antigen was decreased only by chronic darkness. The present study thus provides new insights into the physiological changes associated with long-term exposure to light or darkness, in which the expression levels of various clock gene mRNAs are modulated, reproductive hormones are increased, and the antioxidant enzyme system is ameliorated as mechanisms of adaptation to chronic circadian disruption.