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From broiler breeder hen feed to the egg and embryo: The molecular effects of guanidinoacetate supplementation on creatine transport and synthesis.

ABSTRACT: Supplementation of broiler breeder hens with beneficial additives bears great potential for affecting nutrient deposition into the fertile egg. Guanidinoacetate (GAA) is the endogenous precursor of creatine that is used as a feed additive for improving cellular energy metabolism in animal nutrition. In the present study, we have investigated whether GAA supplementation in broiler breeder feed affects creatine deposition into the hatching egg and molecular mechanisms of creatine transport and synthesis within hens and their progeny. For this, broiler breeder hens of 47 wk of age were supplemented with 0.15% GAA for 15 wk, and samples from their tissues, hatching eggs and progeny were compared with those of control, nonsupplemented hens. A significant increase in creatine content was found within the yolk and albumen of hatching eggs obtained from the GAA group, compared with the control group. The GAA group exhibited a significant increased creatine transporter gene expression compared with the control group in their small intestines and oviduct. In GAA group progeny, a significant decrease in creatine transporter expression at embryonic day 19 and day of hatch was found, compared with control group progeny. At the day of hatch, creatine synthesis genes (arginine glycine amidinotransferase and guanidinoacetate N-methyltransferase) exhibited significant decrease in expression in the GAA group progeny compared with control group progeny. These results indicate that GAA supplementation in broiler breeder feed increases its absorbance and deposition into hatching eggs, subsequently affecting GAA and creatine absorbance and synthesis within broiler progeny.

SUBMITTER: Reicher N

PROVIDER: S-EPMC7597819 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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From broiler breeder hen feed to the egg and embryo: The molecular effects of guanidinoacetate supplementation on creatine transport and synthesis.

Reicher Naama N Epstein Tomer T Gravitz Dor D Cahaner Avigdor A Rademacher Meike M Braun Ulrike U Uni Zehava Z

Poultry science 20200425 7

Supplementation of broiler breeder hens with beneficial additives bears great potential for affecting nutrient deposition into the fertile egg. Guanidinoacetate (GAA) is the endogenous precursor of creatine that is used as a feed additive for improving cellular energy metabolism in animal nutrition. In the present study, we have investigated whether GAA supplementation in broiler breeder feed affects creatine deposition into the hatching egg and molecular mechanisms of creatine transport and syn ...[more]

PMID: 32616254

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Project description:BackgroundGuanidinoacetate (GAA) induces epileptogenesis and neurotoxicity in the brain. As epileptic animal models have been reported to show elevated cerebral GAA levels, the processing mechanism of GAA in the brain is important for maintaining brain homeostasis. We have revealed that GAA in the cerebrospinal fluid (CSF) is removed by incorporation into the choroid plexus epithelial cells (CPxEpic), which form the blood-CSF barrier (BCSFB). However, the processing mechanism of GAA incorporated into CPxEpic remains unknown. We have reported that monocarboxylate transporter 12 (MCT12) functions as an efflux transporter of GAA and creatine, a metabolite of GAA, in the kidneys and liver. Therefore, we aimed to clarify the role of MCT12 in GAA dynamics in CPxEpic.MethodsProtein expression and localization in CPxEpic were evaluated using immunohistochemistry. Metabolic analysis was performed using high-performance liquid chromatography (HPLC) 24 h after the addition of [14C]GAA to TR-CSFB3 cells, which are conditionally immortalized rat CPxEpic. The efflux transport of [14C]creatine was evaluated in TR-CSFB3 cells after transfection with MCT12 small interfering RNA (siRNA). The CSF-to-brain parenchyma transfer of creatine was measured after intracerebroventricular injection in rats.ResultsImmunohistochemical staining revealed that MCT12-derived signals merged with those of the marker protein at the apical membrane of CPxEpic, suggesting that MCT12 is localized on the apical membrane of CPxEpic. The expression levels of guanidinoacetate N-methyltransferase (GAMT), which catalyzes the conversion of GAA to creatine, in TR-CSFB3 cells was also indicated, and GAA was considered to be metabolized to creatine after influx transport into CPxEpic, after which creatine was released into the CSF. Creatine release from TR-CSFB3 cells decreased following MCT12 knockdown. The contribution ratio of MCT12 to the release of creatine was more than 50%. The clearance of CSF-to-brain parenchyma transfer of creatine was 4.65 µL/(min·g brain), suggesting that biosynthesized creatine in CPxEpic is released into the CSF and supplied to the brain parenchyma.ConclusionsIn CPxEpic, GAA is metabolized to creatine via GAMT. Biosynthesized creatine is then released into the CSF via MCT12 and supplied to the brain parenchyma.

Project description:The feed restriction applied during rearing of broiler breeders inflicts chronic hunger, and frustration due to unfulfilled behavioural needs for feeding. To alleviate the welfare problems associated with feed restriction, qualitative feed restriction allows a larger amount of feed to be provided without increasing the energy intake. In the present study, the aim was to investigate the effect of scatter-fed qualitative feed restriction on a range of welfare indicators in broiler breeders at the end of the rearing period. In total, 1,200 female breeder chicks of the genotype Ross 308 were housed in 24 pens: six pens of initially 50 birds per dietary treatment. The treatments were: (1) standard feed (Control), (2) standard feed diluted with oat hulls (Insoluble), (3) standard feed diluted with oat hulls and sugar beet pulp (Mixed), and (4) standard feed plus maize silage (Roughage). At 15 weeks of age, a blood sample was taken from 40 birds (10/treatment) five times within 24 h. The plasma was analysed for corticosterone concentration. At 19 weeks of age, a clinical welfare assessment was performed on all birds before they were sacrificed. From each bird, three feathers were plucked and macroscopically examined for the presence of fault bars. Feather length and weight were also recorded. Mortality was registered on occurrence throughout the rearing period. Treatment affected the plumage condition, footpad dermatitis, plumage dirtiness, vent pasting, and number of severe fault bars (P ? 0.05) but not plasma corticosterone concentration, hock burns, hyperkeratosis and mortality (P ? 0.17). There was an effect of the interactions between treatment and feather type on the total number of fault bars per feather, average position of the fault bars relative to the base of the feather, and growth rates of feather mass and length (P < 0.0001). Overall, the results showed improved welfare of Roughage birds and reduced welfare of Mixed birds, whereas the welfare of Insoluble birds did not seem to differ noticeably from that of Control birds. We recommend to further develop a feeding strategy that includes daily allocation of roughage to broiler breeders during the rearing period.

Project description:BackgroundCreatine synthesis from guanidinoacetate consumes ~50% of s-adenosylmethionine (SAM)-derived methyl groups, accounting for an equivalent proportion of s-adenosylhomocysteine (SAH) and total homocysteine (tHcys) synthesis. Dietary creatine inhibits the synthesis of guanidinoacetate, thereby lowering plasma tHcys in rats.ObjectiveWe tested the hypotheses that creatine supplementation lowers plasma guanidinoacetate, increases blood SAM, lowers blood SAH, and lowers plasma tHcys.MethodsBangladeshi adults were randomly assigned to receive 1 of 4 treatments for 12 wk: placebo (n = 101), 3 g/d creatine (Cr; n = 101), 400 μg/d folic acid (FA; n = 153), or 3 g/d creatine plus 400 μg/d folic acid (Cr+FA; n = 103). The outcomes of plasma guanidinoacetate and tHcys, as well as whole blood SAM and SAH, were analyzed at baseline and week 12 by HPLC. Treatment effects of creatine supplementation were examined with the use of the group comparisons of Cr vs. placebo and Cr+FA vs. FA.ResultsPlasma guanidinoacetate declined by 10.6% (95% CI: 4.9, 15.9) in the Cr group while increasing nonsignificantly in the placebo group (3.7%; 95% CI: -0.8, 8.5) (Pgroup difference = 0.0002). Similarly, plasma guanidinoacetate declined by 9.0% (95% CI: 3.4, 14.2) in the Cr+FA group while increasing in the FA group (7.0%; 95% CI: 2.0, 12.2) (Pgroup difference < 0.0001). Plasma tHcys declined by 23.4% (95% CI: 19.5, 27.1) and 21.0% (95% CI: 16.4, 25.2) in the FA and Cr+FA groups, respectively (Pgroup difference = 0.41), with no significant changes in the placebo or Cr groups (Pgroup difference = 0.35). A decrease in guanidinoacetate over time was associated with a decrease in tHcys over time in the Cr+FA group (β = 0.30; 95% CI: 0.17, 0.43; P < 0.0001).ConclusionsOur findings indicate that whereas creatine supplementation downregulates endogenous creatine synthesis, this may not on average lower plasma tHcys in humans. However, tHcys did decrease in those participants who experienced a decline in plasma guanidinoacetate while receiving creatine plus folic acid supplementation. This trial was registered at clinicaltrials.gov as NCT01050556.

Project description:A supplement of 69 ?g 25-hydroxycholecalciferol (25-OH-D3)/kg feed increased livability in feed restricted (R-hens) broiler breeder hens by 9.9% and by 65.6% in hens allowed ad libitum feed intake (Ad-hens) in a feeding trial from age 26-60 weeks. Hens with higher bodyweight and/or adiposity suffered sudden death (SD) earlier in conjunction with compromised heart rhythms and over-ventilation. In the study with the same flock of hens, we demonstrate that 25-OH-D3 improved hen's livability and heart health by ameliorating systemic hypoxia, acidosis, and cardiac pathological hypertrophy through calcineurin-NFAT4c signaling and MHC- expression in association with reduced plasma triacylglycerol and hepatic steatosis and fibrosis (p < 0.05). In contrast to live hens sampled at 29, 35, and 47 weeks, SD hens exhibited severe cardiac hypertrophy that was either progressive (Ad-groups) or stable (R-groups). Actual and relative liver weights in SD hens from any group declined as the study progressed. Heart weight correlated significantly to total and relative liver weights in SD-hens of both R- and Ad-groups. In contrast to normal counterparts sampled at 35 and 47 weeks, R-hens exhibiting cardiac hypertrophy experienced severe hypoxia and acidosis, with increased bodyweight, absolute and relative weights of liver and heart, hepatic and plasma triacylglycerol content, and cardiac arrhythmia (p < 0.05). The present results demonstrate that pathological cardiac hypertrophy and functional failure are causative factors of SD and this pathogenic progression is accelerated by hepatopathology, particularly during the early age. Increased feed efficiency with rapid gains in BW and fat increase hens' risk for hypoxia, irreversible cardiac hypertrophy, and arrhythmias that cause functional compromise and SD. Additional supplementation of 69 mg/kg feed of 25-OH-D3 to the basal diet is effective to ameliorate cardiac pathogenesis and prevent SD in broiler breeder hens.

Project description:Trace mineral minerals Zn, Cu, and Mn play important roles in breeder production and progeny performance. The objective of this study was to determine maternal supplementation of trace mineral minerals on breeder production and progeny growth and development. A total of 540 broiler breeders, Cobb 500 (Slow feathering; 0-66 weeks old) were assigned to one of three treatment groups with the same basal diet and three different supplemental trace minerals: ITM-inorganic trace minerals in sulfates: 100, 16, and 100 ppm of Zn, Cu, and Mn respectively; MMHAC -mineral methionine hydroxy analog chelate: 50, 8, and 50 ppm of bis-chelated MINTREX®Zn, Cu and Mn (Novus International, Inc.), and TMAAC - trace minerals amino acid complex: 50, 8, and 50 ppm of Zn, Cu, and Mn. At 28 weeks of age, eggs from breeder treatments were hatched for progeny trial, 10 pens with 6 males and 6 female birds per pen were fed a common diet with ITM for 45 days. Breeder production, egg quality, progeny growth performance, mRNA expression of gut health associated genes in breeder and progeny chicks were measured. Data were analyzed by one-way ANOVA; means were separated by Fisher's protected LSD test. A p-Value ≤ 0.05 was considered statistically different and 0.1 was considered numerical trend. Breeders on ITM treatment had higher (p < 0.05) body weight (BW), weight gain and lower (p < 0.05) feed conversion ratio (FCR) from 0 to 10 weeks, when compared to birds fed MMHAC. MMHAC significantly improved egg mass by 3 g (p < 0.05) and FCR by 34 points (0.05 < p < 0.1) throughout the reproductive period (26-66 weeks) in comparison to ITM. MMHAC improved (p < 0.01) egg yolk color versus (vs.) ITM and TMAAC in all periods, except 28 weeks, increased (p < 0.01) eggshell thickness and resistance vs. TMAAC at 58 weeks, and reduced (p < 0.05) jejunal NF-κB gene expression vs. TMAAC at 24 weeks. There was a significant reduction in tibial dry matter weight, Seedor index and resistance for the breeders that received MMHAC and/or TMAAC when compared to ITM at 18 weeks. Lower seedor index but numerically wider tibial circumference was seen in hens fed MMHAC at 24 weeks, and wider tibial circumference but lower tibial resistance in hens fed TMAAC at 66 weeks. Maternal supplementation of MMHAC in breeder hens increased (p < 0.0001) BW vs. ITM and TMAAC at hatching, reduced (p < 0.05) feed intake vs. ITM at d14 and d28, and improved (p < 0.01) FCR and performance index vs. TMAAC at d28, reduced (p < 0.01) NF-κB gene expression and increased (p < 0.05) A20 gene expression vs. TMAAC on d0 and vs. ITM on d14, reduced (p < 0.05) TLR2 gene expression vs. ITM on d0 and vs. TMAAC on d14, increased (p < 0.05) MUC2 gene expression vs. both ITM and TMAAC on d45 in progeny jejunum. Overall, these results suggest that supplementation with lower levels of MHA-chelated trace minerals improved breeder production and egg quality and reduced breeder jejunal inflammation while maintaining tibial development in comparison to those receiving higher inorganic mineral supplementation, and it also carried over the benefits to progeny with better growth performance, less jejunal inflammation and better innate immune response and gut barrier function in comparison to ITM and/or TMAAC.

Dataset Information

From broiler breeder hen feed to the egg and embryo: The molecular effects of guanidinoacetate supplementation on creatine transport and synthesis.

Publications

From broiler breeder hen feed to the egg and embryo: The molecular effects of guanidinoacetate supplementation on creatine transport and synthesis.

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