RNA Profiles of the Korat Chicken Breast Muscle with Increased Carnosine Content Produced through Dietary Supplementation with β-Alanine or L-Histidine
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ABSTRACT:
PROVIDER: PRJNA744469 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15058846_1.fastq.gz | Fastqsanger.gz | |||
| SRR15058846_2.fastq.gz | Fastqsanger.gz | |||
| SRR15058847_1.fastq.gz | Fastqsanger.gz | |||
| SRR15058847_2.fastq.gz | Fastqsanger.gz | |||
| SRR15058848_1.fastq.gz | Fastqsanger.gz |
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Project description:Carnosine is a bioactive food component with several potential health benefits for humans due to its physiological functions. Dietary supplementation with β-alanine or L-histidine can increase the carnosine content of skeletal muscles in chickens. Dietary supplementation with β-alanine or L-histidine has produced a slow-growing chicken variety with high carnosine content in the breast meat; however, the supplementation with L-histidine alone softens the meat toughness, which may affect consumers’ willingness to buy the meat. Gene expression is a key factor that influences meat quality. Understanding the molecular mechanisms that affect carnosine content and meat toughness would allow the production of more value-added slow-growing chickens. We compared global gene expression in chicken breast muscles with differing carnosine contents and meat toughness produced through dietary supplementation with β-alanine or L-histidine. We identified differentially expressed genes involved in regulating myosin, collagen, intramuscular fat, and calpain—factors that may affect meat tenderness. Pathway enrichment analysis indicated that the insulin-related and adipocytokine signaling pathways were altered by dietary supplementation with β-alanine or L-histidine. These data will be useful for future studies on carnosine content and meat toughness in slow-growing chickens.
2021-09-04 | GSE179643 | GEO
Project description:Korat chicken (KRC) is a slow-growing chicken bred in Thailand, whose meat exhibits a unique toughness. A previous study produced KRC breast meat containing high carnosine content through dietary supplementation with β-alanine or L-histidine; however, the KRC that were fed an L-histidine-supplemented diet produced meat that was significantly more tender. Herein, we performed RNA-Seq to identify candidate genes involved in the regulation of carnosine content and meat toughness. Total RNA was isolated from five female KRC breast muscles in each treatment group that KRC fed diets without supplementation, supplemented with β-alanine or L-histidine. Compared to the non-supplemented group, we identified 118 and 198 differentially expressed genes (DEGs) in the β-alanine or L-histidine supplementation groups, respectively. Genes potentially related to meat tenderness-i.e., those regulating myosin, collagen, intramuscular fat, and calpain-were upregulated (LOC107051274, ACSBG1, and CAPNS2) and downregulated (MYO7B, MYBPH, SERPINH1, and PGAM1). However, carnosine synthase gene was not identified. Functional enrichment analysis identified pathways affected by dietary supplementation, including the insulin signaling pathway (β-alanine supplementation) and the insulin resistance and adipocytokine signaling pathways (L-histidine supplementation). The FoxO signaling pathway was identified as a regulatory network for both supplementation groups. The identified genes can be used as molecular markers of meat tenderness in slow-growing chickens.
| S-EPMC8464878 | biostudies-literature
Project description:Carnosine is an endogenous β-alanyl-L-histidine dipeptide endowed of antioxidant and carbonyl scavenger properties, able to significantly prevent the visible signs of aging and photoaging. To deeply investigate the mechanism of action of carnosine on human skin proteome, a 3D scaf-fold-free spheroids model of primary dermal fibroblasts from 50-years-old donor, was here adopted in combination with quantitative proteomics
2022-02-22 | PXD031053 | Pride
Project description:To reveal the effects of carnosine on Caco-2 cells, we have employed whole genome microarray to detect genes that showed significantly different expression when exposed to carnosine. Caco-2 cells were treated with 1 mM carnosine for 3 days. Caco-2 cells were treated with 1 mM carnosine for 3 days. Three independent experiments were performed.
2015-03-31 | E-GEOD-61455 | biostudies-arrayexpress
Project description:To reveal the effects of carnosine on Caco-2 cells, we have employed whole genome microarray to detect genes that showed significantly different expression when exposed to carnosine. Caco-2 cells were treated with 1 mM carnosine for 3 days.
2015-03-31 | GSE61455 | GEO
Project description:A histidine prototrophic strain achieves A600 three-four fold higher than a histidine auxotroph when cultured in nutrient rich media YPA, which is abundant in amino acids. This retaded growth of histidine auxotroph in YPA can also be rescued by supplementing media with exogenous histidine. Here, we aim to study the transcriptomic changes associated with culturing of histidine auxotroph and prototroph in YPA and also the effects of histidine addition to the culture medium of histidine auxotroph.
2022-04-06 | GSE174633 | GEO
Project description:Mitochondrial dysfunction plays a central role in the pathogenesis of neurodegenerative diseases such as Parkinson’s disease (PD). This study tested the hypothesis that the dipeptide carnosine would exert a beneficial effect in the Thy1-aSyn mouse model of PD, which displays mitochondrial dysfunction. Mitochondrial function and gene expression were evaluated in the midbrain after two months of carnosine administration by intranasal (IN) or drinking water routes of exposure. IN carnosine attenuated transcriptional changes in the midbrain in Thy1-aSyn mice. Additionally, IN-carnosine increased expression of mitochondria complexes and enhanced mitochondrial function, suggesting a potential neuroprotective role for IN-carnosine in PD.
2018-12-31 | GSE115769 | GEO
Project description:Oral consumption of histidyl dipeptides such as l-carnosine has been suggested to promote cardiometabolic health, although therapeutic mechanisms remain incompletely understood. We recently reported that oral consumption of a carnosine analog suppressed markers of fibrosis in liver of obese mice, but whether antifibrotic effects of carnosine extend to the heart is not known, nor are the mechanisms by which carnosine is acting. Here, we investigated whether oral carnosine was able to mitigate the adverse cardiac remodeling associated with diet induced obesity in a mouse model of enhanced lipid peroxidation (i.e., glutathione peroxidase 4 deficient mice, GPx4+/−), a model which mimics many of the pathophysiological aspects of metabolic syndrome and T2 diabetes in humans. Wild-type (WT) and GPx4+/− male mice were randomly fed a standard (CNTL) or high fat high sucrose diet (HFHS) for 16 weeks. Seven weeks after starting the diet, a subset of the HFHS mice received carnosine (80 mM) in their drinking water for duration of the study. Carnosine treatment led to a moderate improvement in glycemic control in WT and GPx4+/− mice on HFHS diet, although insulin sensitivity was largely unchanged. Interestingly, while our transcriptomic analysis revealed that carnosine therapy had no significant impact on global gene expression in the heart, carnosine substantially upregulated cardiac GPx4 expression in both WT and GPx4+/− mice on HFHS diet. Carnosine also significantly reduced protein carbonyls and iron levels in myocardial tissue from both genotypes on HFHS diet. Importantly, we observed a robust antifibrotic effect of carnosine therapy in hearts from mice on HFHS diet, which further in vitro experiments suggest is due to carnosine’s ability to suppress collagen-cross-linking. Collectively, this study reveals antifibrotic potential of carnosine in the heart with obesity and illustrates key mechanisms by which it may be acting.
2023-12-19 | GSE250315 | GEO
Project description:PurposeThis study aimed to describe the kinetics of carnosine washout in human skeletal muscle over 16 wk.MethodsCarnosine washout kinetics were studied in 15 young, physically active omnivorous men randomly assigned to take 6.4 g·d-1 of β-alanine (n = 11) or placebo (n = 4) for 8 wk. Muscle carnosine content (M-Carn) was determined before (PRE), immediately after (POST), and 4, 8, 12, and 16 wk after supplementation. High-intensity exercise tests were performed at these same time points. Linear and exponential models were fitted to the washout data, and the leave-one-out method was used to select the model with the best fit for M-Carn decay data. Repeated-measures correlation analysis was used to assess the association between changes in M-Carn and changes in performance.ResultsM-Carn increased from PRE to POST in the β-alanine group only (+91.1% ± 29.1%; placebo, +0.04% ± 10.1%; P < 0.0001). M-Carn started to decrease after cessation of β-alanine supplementation and continued to decrease until week 16 (POST4, +59% ± 40%; POST8, +35% ± 39%; POST12, +18% ± 32%; POST16, -3% ± 24% of PRE M-Carn). From week 12 onward, M-Carn was no longer statistically different from PRE. Both linear and exponential models displayed very similar fit and could be used to describe carnosine washout, although the linear model presented a slightly better fit. The decay in M-Carn was mirrored by a similar decay in high-intensity exercise tolerance; M-Carn was moderately and significantly correlated with total mechanical work done (r = 0.505; P = 0.032) and time to exhaustion (r = 0.72; P < 0.001).ConclusionsCarnosine washout takes 12-16 wk to complete, and it can be described either by linear or exponential curves. Changes in M-Carn seem to be mirrored by changes in high-intensity exercise tolerance. This information can be used to optimize β-alanine supplementation strategies.
| S-EPMC8048732 | biostudies-literature