Anabolic effects of cheddar cheese consumption in human skeletal muscle
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE163279 | GEO | 2021/01/31
REPOSITORIES: GEO
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Project description:With the aim of investigating the genome-wide postprandial effects of single servings ingestion of milk and yogurt on gene expression in the blood cells of human subjects and to identify the downstream physiological processes regulated by the differentially expressed genes we conducted a randomized, controlled, single blinded, crossover study on 6 healthy male individuals. 540g of milk or yogurt was ingested after an overnight fasting. Blood samples were collected before (0h) and 2h, 4h, 6h after the ingestion and the blood cell transcriptome was analyzed using a linear kinetic analysis.
2010-10-01 | E-MEXP-2571 | biostudies-arrayexpress
Project description:Anabolic effects of cheddar cheese consumption in human skeletal muscle
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2011-11-21 | E-GEOD-27285 | biostudies-arrayexpress
Project description:L. helveticus is used to modulate cheese flavor and as a starter organism in certain cheese varieties. Our group has compiled a draft (4x) sequence for the 2.4 Mb genome of an industrial strain L. helveticus CNRZ32. The primary aim was to investigate expression of 168 completely sequenced genes during growth in milk and MRS medium using microarrays. Oligonucleotide probes against each of the completely sequenced genes were compiled on maskless photolithography-based DNA microarrays. Additionally, the entire draft genome sequence was used to produce tiled microarrays where the non-interrupted sequence contigs were covered by consecutive 24-mer probes. Keywords: growth conditions response
2007-02-14 | GSE7005 | GEO
Project description:mTORC1 (mechanistic target of rapamycin complex 1) is a metabolic sensor that promotes growth when nutrients are abundant. Ubiquitous inhibition of mTORC1 extends lifespan in multiple organisms but also disrupts several anabolic processes resulting in stunted growth, slowed development, reduced fertility, and disrupted metabolism. However, it is unclear if these pleotropic effects of mTORC1 inhibition can be uncoupled from longevity. Here, we utilize the auxin-inducible degradation (AID) system to restrict mTORC1 inhibition to C. elegans neurons. We find that neuron-specific degradation of RAGA-1, an upstream activator of mTORC1, or LET-363, the ortholog of mammalian mTOR, is sufficient to extend lifespan in C. elegans. Unlike raga-1 loss of function genetic mutations or somatic AID of RAGA-1, neuronal AID of RAGA-1 robustly extends lifespan without impairing body size, developmental rate, brood size or neuronal function. Moreover, while somatic degradation of RAGA-1 alters the expression of thousands of genes, demonstrating the widespread effects of mTORC1 inhibition, neuronal degradation of RAGA-1 only results in around 200 differentially expressed genes with a specific enrichment in metabolism and stress response. Notably, our work demonstrates that targeting mTORC1 specifically in the nervous system in C. elegans uncouples longevity from growth and reproductive impairments, and that many canonical effects of low mTORC1 activity are not required to promote healthy aging. These data challenge previously held ideas about the mechanisms of mTORC1 lifespan extension and underscore the potential of promoting longevity by neuron-specific mTORC1 modulation.
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Project description:All living cells require a minimal iron threshold to sustain anabolic metabolism. However, the mechanisms by which cells sense iron to regulate anabolic processes are unclear. Here, we report a universal eukaryotic pathway for iron sensing in which molecular iron is required to sustain active histone demethylation and maintain the expression of critical components of the pro-anabolic mTORC1 pathway. Specifically, we identify the iron-binding histone-demethylase KDM3B as an intrinsic iron sensor that regulates mTORC1 activity by demethylating H3K9me2 at enhancers of genes encoding high-affinity leucine transporters and RAPTOR. By directly suppressing leucine availability and RAPTOR levels, iron deficiency (ID) supersedes other nutrient inputs into mTORC1. This process occurs in vivo, and is not an indirect effect by canonical iron-utilizing pathways. Elevated expression of KDM3B targets is associated with reduced survival in a subset of human cancers and ID represses mTORC1 in patient-derived tumor cells and sensitizes cancer cells to chemotherapy. These data demonstrate a novel mechanism of eukaryotic iron sensing through dynamic chromatin remodeling and repression of mTORC1 mediated anabolism. Due to ancestral eukaryotes sharing homologues of KDMs and mTORC1 core components, this pathway likely predated the emergence of the other kingdom-specific nutrient sensors for mTORC1
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Project description:Background : Although the chemical, physical, and nutritional properties of bovine milk have been extensively studied, few studies have attempted to characterize the milk synthesizing genes associated with milk yielding traits. In addition, no previous attempts have been made to detect quantitative traits such as milk production related traits, associated genes on RNA-seq experiment with several biological replicates. Research in this field is necessary as bovine milk is a primary source of nutrition for humans. Results : We investigated advantages of using linear models with continuous response variables over converted group variables in a Holsteins’ milk. Suggested methods were more suitable in detection of significant genes in our analysis; the proportion of false discoveries to total significant genes was observed to be much lower compared to the precedent approaches we employed. These were observed through mock comparison studies and quantitative real time PCR (qRT-PCR). Conclusion : Several milk production related genes and pathways were identified from the suggested methods. Given the current trend in RNA-seq pricing, we expect our methods to be successfully applied in various RNA-seq studies with numerous biological replicates that handle continuous response traits.
2016-04-23 | GSE60575 | GEO
Project description:This is the first metaproteomics-based featuring of the microbial community harbured in the traditional raw milk Caprino Nicastrese cheese
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Project description:All living cells require a minimal iron threshold to sustain anabolic metabolism. However, the mechanisms by which cells sense iron to regulate anabolic processes are unclear. Here, we report a universal eukaryotic pathway for iron sensing in which molecular iron is required to sustain active histone demethylation and maintain the expression of critical components of the pro-anabolic mTORC1 pathway. Specifically, we identify the iron-binding histone-demethylase KDM3B as an intrinsic iron sensor that regulates mTORC1 activity by demethylating H3K9me2 at enhancers of a high-affinity leucine transporter and RAPTOR. By directly suppressing leucine availability and RAPTOR levels, iron deficiency (ID) supersedes other nutrient inputs into mTORC1. This process occurs in vivo, and is not an indirect effect by canonical iron-utilizing pathways. These data demonstrate a novel mechanism of eukaryotic iron sensing through dynamic chromatin remodeling and repression of mTORC1 mediated anabolism. Due to ancestral eukaryotes sharing homologues of KDMs and mTORC1 core components, this pathway likely predated the emergence of the other kingdom-specific nutrient sensors for mTORC1.
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2022-12-11 | E-MTAB-11581 | biostudies-arrayexpress