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Gpcpd1-GPC metabolic pathway is dysfunctional in aging and its deficiency severely perturbs glucose metabolism

ABSTRACT: Gpcpd1-GPC metabolic pathway is dysfunctional in aging and its deficiency severely perturbs glucose metabolism

PROVIDER: PRJNA1027761 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26377423.fastq.gz	Fastqsanger.gz
	SRR26377424.fastq.gz	Fastqsanger.gz
	SRR26377425.fastq.gz	Fastqsanger.gz
	SRR26377426.fastq.gz	Fastqsanger.gz
	SRR26377427.fastq.gz	Fastqsanger.gz

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Gpcpd1-GPC metabolic pathway is dysfunctional in aging and its deficiency severely perturbs glucose metabolism

Project description:Skeletal muscle plays a central role in the regulation of systemic metabolism during lifespan. With aging, muscle mediated metabolic homeostasis is perturbed, contributing to the onset of multiple chronic diseases. Our knowledge on the mechanisms responsible for this age-related perturbation is limited, as it is difficult to distinguish between correlation and causality of molecular changes in muscle aging. Glycerophosphocholine phosphodiesterase 1 (GPCPD1) is a highly abundant muscle enzyme responsible for the hydrolysis of the lipid glycerophosphocholine (GPC). The physiological function of GPCPD1 remained largely unknown. Here, we report that the GPCPD1-GPC metabolic pathway is dramatically perturbed in the aged muscle. Muscle-specific inactivation of Gpcpd1 resulted in severely affected glucose metabolism, without affecting muscle development. This pathology was muscle specific and did not occur in white fat-, brown fat- and liver-deficient Gpcpd1 deficient mice. Moreover, in the muscle specific mutant mice, glucose intolerance was markedly accelerated under high sugar and high fat diet. Mechanistically, Gpcpd1 deficiency results in accumulation of GPC, without any other significant changes in the global lipidome. This causes an “aged-like” transcriptomic signature in young Gpcpd1 deficient muscles and impaired insulin signaling. Finally, we report that GPC levels are markedly perturbed in muscles from both aged humans and patients with Type 2 diabetes, with a high correlation between GPC levels and increased chronological age. Our findings show the novel and critical physiological function of GPCPD1-GPC metabolic pathway to glucose metabolism, and the perturbation of this pathway with aging, which may contribute to glucose intolerance in aging.

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Project description:CD14+ purified bovine monoctye stimulation with CpG ODN 2007 vs. GpC ODN 2007, CpG 2007 vs. Control, GpC 2007 vs. Control and Media vs Control (Control is unstimluated CD14+ purified bovine monocytes at time zero). Before stimulation, the CD14+ purified bovine monocytes were rested for 20 h. Then the cells were stimulated for 4hrs.

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Project description:When GPC transcription factor in hexaploid wheat is down-regulated by stable RNA interference (GPC RNAi), senescence is significantly delayed and grain protein content together with the overall nutrient partitioning to the grain is greatly reduced. mRNA-seq was used to catalogue the genes that are regulated by the GPC transcription factor during monocarpic senescence. cDNA was prepared from wild type bread wheat plants and GPC RNAi plants 12 days after anthesis and sequenced by Illumina. Four biological replications per genotypes were sequenced. To determine gene expression levels, reads were aligned to a reference transcriptome generated by assemblying 454-reads obtained from the same biological material (454 assembled sequences: TSA project 59945 - accession numbers: HP608076-HP639668).

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