Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integrated in vivo quantitative proteomics and nutrient tracing reveals age-related metabolic rewiring of pancreatic beta-cell function

ABSTRACT: Integrated in vivo quantitative proteomics and nutrient tracing reveals age-related metabolic rewiring of pancreatic beta-cell function

PROVIDER: PRJNA413145 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6130330.fastq.gz	Fastqsanger.gz
	SRR6130331.fastq.gz	Fastqsanger.gz
	SRR6130332.fastq.gz	Fastqsanger.gz
	SRR6130327.fastq.gz	Fastqsanger.gz
	SRR6130328.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Integrated in vivo quantitative proteomics and nutrient tracing reveals age-related metabolic rewiring of pancreatic beta-cell function

Project description:Aging is associated with fundamental changes in pancreatic β-cell physiology; yet, the mechanisms that drive these age-related changes are poorly understood. We performed comprehensive proteomic profiling of pancreatic islets from adolescent and old mice. The analysis revealed striking differences in abundance of enzymes controlling glucose metabolism not reflected at the transcript level. We show that these changes in protein abundance are associated with increased activity of the amplifying pathway of insulin secretion. The amplifying pathway stimulates insulin secretion through coupling factors produced during glucose metabolism. Nutrient tracing and targeted metabolomics demonstrate accelerated accumulation of glucose-derived metabolites and coupling factors in aged islets, indicating that age-related changes in glucose metabolism contribute to the improved response of β-cells to glucose with age. Together, our study provides the first in-depth characterization of changes in the islet proteome during aging and establishes metabolic rewiring as an important mechanism for age-associated changes in β-cell function.

2018-12-03 | GSE104591 | GEO

Integrated in vivo quantitative proteomics and nutrient tracing reveals age-related metabolic rewiring of pancreatic B-cell function

Project description:Aging is associated with fundamental changes in pancreatic B-cell physiology; yet, the mechanisms that drive these age-related changes are poorly understood. We performed comprehensive proteomic profiling of pancreatic islets from adolescent and old mice. The analysis revealed striking differences in abundance of enzymes controlling glucose metabolism not reflected at the transcript level. We show that these changes in protein abundance are associated with increased activity of the amplifying pathway of insulin secretion. The amplifying pathway stimulates insulin secretion through coupling factors produced during glucose metabolism. Nutrient tracing and targeted metabolomics demonstrate accelerated accumulation of glucose-derived metabolites and coupling factors in aged islets, indicating that age-related changes in glucose metabolism contribute to the improved response of B-cells to glucose with age. Together, our study provides the first in-depth characterization of changes in the islet proteome during aging and establishes metabolic rewiring as an important mechanism for age-associated changes in B-cell function.

2017-10-03 | MSV000081577 | MassIVE

Integrated In Vivo Quantitative Proteomics and Nutrient Tracing Reveals Age-Related Metabolic Rewiring of Pancreatic β Cell Function.

Project description:Pancreatic β cell physiology changes substantially throughout life, yet the mechanisms that drive these changes are poorly understood. Here, we performed comprehensive in vivo quantitative proteomic profiling of pancreatic islets from juvenile and 1-year-old mice. The analysis revealed striking differences in abundance of enzymes controlling glucose metabolism. We show that these changes in protein abundance are associated with higher activities of glucose metabolic enzymes involved in coupling factor generation as well as increased activity of the coupling factor-dependent amplifying pathway of insulin secretion. Nutrient tracing and targeted metabolomics demonstrated accelerated accumulation of glucose-derived metabolites and coupling factors in islets from 1-year-old mice, indicating that age-related changes in glucose metabolism contribute to improved glucose-stimulated insulin secretion with age. Together, our study provides an in-depth characterization of age-related changes in the islet proteome and establishes metabolic rewiring as an important mechanism for age-associated changes in β cell function.

| S-EPMC6317899 | biostudies-literature

Nutrient Starvation-induced Hda1C Rewiring: coordinated regulation of transcription and translation

Project description:Nutrient Starvation-induced Hda1C Rewiring: coordinated regulation of transcription and translation

| PRJNA1159102 | ENA

Gut bacterial nutrient preferences quantified in vivo

Project description:We quantitatively examine inputs and outputs of the mouse gut microbiome, using isotope tracing. To determine nutrient preferences across bacteria, we traced into genus-specific bacterial protein sequences. By in vivo isotope tracer feeding, mapped the contribution of different dietary nutrients vs circulating nutrients contribution to different gut bacterial genera.

2022-08-17 | PXD031015 | Pride

Nutrient Starvation-induced Hda1C Rewiring: coordinated regulation of transcription and translation

Project description:In yeast, Hda1 histone deacetylase complex (Hda1C) plays an important role in transcriptional regulation by modulating histone acetylation. We here explored the dynamics of Hda1C binding in nutrient-rich and -starved conditions. Chromatin immunoprecipitation sequencing revealed that starvation alters RNA Pol II and Hda1C binding to coding genes in a highly correlated manner. Interestingly, we discovered RNA Pol II transcription-independent recruitment of Hda1C to intergenic regions, particularly the upstream regulatory sequences (URS) of ribosomal protein (RP) genes, which are enriched with Rap1 binding sites. Under nutrient starvation, Rap1 contributes to the recruitment of Hda1C to these URS regions, where Hda1C deacetylates histones, thereby fine-tuning basal gene expression and delaying RP gene reactivation. Furthermore, Hda1C is also required for RNA Pol I transcription of rRNAs and RNA Pol III transcription of tRNA genes, especially in nutrient-limited conditions. Significantly, Hda1C mutants are sensitive to translation inhibitors and display altered ribosome profiles. Thus, Hda1C may coordinate transcriptional regulation within the nucleus with translation control in the cytoplasm and could be a key regulator of gene expression responses to nutrient stress.

2025-04-23 | GSE276792 | GEO

Nutritional Status and Nutrient Supply in Hospitalised Surgical Patients

Project description:Prospective single arm, single center observational study to assess the nutritional status and the nutrient supply during hospitalization for elective gastrointestinal surgery.

| 2293083 | ecrin-mdr-crc

Charting the age-altered thymic epithelial cell differentiation by lineage tracing from a beta 5-t expressing TEC progenitor

Project description:TEC progenitors that express beta 5-t contribute to both the cortical and medullary TEC compartments. Our initial experiments across ageing thymi identified a population of potential progenitor TECs which expanded with age, and appears to be a progenitor population for mTEC. These lineage tracing experiments are designed to chart the altered differentiation and senescence of mTEC progenitors with age.

2020-09-14 | E-MTAB-8737 | biostudies-arrayexpress

Nutrient regulated control of lysosome function by signaling lipid conversion

Project description:Lysosomes serve dual antagonistic functions in cells by mediating anabolic growth signaling and the catabolic turnover of macromolecules. How these janus-faced activities are regulated in response to cellular nutrient status is poorly understood. We show here that lysosome morphology and function are reversibly controlled by a nutrient-regulated signaling lipid switch that triggers the conversion between motile mTOR complex 1 (mTORC1) signaling-active and static mTORC1-inactive degradative lysosomes clustered at the cell center. Starvation-triggered relocalization of phosphatidylinositol 4-phosphate [PI(4)P] metabolizing enzymes reshapes the lysosomal surface proteome to facilitate lysosomal proteolysis and to repress mTORC1-signaling by erasing phosphatidylinositol 3-phosphate [PI(3)P], which marks motile signaling-active lysosomes in the cell periphery. Interference with this PI(3)P/ PI(4)P lipid switch module impairs the adaptive response of cells to altering nutrient supply. Our data unravel a key function for lysosomal phosphoinositide metabolism in rewiring organellar membrane dynamics in response to cellular nutrient status.

2025-02-10 | PXD038428 | Pride

Nutrient-driven dedifferentiation of enteroendocrine cells promotes adaptive intestinal growth

Project description:Post-developmental organ resizing improves organismal fitness under constantly changing nutrient environments. Although stem cell abundance is a fundamental determinant of adaptive resizing, our understanding of its underlying mechanisms remains primarily limited to the regulation of stem cell division. Here, we demonstrate that nutrient fluctuation induces dedifferentiation in the Drosophila adult midgut to drive adaptive intestinal growth. From lineage tracing and single-cell RNA sequencing, we identify a subpopulation of enteroendocrine (EE) cells that convert into functional intestinal stem cells (ISCs) in response to dietary glucose and amino acids by activating the JAK-STAT pathway. Genetic ablation of EE-derived ISCs severely impairs ISC expansion and midgut growth despite the retention of resident ISCs, and in silico modeling further indicates that EE dedifferentiation enables an efficient increase in the midgut cell number while maintaining epithelial cell composition. Our findings identify a physiologically induced dedifferentiation that ensures ISC expansion during adaptive organ growth in concert with nutrient conditions.

2023-08-12 | GSE207662 | GEO