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Proteomics and phosphoproteomics analyses in obesity and type 2 diabetes

ABSTRACT: Proteomics strategies are widely used to examine obesity and type 2 diabetes (T2D). Patients with obesity, with T2D and sex- and age-matched controls were recruited. Proteomics and phosphoproteomics identification and quantitation were performed in serum samples. Statistical analysis along with network analysis was carried out.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Serum

DISEASE(S): Obesity,Type 2 Diabetes Mellitus

SUBMITTER: Erdenetsetseg Nokhoijav

LAB HEAD: Éva Csősz

PROVIDER: PXD058424 | Pride | 2026-01-05

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	DDA_SDRF.sdrf.tsv	Tabular
	Homo_sapiens_sp_canonical_TaxID_9606.fasta	Fasta
	L_U_240229_10xS1_HpH1_05.raw	Raw
	L_U_240229_10xS1_HpH2_06.raw	Raw
	L_U_240229_10xS1_HpH3_07.raw	Raw

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1 - 5 of 83

Publications

Comprehensive Insights into Obesity and Type 2 Diabetes from Protein Network, Canonical Pathway, Phosphorylation and Antimicrobial Peptide Signatures of Human Serum.

Bertalan Petra Magdolna PM Nokhoijav Erdenetsetseg E Pap Ádám Á Neagu George C GC Káplár Miklós M Darula Zsuzsanna Z Kalló Gergő G Prokai Laszlo L Csősz Éva É

Proteomes 20251217 4

<h4>Background</h4>Obesity is a major risk factor for type 2 diabetes (T2D); however, the molecular links between these conditions are not fully understood.<h4>Methods</h4>We performed an integrative serum proteomics study on samples from 134 individuals (healthy controls, patients with obesity and/or T2D) using both data-independent (DIA) and data-dependent (DDA) liquid chromatography-mass spectrometry approaches, complemented by phosphopeptide enrichment, kinase activity prediction, network an ...[more]

PMID: 41441338

Similar Datasets

Proteomics and phosphoproteomics analyses in obesity and type 2 diabetes

Project description:Proteomics strategies are widely used to examine obesity and type 2 diabetes (T2D). Patients with obesity, with T2D and sex- and age-matched controls were recruited. Proteomics and phosphoproteomics identification and quantitation were performed in serum samples. Statistical analysis along with network analysis was carried out.

2026-01-05 | PXD058421 | Pride

Proteomics and phosphoproteomics analyses in obesity and type 2 diabetes

2026-01-05 | PXD058428 | Pride

DNA methylation and gene expression analyses in adipose tissue to identify new loci associated with T2D development in obesity

Project description:Our study seeked to identify changes in DNA methylation and gene expression that might underlie type 2 diabetes susceptibility. We investigated DNA methylation and gene expression in VAT biopsies from 19 women with obesity, without (n=9) or with T2D (n=10). We analyzed and compared the methylome and transcriptome of visceral adipose tissue biopsies of women with obesity, with and without type 2 diabetes. Differential methylation and expression where then paired to test for Pearson's correlation to measure their relationship.

2023-01-01 | E-MTAB-11841 | biostudies-arrayexpress

Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using TALLYHO x C57BL6 F2 mice

Project description:Type 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The TALLYHO/JngJ (TH) mouse is a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia. To determine the genetic factors that contribute to these T2D related characteristics in TH mice, we interbred TH mice with C57BL/6J (B6) mice. The parental, F1, and F2 mice were phenotyped at 8, 12, 16, 20, and 24 weeks of age for 4-hour fasting plasma triglyceride, cholesterol, insulin, and glucose levels, as well as body weights. Fat pad and carcass weights were measured at 24 weeks after sacrificing the mice. The F2 mice were genotyped genome-wide for 68 markers. Of 393 genotyped F2 mice, 16 were chosen from the extremes of the triglyceride distribution (8 high and 8 low), and liver, pancreas, muscle and adipose tissue were measured for gene expression. Gene expression quantitative trait locus (eQTL) analysis aided in selection of candidates underlying hyperlipidemia, diabetes and obesity QTLs. We identified several genetic loci that affected quantitative variation in plasma lipid and glucose levels and obesity traits. 16 (8 high and 8 low) out of 393 F2 mice were chosen from the extremes of the triglyceride distribution, excluding overtly diabetic mice, and liver, pancreas, muscle and adipose tissue were measured for gene expression. In addition to data from the 64 microarrays on the 16 mice, a supplemental file with phenotypes and marker genotypes is provided for all mice as a supplementary file on the Series record (below). Mouse identification numbers are included to connect the data files.

2010-12-01 | E-GEOD-24637 | biostudies-arrayexpress

A Transcriptomic and Proteomic Atlas of Obesity and Type 2 Diabetes in Cynomolgus Monkeys

Project description:Obesity and type 2 diabetes (T2D) remain major global healthcare challenges and developing therapeutics necessitate using nonhuman primate models. Here, we present transcriptomic and proteomic analyses of all the major organs of cynomolgus monkeys with spontaneous obesity or T2D in comparison to healthy controls. Molecular changes occur predominantly in the adipose tissues of obesity individuals, while extensive expression perturbations of T2D individuals are observed in many tissues, such as liver, kidney, brain, and heart. Immune response-related pathways are upregulated in obesity and T2D, whereas metabolism and mitochondrial pathways are downregulated. Incorporating human single-cell RNA sequencing findings corroborates the role of macrophages and monocytes in obesity. Moreover, we highlight some potential therapeutic targets including SLC2A1 and PCSK1 in obesity as well as SLC30A8 and SLC2A2 in T2D. Our findings provide insights into the tissue-specific molecular foundations of obesity and T2D and reveal the mechanistic links between these two metabolic disorders.

2023-06-22 | GSE188418 | GEO

Proteomic Atlas of Obesity and Type 2 Diabetes in Cynomolgus Monkeys

2023-06-23 | PXD036423 | Pride

Methylated DNA Immunoprecipitation (MeDIP) using a custom type 2 diabetes and related phenotypes array

Project description:Custom array designed to tile Linkage Disequilibrium Blocks of T2D GWAS SNPs, monogenic candidates for T2D and Obesity, and all plausible imprinted loci from human and mouse data. Case Control comparison of MeDIP for Type 2 Diabetes. MeDIP versus Input fraction.

2010-12-01 | E-GEOD-20553 | biostudies-arrayexpress

RNA-sequencing of human skeletal myocytes from healthy, obese, and type 2 diabetic subjects

Project description:Skeletal muscle is one of the primary tissues involved in the development of type 2 diabetes (T2D). Obesity is tightly associated with T2D, making it challenging to isolate specific effects attributed to the disease alone. By using an in vitro myocyte model system we were able to isolate the inherent properties retained in myocytes originating from donor muscle precursor cells, without being confounded by varying extracellular factors present in the in vivo environment of the donor. We generated and characterized transcriptional profiles of myocytes from 24 human subjects, using a factorial design with two levels each of the factors T2D (healthy or diseased) and obesity (non-obese or obese), and determined the influence of each specific factor on genome-wide transcription. We identified a striking similarity of the transcriptional profiles associated independently with T2D or obesity. Obesity thus presents an inherent phenotype in skeletal myocytes, similar to that induced by T2D. Through bioinformatics analysis we found a candidate epigenetic mechanism, H3K27me3 histone methylation, mediating the observed transcriptional signatures. Functional characterization of the expression profiles revealed dysregulated myogenesis and down-regulated muscle function in connection with T2D and obesity, as well as up-regulation of genes involved in inflammation and the extracellular matrix. Further on, we identified a metabolite subnetwork involved in sphingolipid metabolism and affected by transcriptional up-regulation in T2D. Collectively, these findings pinpoint transcriptional changes that are hard-wired in skeletal myocytes in connection with both obesity and T2D.

2017-04-22 | GSE81965 | GEO

Integratome analysis of adipose tissues reveals abnormal epigenetic regulation of adipogenesis, inflammation, and insulin signaling in obese individuals with type 2 diabetes

Project description:Type 2 diabetes (T2D) is associated with cardiovascular-renal complications and premature death. Although most patients with T2D are obese, not all obese individuals develop T2D. Thus, an understanding of the mechanistic relationships between obesity and T2D is crucial. In this study, using subcutaneous (SAT) and visceral adipose tissues (VAT) from obese individuals with or without T2D collected during metabolic surgery, integration of the transcriptomes and methylomes of VAT and SAT with publicly available tissue-specific regulatory networks, we discovered the close relation between T2D and inflammatory response in both SAT and VAT in obese individuals, although less differences were observed respectively in transcriptome or methylome. Specifically, a HOX gene family-enriched functional epigenetic sub-network in T2D-SAT, as well as a novel such sub-network was discovered, which involved multiple genes implicated in activation of obesity-induced inflammatory response. Our integrated approach of using biosamples, multi-omic data and public databases to understand complex diseases for discovery of novel biology, including biomarkers and drug targets, can be applied to diseases other than T2D and obesity.

2021-12-20 | GSE162166 | GEO

The Role of Maternal Obesity in Offspring Cardiovascular Development and Congenital Heart Defects

Project description:Background: Congenital heart disease (CHD) is a leading cause of death in newborns, yet many of its molecular mechanisms remain unknown. Both maternal obesity and diabetes increase the risk of CHD in offspring, with recent studies suggesting these conditions may have distinct teratogenic mechanisms. The global prevalence of obesity is rising, and while maternal obesity is a known risk factor for fetal CHD, the specific mechanisms are largely unexplored. Methods: We used a murine model of diet-induced maternal obesity, without diabetes, to produce dams that were overweight but had normal blood glucose levels. Embryos were generated and their developing hearts analyzed. Transcriptome analysis was performed using single-nuclei (snRNAseq) and bulk RNA sequencing (RNA-seq). Global and phospho-enriched proteome analysis was performed using tandem-mass tag mass spectroscopy (TMT-MS). Immunobloting and histologic evaluation were also performed. Results: Analysis revealed disrupted oxidative phosphorylation and reactive oxygen species formation, with reduced antioxidant capacity, evidenced by downregulation of genes Sod1 and Gp4x, and disrupted Hif1a signaling. Evidence of oxidative stress, cell death signaling, and alteration in Rho GTPase and actin cytoskeleton signaling was also observed. Genes involved in cardiac morphogenesis, including Hand2, were downregulated, and fewer mature cardiomyocytes were present. Histologic analysis confirmed increased cardiac defects in embryos exposed to maternal obesity. Conclusion: These findings demonstrate maternal obesity alone can result in cardiac defects through mechanisms similar to those associated with maternal hyperglycemia. This study provides valuable insights into the role of maternal obesity, a growing and modifiable risk factor, in the development of the most common birth defect, CHD.

2025-06-30 | PXD062087 | Pride

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