ArticleDiabetology & metabolic syndrome2025
Depot-specific acetylation profiles of adipose tissues-therapeutic targets for metabolically unhealthy obesity.
Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundAdipose tissue plays a critical role in the development of metabolically unhealthy obesity (MUO), with distinct adipose depots demonstrating functional differences. This study aimed to investigate the unique characteristics of subcutaneous (SA) and visceral adipose tissue (VA) in MUO.
methodsPaired omental VA and abdominal SA samples were obtained from four male patients with MUO and subjected to Four-Dimensional Data Independent Acquisition (4D-DIA) proteomic and lysine acetylation (Kac) analyses. Differentially expressed proteins and differentially modified Kac sites were identified, quantified, integrated, and subjected to functional analyses. Overlap analysis was performed between our datasets and previously published proteomic datasets in obesity populations. Additionally, differentially modified Kac sites on histones and their related enzymes were identified.
resultsA total of 281 differentially expressed proteins and 147 differentially modified Kac sites were identified among 6,201 quantifiable proteins and 1,826 quantifiable Kac sites. Upregulated proteins and acetylated proteins in SA were predominantly enriched in extracellular matrix (ECM) remodeling pathways, while those in VA were enriched in energy metabolism and disease-related pathways. Differential ECM remodeling adaptability between SA and VA was primarily mediated by fibranexin and integrin, with COL6A1, COL6A3, and ITGA5 identified as differentially acetylated proteins overlapping between our dataset and previous studies. Potential unique proteins in MUO were enriched in inflammatory processes and closely associated with acetylated modifications. Specific differentially acetylated sites on histones, including H1.2K63, H1XK90, and H3.7K80, showed increased acetylation in VA, with N-deacetylase/N-sulfotransferase 1 (NDST1) identified as the associated enzyme.
conclusionsThis study provided a comprehensive dataset on the proteomic and acetylomic profiles of SA and VA, laying a foundation for investigating the pathogenesis and potential therapeutic approaches for MUO. SA was characterized by pronounced ECM remodeling regulation, while VA exhibited poorer adaptability and more prominent metabolic functional changes. These differential processes were influenced not only by protein expression levels but, more importantly, by acetylated modifications. The regulation of acetylated modifications in white adipose tissue (WAT), particularly for the differential Kac sites enriched in ECM remodeling and inflammation-related pathways, may serve as an effective intervention strategy for MUO, with NDST1 emerging as a promising therapeutic target.
trial registrationNot applicable since this study did not involve clinical intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.