Evidence map›Paper›PMID 39979938›Full record

ArticleJournal of translational medicine2025

Intra and inter-organ communication through extracellular vesicles in obesity: functional role of obesesomes and steatosomes.

N Lago-Baameiro, T Camino, A Vazquez-Durán, A Sueiro, I Couto, F Santos, J Baltar, J M Falcón-Pérez, M Pardo

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

N Lago-BaameiroGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain.
T CaminoGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain.
A Vazquez-DuránGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain.
A SueiroGrupo Endocrinología Molecular y Celular, Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Spain.
I CoutoGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain.
F SantosGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain.
J BaltarGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain.
J M Falcón-PérezExosomes Laboratory and Metabolomics Platform, CIC bioGUNE-BRTA, CIBERehd, Derio, Spain.
M PardoGrupo Obesidómica, Área de Endocrinología, Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS), Complexo Hospitalario Universitario de Santiago de Compostela/SERGAS, Santiago de Compostela, Travesía da Choupana s/n, 15706, Santiago de Compostela, A Coruña, Spain. maruxapardo@hotmail.com.ORCID 0000-0002-9967-1650

Funding

Axencia Galega de Innovación IN607D2022/01Instituto de Salud Carlos III PI19/00305Instituto de Salud Carlos III PI22/00196
6 · The paper itself

Abstract

backgroundExtracellular vesicles (EVs) represent a sophisticated mechanism of intercellular communication that is implicated in health and disease. Specifically, the role of EVs in metabolic regulation and their implications in metabolic pathologies, such as obesity and its comorbidities, remain unclear.

methodsExtracellular vesicles (EVs) were isolated through serial ultracentrifugation from murine adipocytes treated with palmitate or oleic acid, whole visceral and subcutaneous adipose tissue (obesesomes) of bariatric surgery obese donors, and human hepatocytes under steatosis (steatosomes) for functional in vitro experiments. Functional effects on inflammation and glucose and lipid metabolism of target cells (human and murine macrophages and hepatocytes) were assessed using ELISA, RT-PCR, and immunodetection. Isolated EVs from human steatotic (steatosomes) and control hepatocytes (hepatosomes) were characterized for quantity, size, and tetraspanin profile by NTA and Single Particle Interferometric Reflectance Imaging Sensor (SP-IRIS), and their protein cargo analyzed by qualitative (DDA) and quantitative (DIA-SWATH) proteomics using LC-MS/MS. Proteins identified by proteomics were validated by capturing EVs on functionalized chips by SP-IRIS. RESULTS AND

conclusionsIn this study, we investigated the role of EVs in the local communication between obese adipocytes and immune cells within adipose tissue, and the interaction of steatotic and healthy hepatocytes in the context of fatty liver disease progression. Furthermore, we analyzed obese adipose tissue-to-liver interactions through EV-obesesomes to elucidate their role in obesity-associated hepatic metabolic dysregulation. Our findings reveal that obesesomes promote inflammation and the secretion of pro-inflammatory cytokines upon interaction with macrophages, exerting a significant impact on reducing insulin resistance and altering lipid and glucose metabolism upon interaction with hepatocytes; in both cases, EVs from palmitate-loaded adipocytes and obesesomes from human visceral adipose depots demonstrated the most deleterious effect. Additionally, EVs secreted by steatotic hepatocytes (steatosomes) induced insulin resistance and altered lipid and glucose metabolism in healthy hepatocytes, suggesting their involvement in MASLD development. Proteomic analysis of steatosomes revealed that these vesicles contain liver disease-associated proteins, rendering them significant repositories of real-time biomarkers for the early stages and progression of MASLD.

Indexed as

Cell CommunicationExtracellular VesiclesFatty LiverObesityAdipocytesAnimalsHepatocytesHumansInflammationLipid MetabolismMacrophagesMaleMiceMice, Inbred C57BLProteomicsExtracellular vesiclesInflammationLiver steatosisMASLDObesity

Identifiers

PMID39979938
PMCPMC11844161

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

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 Socratic graph.