Evidence map›Paper›PMID 40696281›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

Depot-specific metabolic and inflammatory profiles in perirenal and renal sinus adipose tissue.

Maria J Pereira, Argyri Mathioudaki, Susanne Hetty, Amir Sedigh, Jan W Eriksson, Maria K Svensson

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Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Maria J Pereira *Department of Medical Sciences, Clinical Diabetology and Metabolism, Uppsala University, Uppsala, Sweden.ORCID 0000-0001-5498-3899
Argyri Mathioudaki *Department of Medical Sciences, Clinical Diabetology and Metabolism, Uppsala University, Uppsala, Sweden.ORCID 0000-0003-0200-0760
Susanne HettyDepartment of Medical Sciences, Clinical Diabetology and Metabolism, Uppsala University, Uppsala, Sweden.
Amir SedighDepartment of Surgical Sciences, Transplantation Surgery, Uppsala University, Uppsala, Sweden.ORCID 0000-0003-0238-0839
Jan W ErikssonDepartment of Medical Sciences, Clinical Diabetology and Metabolism, Uppsala University, Uppsala, Sweden.ORCID 0000-0002-2639-9481
Maria K SvenssonDepartment of Medical Sciences, Renal Medicine, Uppsala University, Uppsala University Hospital, Uppsala, 751 85, Sweden. maria.k.svensson@medsci.uu.se.ORCID 0000-0001-7545-5585

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlterations in kidney-associated adipose tissue depots, specifically renal sinus (RSAT) and perirenal adipose tissue (PRAT), may contribute to metabolic, cardiovascular, and chronic kidney diseases. We compared transcriptomic profiles and phenotypes, including adipocyte size, glucose uptake, and insulin action in RSAT and PRAT from healthy individuals.

methodsSubcutaneous (SAT), omental (OAT) and renal adipose tissue biopsies were collected from healthy kidney donors (20 women, 20 men; BMI 20 to 36 kg/m

resultsPRAT exhibited significantly larger adipocytes and higher insulin-stimulated glucose uptake than RSAT. Of 1113 significantly differentially expressed genes (DEGs) (PRAT: 571 down- and 542 upregulated), thermogenic and metabolic genes (UCP1, CIDEA, and CKMT1B) were enriched in PRAT, while inflammation-related genes (NFKBIA, BIRC3, and IRF1) in RSAT. Pathway analysis indicated activation of metabolic pathways (TCA cycle and oxidative phosphorylation), in PRAT, which contrasts with the immune and inflammatory pathways in RSAT and OAT. Immune cell gene signatures revealed an anti-inflammatory environment in PRAT (eosinophils and activated NK cells), and a pro-inflammatory profile in RSAT (M0 macrophages). Immunohistochemistry confirmed higher CD68- and IL1B-positive cells in RSAT than in PRAT. When overweight individuals were compared to lean, genes related to the VEGF signaling were upregulated in PRAT and Ras signaling in RSAT. Additionally, metabolic pathways linked to the TCA cycle as well as carbon and fatty acid metabolism were downregulated.

conclusionsThe different kidney-associated adipose tissue depots exhibit distinct gene expression and functional profiles. PRAT displays higher expression of thermogenic markers and less inflammatory profile compared to RSAT and also OAT. In contrast, RSAT exhibits an inflammatory and macrophage-enriched profile, more closely resembling OAT. This study highlights the heterogeneity of the kidney-associated adipose tissue depots and could suggest that an excessive amount of RSAT may impact development of metabolic, cardiovascular, and chronic kidney diseases.

Indexed as

Adipose TissueInflammationKidneyAdipocytesAdultFemaleGene Expression ProfilingGlucoseHumansMaleMiddle AgedTranscriptomeGlucoseAdipocyteGlucose uptakeKidneyOmental adipose tissuePerirenal adipose tissueRenal sinus adipose tissueTranscriptomics

Identifiers

PMID40696281
PMCPMC12285007

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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.