Adipocytes regulate monocyte development through the OGT-NEFA-CD36/FABP4 pathway in high-fat diet-induced obesity.
He N., Li Y., Liu F., Dong X., Ma D.
Animal Study, published in Cell Death Dis (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Cell Death Dis (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40389445
- PMCID
- PMC12089399
- DOI
- 10.1038/s41419-025-07721-x
- Citations
- 3
Abstract (original English)
Obesity, resulting from excessive adipocyte accumulation, is a primary risk for various diseases. Although its impact on hematopoietic stem cell (HSC) function has been reported, its effects on HSC differentiation remain controversial. O-GlcNAc transferase (OGT), which catalyzes the attachment of N-acetylglucosamine to serine and threonine residues in proteins, acts as a metabolic sensor capable of regulating diverse physiological processes. This study demonstrates that obesity is associated with higher peripheral monocyte levels. Adipocyte OGT is crucial for monocyte development in high-fat diet (HFD)-induced obesity, promoting an increase in peripheral blood monocytes through transcriptional activation of nonesterified fatty acids (NEFA), a critical energy substrate. Loss of adipocyte OGT decreases serum NEFA levels, reduces white adipose tissue, and inhibits HSC differentiation into monocytes in HFD-induced obesity. Mechanistically, the regulated effect of adipocyte OGT on monocyte development may be mediated by NEFA-cluster of differentiation 36/fatty acid binding protein 4 (CD36/FABP4) pathway in HSCs in HFD-induced obesity. These findings establish the critical role of adipocyte OGT in hematopoietic homeostasis and monocyte development.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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