Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Orbital Fat is an Observation Model to Provide Insights into Adipocyte Hypertrophy and Hyperplasia During White Adipose Tissue Expansion

Cheng Y., Zhang K., Liu J., Liu G.

Laboratory Study on Type 2 Diabetes, published in Diabetes Metab Syndr Obes (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
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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
Laboratory Study
Journal
Diabetes Metab Syndr Obes (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40862228
PMCID
PMC12375334
DOI
10.2147/dmso.s521845

Abstract (original English)

Introduction Obesity is a global health problem characterized by excessive white adipose tissue (WAT) distribution. Adipocyte hypertrophy (increased cell size) and hyperplasia (differentiation into new adipocytes from pre-adipocytes) are two ways for WAT to expand. The precedence of hypertrophy over hyperplasia leads to an enlarged adipocyte size, which is associated with multiple metabolic dysfunctions. Compared with abdominal subcutaneous fat (SF), orbital fat (OF) has smaller adipocytes with less inflammatory infiltration, better vascularization, and higher adipogenic and proliferative capacities, reflecting a healthy metabolic state. Polyunsaturated fatty acids (PUFAs) can stabilize energy homeostasis via G protein-coupled receptor 120 (GPR120) to alleviate insulin resistance and inflammation. Methods We used lipidomics analysis to reveal a greater accumulation of two PUFAs-arachidonic acid (AA) and docosapentaenoic acid (DPA) in OF than in SF and then hypothesized that AA/DPA is one factor regulating WAT morphological and biological heterogeneity. Results Mechanistically, the existing literature evidence suggests that AA/DPA signals may stimulate the co-activation and interaction of GPR120 and peroxisome proliferator-activated receptor γ (PPARγ), at least partially contributing to adipose metabolic health. Conclusion As the differential metabolites between OF and SF, AA an

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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