Level C· Early human research exploring benefitsCohort StudyEurope PMCOpen access

The role of impaired adipogenesis in insulin resistance among non-obese individuals

Almuraikhy S., Alser M., Naja K., Anwardeen N., Taha S., John J.

Cohort Study on Type 2 Diabetes, published in Front Physiol (2025) — summary generated from the PubMed abstract.

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Level C· Early human research exploring benefitsEvidence level of this study

Early human evidence such as case series or small samples is exploring possible benefits.

  • 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
Cohort Study
Journal
Front Physiol (2025)
Reported sample size
—
Source database
Europe PMC
PMID
41574186
PMCID
PMC12819270
DOI
10.3389/fphys.2025.1739215

Abstract (original English)

Introduction Adipogenesis is an essential process for energy storage, hormone regulation, and overall metabolic health. Previous work showed that impaired adipogenesis plays an important role in the development of obesity-associated insulin resistance. This project investigates the role of impaired adipogenesis in the development of insulin resistance among non-obese (lean/overweight) individuals under physiological and pathological microenvironments. Methods Subcutaneous adipose tissue samples were obtained from insulin-sensitive and insulin-resistant non-obese cohorts undergoing maxillofacial or body contouring surgeries. Preadipocytes were isolated and examined for proliferation and adipogenic capacity, insulin signaling, and inflammatory markers. These assessments were conducted under basal conditions and following treatment with either tumor necrosis factor alpha (TNF-α) to induce insulin resistance or metformin to promote insulin sensitivity. Results Insulin-resistant participants, in comparison to insulin-sensitive counterparts, showed lower adipogenic capacity, higher susceptibility to the anti-adipogenic and pro-inflammatory effect of TNF-α potentially due to hyperphosphorylation of insulin receptor substrate-1. Discussion This highlights the role of impaired adipogenesis in the pathogenesis of insulin resistance among non-obese individuals. Further research is needed

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

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Early human evidence such as case series or small samples is exploring possible benefits.

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