Evidence map›Paper›PMID 41574186›Full record

ArticleFrontiers in physiology2025

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

Shamma Almuraikhy, Maha Alser, Khaled Naja, Najeha Anwardeen, Samir Taha, Jomon John, Sharique Halim, Saif Badran, Mohamed Badie Ahmed, Salma Jarrar and 6 more

Abstract read
In one paragraph

Article in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Shamma AlmuraikhyBiomedical Research Center, Qatar University, Doha, Qatar.
Maha AlserBiomedical Research Center, Qatar University, Doha, Qatar.
Khaled NajaBiomedical Research Center, Qatar University, Doha, Qatar.
Najeha AnwardeenBiomedical Research Center, Qatar University, Doha, Qatar.
Samir TahaOral and Maxillofacial Surgery, Al-Wakra Hospital, Hamad Medical Corporation, Doha, Qatar.
Jomon JohnOral and Maxillofacial Surgery, Al-Wakra Hospital, Hamad Medical Corporation, Doha, Qatar.
Sharique HalimOral and Maxillofacial Surgery, Al-Wakra Hospital, Hamad Medical Corporation, Doha, Qatar.
Saif BadranDivision of Plastic and Reconstructive Surgery, Washington University School of Medicine, Saint Louis, MO, United States.
Mohamed Badie AhmedPlastic Surgery Department, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Salma JarrarPlastic Surgery Department, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Ghanem AljassemPlastic Surgery Department, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Fatima Saoud Al-MohannadiPlastic Surgery Department, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Suhail DoiCollege of Medicine, QU Health Cluster, Qatar University, Doha, Qatar.
Asmaa Abdel-AzizDepartment of Biomedical Science, College of Health Sciences, Qatar University, Doha, Qatar.
Yousra Jalal ElafDepartment of Biomedical Science, College of Health Sciences, Qatar University, Doha, Qatar.
Mohamed A ElrayessBiomedical Research Center, Qatar University, Doha, Qatar.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 to understand the impact of impaired adipogenesis and the potential therapeutic interventions targeting adipogenesis to improve insulin sensitivity in non-obese individuals.

Indexed as

adipogenesisinsulin resistancemetforminnon-obesetumor necrosis factor alpha

Identifiers

PMID41574186
PMCPMC12819270

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.