Level B· Emerging clinical evidence with positive signalsClinical TrialPubMed

Dysregulated adipose tissue expansion and impaired adipogenesis in Prader-Willi syndrome children before obesity-onset.

Chao Y., Gao L., Wang X., Cai Y., Shu Y., Zou X.

Clinical Trial, published in Metabolism (2022) — summary generated from the PubMed abstract.

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Level B· Emerging clinical evidence with positive signalsEvidence level of this study

Several human studies show positive signals, while research methods and sample sizes continue to develop.

  • 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
Read the A–D evidence level guide

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
Clinical Trial
Journal
Metabolism (2022)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
36007622
DOI
10.1016/j.metabol.2022.155295
Citations
6

Abstract (original English)

Objective Prader-Willi syndrome (PWS) is a rare genetic imprinting disorder resulting from the expression loss of genes on the paternally inherited chromosome 15q11-13. Early-onset life-thriving obesity and hyperphagia represent the clinical hallmarks of PWS. The noncoding RNA gene SNORD116 within the minimal PWS genetic lesion plays a critical role in the pathogenesis of the syndrome. Despite advancements in understanding the genetic basis for PWS, the pathophysiology of obesity development in PWS remains largely uncharacterized. Here, we aimed to investigate the signatures of adipose tissue development and expansion pathways and associated adipose biology in PWS children without obesity-onset at an early stage, mainly from the perspective of the adipogenesis process, and further elucidate the underlying molecular mechanisms. Methods We collected inguinal (subcutaneous) white adipose tissues (ingWATs) from phase 1 PWS and healthy children with normal weight aged from 6 M to 2 Y. Adipose morphology and histological characteristics were assessed. Primary adipose stromal vascular fractions (SVFs) were isolated, cultured in vitro, and used to determine the capacity and function of white and beige adipogenic differentiation. High-throughput RNA-sequencing (RNA-seq) was performed in adipose-derived mesenchymal stem cells (AdMSCs) to analyze transcriptome signatures in PWS subjects.

What this study does not prove

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

Evidence level

Several human studies show positive signals, while research methods and sample sizes continue to develop.

How we grade evidence
AdipogenesisAdipose Tissue, WhiteChildHumansHyperphagiaObesityPPAR gammaPrader-Willi SyndromeRNA PrecursorsRNA, Small Nucleolar

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