Related Experiment Video
Updated: Jun 25, 2025
06:08
Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator
Published on: May 19, 2023
2.1K
Pathological analysis of Prader-Willi syndrome using adipocytes
Urara Kishimura1, Shuhei Soeda1, Daiki Ito1
1Laboratory of Neurochemistry, College of Pharmaceutical Sciences, Ritsumeikan University, Shiga, 525-8577, Japan.
Biochemical and Biophysical Research Communications
|May 22, 2024
Summary
Prader-Willi syndrome (PWS) adipocytes show increased lipid accumulation and impaired glucose metabolism. This epigenetic disorder affects fat cells, contributing to obesity and metabolic challenges in affected individuals.
Area of Science:
- Genetics
- Epigenetics
- Cell Biology
Background:
- Prader-Willi syndrome (PWS) is a complex epigenetic disorder.
- It results from the deficiency of paternally expressed genes on chromosome 15q11-q13.
- PWS is associated with endocrine dysfunction, including obesity and hyperphagia, but the molecular mechanisms are unclear.
Purpose of the Study:
- To investigate the adipocytic characteristics of PWS-induced pluripotent stem cells (iPSCs).
- To understand the molecular pathology of obesity in Prader-Willi syndrome.
Main Methods:
- Generated and analyzed two types of PWS-iPSC lines: iPWS (gene deletion) and M-iPWS (abnormal methylation).
- Examined adipocyte differentiation and characteristics, including lipid droplet accumulation and glucose uptake.
- Measured transcript levels of adipocyte protein 2 (aP2).
Main Results:
- Decreased transcript levels of aP2 were observed in both iPWS and M-iPWS adipocytes.
- PWS adipocytes exhibited increased lipid droplet accumulation compared to normal adipocytes.
- Glucose uptake upon insulin stimulation was attenuated in PWS adipocytes.
Conclusions:
- PWS adipocytes display significantly increased lipid content.
- Defective glucose metabolism is a key feature of PWS adipocytes.
- These findings provide insights into the molecular mechanisms underlying obesity in Prader-Willi syndrome.
