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Updated: Mar 19, 2026

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
Published on: March 28, 2013
EXPRESSION OF PEROXISOME-PROLIFERATOR ACTIVATED RECEPTORS-γ IN DIABETICS, OBESE AND NORMAL SUBJECTS
Levels of Peroxisome Proliferator Activated Receptors-Gamma (PPAR-γ) are significantly lower in patients with type 2 diabetes mellitus and obesity. This finding highlights PPAR-γ
Area of Science:
- Endocrinology
- Metabolic Disorders
- Molecular Biology
Background:
- Type 2 diabetes mellitus (T2DM) research increasingly focuses on Peroxisome-Proliferator Activated Receptors (PPARs) and their role in Insulin Resistance Syndrome (IRS).
- PPARs are implicated in the pre-diabetic lesions and are characteristic of established T2DM.
- This study investigates the status of PPAR-γ in adipose tissue of T2DM patients compared to controls.
Purpose of the Study:
- To identify abnormal PPAR-γ expression in adipose tissue of T2DM patients.
- To compare PPAR-γ levels between T2DM patients, obese individuals, and normal controls.
Main Methods:
- A cross-sectional study conducted from 2012-2014 at Ayub Medical College, Abbottabad.
- Participants were divided into three groups: T2DM patients, non-diabetic obese individuals, and normal subjects (aged 40-65 years).
- Transcription Factor Assay for Peroxisome Proliferator Activated Receptor Gamma (PPAR-γ) was performed using ELISA on nuclear extracts from adipose tissue.
Main Results:
- The mean age of participants was 48.93 ± 6.52 years.
- Mean PPAR-γ values were 1.72 ± 0.28 in normal controls, 1.28 ± 0.18 in obese individuals, and 1.28 ± 0.18 in T2DM patients.
- A significant difference (p < 0.05) in mean PPAR-γ values was observed between the groups.
Conclusions:
- Patients with type 2 diabetes mellitus exhibit significantly lower levels of PPAR-γ in adipose tissue compared to normal controls.
- Obese individuals also show significantly reduced PPAR-γ levels compared to normal controls.
- These findings suggest a potential role for reduced PPAR-γ in the pathogenesis of T2DM and obesity.
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