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Obesity is associated with a decrease in expression but not with the hypermethylation of thermogenesis-related genes
Alina Kurylowicz1, Marta Jonas2, Wojciech Lisik3
1Department of Human Epigenetics, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawinskiego Street, 02-106, Warsaw, Poland. akurylowicz@imdik.pan.pl.
Journal of Translational Medicine
|January 28, 2015
Summary
Obese individuals exhibit reduced expression of key thermogenesis-related genes in adipose tissue. This downregulation, not explained by promoter methylation, may impair the body's ability to burn calories.
Area of Science:
- Metabolic research
- Obesity studies
- Gene expression analysis
Background:
- Impaired thermogenesis is linked to obesity development.
- Investigating gene expression and methylation in obesity is crucial for understanding metabolic dysfunction.
Purpose of the Study:
- To examine alterations in thermogenesis-related gene expression in adipose tissue of obese individuals.
- To determine if excessive promoter methylation contributes to altered gene expression in obesity.
Main Methods:
- Real-time PCR was used to measure gene expression of beta adrenergic receptors (ADRBs), thyroid hormone receptors (THRs), 5'-iodothyronine deiodinases (DIOs), and uncoupling proteins (UCPs).
- Analysis was conducted on visceral and subcutaneous adipose tissues from obese and slim individuals.
- Methylation-sensitive digestion/real-time PCR assessed gene promoter methylation status.
Main Results:
- Significant downregulation of ADRB2, ADRB3, THRA, THRB, DIO2, and UCP2 expression was observed in obese patients' adipose tissues compared to controls.
- Obese individuals showed lower expression of ADRB2, ADRB3, and DIO2 in visceral adipose tissue versus subcutaneous adipose tissue.
- No significant differences in mean methylation levels were found between high and low gene expression tissues, indicating no correlation between methylation and expression.
Conclusions:
- Reduced expression of thermogenesis-related genes in adipose tissue may decrease responsiveness to hormonal and adrenergic signals.
- This downregulation could lead to a diminished capacity for thermogenesis in obese individuals.
- Promoter methylation does not appear to be the primary mechanism driving these expression changes in obesity.
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