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Obesity and endoplasmic reticulum (ER) stresses
Yamini B Tripathi1, Vivek Pandey
1Department of Medicinal Chemistry, Institute of Medical Sciences, Banaras Hindu University Varanasi, India.
Frontiers in Immunology
|August 15, 2012
Summary
Obesity causes adipose cells to release inflammatory signals, leading to chronic inflammation and oxidative stress. This review details how obesity triggers cellular stress, impacting organs and contributing to metabolic syndrome.
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Obesity is characterized by adipose cells acting as a source of inflammation.
- Systemic inflammation and oxidative stress in obesity are linked to damage in vital organs.
- High nutritional intake induces high metabolic processes, leading to cellular stress.
Purpose of the Study:
- To review the triggering factors and mechanisms of obesity-mediated cellular stress.
- To explore the relationship between obesity, inflammation, and endoplasmic reticulum (ER) stress.
- To describe the interplay between adipocytes and non-adipocyte cells in metabolic syndrome (MS).
Main Methods:
- Literature review of obesity-mediated inflammation and cellular stress.
- Analysis of the mechanisms linking metabolic processes to ER and mitochondrial stress.
- Examination of the adipocyte-non-adipocyte cell interaction in metabolic syndrome.
Main Results:
- Adipose tissue dysfunction is a key driver of low-grade systemic inflammation in obesity.
- Obesity-induced metabolic overload leads to endoplasmic reticulum (ER) and mitochondrial stress.
- A complex effect-response cycle exists between adipocytes and other cells, contributing to metabolic syndrome.
Conclusions:
- Obesity promotes a pro-inflammatory state through adipose tissue, exacerbating cellular stress.
- Understanding the mechanisms of obesity-induced stress is crucial for addressing metabolic syndrome.
- Targeting the inflammatory and stress pathways in obesity may offer therapeutic strategies.
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