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Obesity and inflammation: lessons from bariatric surgery
Charlene Compher1, Karen O Badellino
1University of Pennsylvania School of Nursing, Philadelphia, PA 19104-6096, USA. compherc@nursing.upenn.edu
JPEN. Journal of Parenteral and Enteral Nutrition
|November 1, 2008
Summary
Obesity triggers inflammation through adipose tissue releasing cytokines, worsening insulin resistance. Weight loss can reduce inflammation and improve insulin sensitivity by increasing adiponectin.
Area of Science:
- Endocrinology
- Immunology
- Metabolic Syndrome
Background:
- Obesity is linked to chronic inflammation and related health issues.
- Adipose tissue plays a key role in mediating obesity-associated inflammation.
Purpose of the Study:
- To provide an updated review on the relationship between obesity, adipose tissue, and inflammation.
- To explore the mechanisms linking obesity, inflammation, and insulin resistance.
Main Methods:
- Literature review using keywords: adipose, inflammation, obesity, insulin resistance.
- Synthesis of findings on cytokine production and adipokine secretion from adipose tissue.
Main Results:
- Adipose tissue, particularly visceral fat, secretes proinflammatory cytokines (e.g., IL-6, TNF-alpha).
- This inflammatory state correlates with insulin resistance.
- Weight loss reduces inflammation and insulin resistance, increasing anti-inflammatory adiponectin.
Conclusions:
- The interplay between obesity, inflammation, and insulin resistance is significant.
- Further research is needed to clarify the long-term benefits of weight loss and the impact of anti-inflammatory interventions in obese individuals.
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