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Updated: May 10, 2026

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Control of Eating Behavior Using a Novel Feedback System
Published on: May 8, 2018
Stressing the brain, fattening the body
Ling Yang1, Gökhan S Hotamisligil
1Harvard School of Public Health, Department of Genetics and Complex Diseases, Boston, MA 02115, USA.
Cell
|October 16, 2008
Summary
Obesity causes chronic inflammation in the body and brain. Central nervous system inflammation disrupts hypothalamic function, leading to leptin resistance via IKK and endoplasmic reticulum stress.
Area of Science:
- Neuroscience
- Immunology
- Endocrinology
Background:
- Obesity is linked to chronic inflammation in peripheral tissues.
- The role of central nervous system (CNS) inflammation in obesity-related disorders is increasingly recognized.
Discussion:
- Zhang et al. (2008) reveal CNS inflammation in obesity.
- This inflammation disrupts hypothalamic function, a key regulator of appetite and metabolism.
- The study identifies activation of IKK and endoplasmic reticulum (ER) stress as mediators.
Key Insights:
- Inflammation in the brain contributes to metabolic dysfunction.
- Activation of IKK and ER stress pathways in the hypothalamus leads to leptin resistance.
- This provides a molecular link between inflammation and impaired appetite signaling.
Outlook:
- Targeting CNS inflammatory pathways may offer novel therapeutic strategies for obesity.
- Further research into the interplay between ER stress and neuroinflammation in metabolic disease is warranted.
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