May 2005 | Kathryn E. Woll and Gökhan S. Hotamisligil
The article by Kathryn E. Wellen and Gökhan S. Hotamisligil explores the intricate relationship between inflammation, stress, and diabetes, highlighting the molecular and cellular underpinnings of obesity-induced inflammation. It discusses how obesity leads to chronic low-level inflammation, which in turn contributes to insulin resistance and diabetes. The authors review the signaling pathways that link metabolism and inflammation, such as the activation of inflammatory kinases like JNK and IKK, and the role of lipids in regulating these pathways. They also examine the mechanisms by which the inflammatory response is initiated in obesity, including endoplasmic reticulum (ER) stress and oxidative stress. The article suggests that inflammation may be a primary driver of obesity-linked insulin resistance rather than a consequence. Finally, it proposes a model for the integration of inflammatory and metabolic pathways in metabolic diseases and discusses potential therapeutic strategies targeting these pathways.The article by Kathryn E. Wellen and Gökhan S. Hotamisligil explores the intricate relationship between inflammation, stress, and diabetes, highlighting the molecular and cellular underpinnings of obesity-induced inflammation. It discusses how obesity leads to chronic low-level inflammation, which in turn contributes to insulin resistance and diabetes. The authors review the signaling pathways that link metabolism and inflammation, such as the activation of inflammatory kinases like JNK and IKK, and the role of lipids in regulating these pathways. They also examine the mechanisms by which the inflammatory response is initiated in obesity, including endoplasmic reticulum (ER) stress and oxidative stress. The article suggests that inflammation may be a primary driver of obesity-linked insulin resistance rather than a consequence. Finally, it proposes a model for the integration of inflammatory and metabolic pathways in metabolic diseases and discusses potential therapeutic strategies targeting these pathways.