Inflammation, stress, and diabetes
Kathryn E. Wellen, Gökhan S. Hotamisligil
Kathryn E. Wellen, Gökhan S. Hotamisligil
Published May 2, 2005
Citation Information: J Clin Invest. 2005;115(5):1111-1119. https://doi.org/10.1172/JCI25102.
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Inflammation, stress, and diabetes

Abstract

Over the last decade, an abundance of evidence has emerged demonstrating a close link between metabolism and immunity. It is now clear that obesity is associated with a state of chronic low-level inflammation. In this article, we discuss the molecular and cellular underpinnings of obesity-induced inflammation and the signaling pathways at the intersection of metabolism and inflammation that contribute to diabetes. We also consider mechanisms through which the inflammatory response may be initiated and discuss the reasons for the inflammatory response in obesity. We put forth for consideration some hypotheses regarding important unanswered questions in the field and suggest a model for the integration of inflammatory and metabolic pathways in metabolic disease.

Authors

Kathryn E. Wellen, Gökhan S. Hotamisligil

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Nutrient and pathogen sensing or response systems have important overlap...
Nutrient and pathogen sensing or response systems have important overlapping features, and their modulation by obesity or infection can lead to overlapping physiological outcomes. For example, the chronic inflammation of obesity leads to elevated plasma lipid levels and the development of insulin resistance, eventually resulting in fatty liver disease, atherosclerosis, and diabetes. Infection typically leads to a more transient and robust inflammatory response and short-term hyperlipidemia that aids in the resolution of the infection. In some circumstances of chronic infection, however, insulin resistance, diabetes, and atherosclerosis can result.