Inflammation, Insulin Resistance, and Type 2 Diabetes: Back to the Future?
- From the Section on Diabetes, Endocrinology and Metabolism, Pennington Biomedical Research Center/Louisiana State University, Louisiana State University School of Medicine, Baton Rouge and New Orleans, Louisiana
- Corresponding author: William T. Cefalu,
In this issue of Diabetes, two articles highlight the emergence of inflammation's contribution to insulin resistance and to chronic diseases in humans. The common feature in each article is the inflammation–obesity–insulin resistance connection, but each article approaches the investigation from a completely different perspective. Specifically, the study of Ortega Martinez de Victoria et al. (1) comments on factors related to macrophage activation in adipocytes as a source for cytokines for systemic inflammatory effects. In contrast, the study of Haus et al. (2) provides data on systemic effects resulting from inflammatory activation, namely, the relationship of cytokines with circulating lipid intermediates.
Approximately 2,000 years ago, Aulus (Aurelius) Cornelius Celsus, a Roman physician, was credited with the first recording of the cardinal signs of inflammation, which included calor (warmth), dolor (pain), tumor (swelling), and rubor (redness and hyperemia) (3). This general description of inflammation appears to have served clinical medicine well for most of the 2,000 years since it was first described. Until the recent past, no one would have ever envisioned that inflammation would be considered a root cause of the pathogenesis of metabolic abnormalities associated with obesity or a potential molecular target for diabetes therapies. But these statements for the inflammatory pathway represent present-day reality for basic and clinical human investigation.
The association of inflammation with carbohydrate metabolism can actually be traced back to reports from the 1800s. Shoelson et al. (4) describe these reports in a historical review. Specifically, they cite reports from over a century ago in which high-dose salicylates appeared to decrease glycosuria in individuals classified as diabetic (presumably type 2 diabetes). The works of Ebstein in 1876 and Williamson in 1901 were also cited. These works …