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.
1. 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.
2. 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.
The precise physiological events leading to initiation of the inflammatory response in obesity remain incompletely understood.
1. However, one emerging hypothesis, as recently evaluated by Regazzetti et al. (10), envisions hypoxia as a novel mechanism participating in insulin resistance in adipose tissue of obese patients. It has been suggested that hypertrophic adipocytes become hypoperfused, creating regional areas of microhypoxia leading to increased expression of hypoxia-inducible factor-1.
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