Although it is becoming clear that inflammation induced by obesity is an important factor linking obesity to type 2 diabetes, the effects of one of the most abundant soluble factors known to have both anti-inflammatory and anti-diabetic effects (adiponectin) remain to be completely determined.
But now, in a study appearing online on January 25 in advance of publication in the February print issue of the Journal of Clinical Investigation, researchers from Boston University show that in mice, adiponectin facilitates the uptake, by immune cells known as macrophages, of cells dying by a process known as apoptosis.
Kenneth Walsh and colleagues found that mice lacking adiponectin were impaired in their ability to clear apoptotic cells when there were very high numbers of apoptotic cells present. By contrast, mice administered adiponectin exhibited enhanced macrophage uptake of apoptotic cells when there were very high numbers of apoptotic cells present. Further analysis showed that adiponectin bound the apoptotic cells and provided a bridge between the apoptotic cells and a protein on the surface of the macrophages known as calreticulin. As the accumulation of large numbers of apoptotic cells triggers inflammation, the authors of this study have identified another anti-inflammatory mechanism of adiponectin.
This might contribute to the link between inflammation and diabetes because adiponectin levels are decreased in individuals who are obese.