Individuals who are obese are predisposed to a variety of metabolic conditions, including type 2 diabetes.
A characteristic of the fat tissue (adipose tissue) of individuals who are obese is that it is inflamed, and understanding the relationship between such inflammation and the onset of the metabolic conditions is of importance in combating what has become a large public health problem.
In a new mouse study, Gökhan Hotamisligil and colleagues, at the Harvard School of Public Health, Boston, found that interactions between adipocytes (fat cells) and inflammatory cells called macrophages seem to underlie the inflammation-related metabolic deterioration associated with obesity.
In the study, when adipocytes isolated from mice lacking proteins known as FABPs, which are molecules that govern metabolic and inflammatory responses, were cultured with normal macrophages, the macrophages expressed reduced levels of inflammatory molecules.
Likewise, when macrophages isolated from mice lacking FABPs were cultured with normal adipocyes, the adipocytes responded more to insulin and took up more glucose. Similar results, indicating that FABPs from both adipocytes and macrophages contribute to the inflammatory basis for metabolic deterioration, were obtained in vivo.
The authors therefore suggest that this FABP-related pathway may be a novel target for metabolism-related disorders.
Journal reference: Adipocyte/macrophage fatty acid--binding proteins contribute to metabolic deterioration through actions in both macrophages and adipocytes in mice. Journal of Clinical Investigation. June 12, 2008.
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