Obesity is one of the biggest risk factors for type 2 diabetes.
One reason for this is thought to be the chronic inflammation characterized by macrophage infiltration into adipose tissue that accompanies obesity, because it has been linked to the development of insulin resistance (which in turn often leads to type 2 diabetes).
New data generated in mice by Dennis Bruemmer and colleagues at the University of Kentucky College of Medicine, Lexington, provides support for this hypothesis.
Osteopontin is an extracellular matrix protein and proinflammatory cytokine that is required for macrophage infiltration of a tissue during an immune response. Bruemmer and colleagues found that although mice lacking osteopontin became obese when fed a high-fat diet, they did not become as insulin resistant as normal mice fed the same diet.
This decrease in insulin resistance was associated with decreased accumulation of macrophages in the adipose tissue leading the authors to conclude that osteopontin has a key role in linking obesity to the development of insulin resistance in mice.
Article: "Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice," Journal of Clinical Investigation
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