In the current paper, the researchers found in cultured cells and mouse experiments that Fox01 stimulates inflammatory white blood cells called macrophages, which migrate to the liver and adipose, or fat, tissue in insulin-resistant states, to increase production of a cytokine called interleukin-1 beta (IL-1B). The cytokine in turn interferes with insulin signaling. Insulin typically inhibits Fox01, setting up a feedback loop in healthy tissues that helps regulate insulin levels.

"The findings suggest that when there is a lack of insulin or when cells such as macrophages are resistant to its presence, there are no brakes on Fox01's stimulation of IL-1B and its further interference with insulin signaling," Dr. Dong said. "That might explain why chronic inflammation often is coupled with obesity and type 2 diabetes. Also, a drug that acts on Fox01 might be able to better control blood sugar."

According to the ADA, an estimated 24 million Americans have type 2 diabetes, formerly known as adult-onset diabetes. As obesity becomes more common, however, the prevalence is rising in children. In type 2 diabetes, the body becomes resistant to the effect of insulin, leading to elevated blood sugar levels.

Source: University of Pittsburgh Schools of the Health Sciences