Signal from Fat Tissues Improves Insulin Secretion in Diabetic Mice, Suggests Potential Therapy

Researchers have discovered that adipsin, a cell signaling protein made by fat cells, plays a critical, previously unsuspected role in stimulating insulin secretion to control blood sugar, according to a report from Dana-Farber Cancer Institute.

Bruce Spiegelman, PhD, senior author of the report in Cell, said the discovery could have implications for treatment of type 2 diabetes, a growing epidemic affecting an estimated 382 million people around the world.

Per-Olof Berggren, PhD, and professor at Karolinska Institutet in Stockholm, Sweden, and a co-investigator of the study, added that adipsin “might be the long-sought molecule linking fat tissue metabolism to pancreatic beta cell function.”

In an experiment with obese, diabetic mice that lacked adipsin, replacing the protein improved the health of beta cells in the pancreas, which normally secrete insulin but malfunction in severe diabetes.

The mice had been genetically altered to lack adipsin, but the scientists also discovered that adipsin is deficient in human patients with severe type 2 diabetes.

“This suggests a new approach to treating type 2 diabetes in patients whose pancreatic beta cells work poorly, leaving them dependent on injected insulin,” said Spiegelman, of Dana-Farber’s Cancer Biology Department and a professor at Harvard Medical School.

“If humans respond similarly to the mice in this study,” he said, “correcting their deficiency of adipsin would improve beta cell function and perhaps maintain enough natural insulin production to avoid or delay having to take additional insulin.”

Checking for adipsin levels in diabetic patients might help doctors predict which individuals are at highest risk of impending beta cell failure so that treatment could be started earlier, the authors noted.

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