Diabetic Pancreases Sending Mixed Signals

Type 2 diabetes patients have altered insulin signals

(RxWiki News) The body of diabetes patients either cannot produce enough insulin or ignores insulin, a hormone that controls blood sugar. New research reveals what may be causing this problem.

For the first time in humans, researchers have shown that insulin signaling is changed in the pancreas of people with type 2 diabetes. These faulty signals affect both the quantity and quality of beta cells (the cells in the pancreas that produce insulin).

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The study was conducted by Franco Folli, M.D., Ph.D., of the University of Texas Health Science Center in San Antonio, and Rohit Kulkarni, M.D., Ph.D., of the Joslin Diabetes Center at Harvard Medical School, and their colleagues.

Before this study, it was already known that the beta cells die off in type 2 diabetes patients. According to Drs. Folli and Kulkarni, their findings show that the beta cells try to reproduce themselves but fail because of the changed insulin signals.

In most organs throughout the body, except the central nervous system, a dead cell is replaced by a new cell that does the same job. This remains true for the cells in the pancreas: when one beta cell dies, another should be replicated to perform the same insulin-producing function. However, the ability of beta cells to replicate is diminished in people with type 2 diabetes.

By examining the pancreases of dead organ donors, the researchers found that beta cells cannot replicate in these diabetes patients because of altered insulin signals.

The inability of beta cells to replicate themselves leads to a huge problem with insulin secretion in the later stages of type 2 diabetes, Drs. Folli and Kulkarni explain. Poor insulin secretion is one of the hallmarks of type 2 diabetes.

The researchers also found that beta cell receptors (molecules that receive signals from hormones) are extremely important for maintaining a healthy number of beta cells.

The results of the study are published in the journal PLoS ONE

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Review Date: 
December 13, 2011