Swapping alpha cells for beta cells to treat diabetes


Date: 10.03.2021

Blocking cell receptors for glucagon, the counter-hormone to insulin, cured mouse models of diabetes by converting glucagon-producing cells into insulin producers instead, a team reports in a new study. The findings could offer a new way to treat both Type 1 and Type 2 diabetes in people, a team led by UT Southwestern reports in a new study.

More than 34 million Americans have diabetes, a disease characterized by a loss of beta cells in the pancreas. Beta cells produce insulin, a hormone necessary for cells to absorb and use glucose, a type of sugar that circulates in the blood and serves as cellular fuel.

In Type 2 diabetes, the body's tissues develop insulin resistance, prompting beta cells to die from exhaustion from secreting excess insulin to allow cells to take in glucose. In Type 1 diabetes, which affects about 10 percent of the diabetic population, beta cells die from an autoimmune attack. Both kinds of diabetes lead to severely elevated blood sugar levels that eventually cause a host of possible complications, including loss of limbs and eyesight, kidney damage, diabetic coma, and death.

Most treatments for diabetes focus on insulin, but its counterpart -- the hormone glucagon that is produced by alpha cells in the pancreas -- has received comparatively little attention, says study leader May-Yun Wang, Ph.D., assistant professor of internal medicine at UTSW. Glucagon binds to receptors on cells in the liver, prompting this organ to secrete glucose. Some recent studies have suggested that depleting glucagon or blocking its receptor can help research animals or humans with diabetes better manage their glucose levels. But how this phenomenon occurs has been unknown.

To answer this question, Wang and her colleagues, including William L. Holland, Ph.D., a former assistant professor of internal medicine at UTSW who is now at the University of Utah, and Philipp E. Scherer, Ph.D., professor of internal medicine and cell biology at UTSW and director of UTSW's Touchstone Center for Diabetes Research, used monoclonal antibodies -- humanmade proteins that act like human antibodies and help the immune system identify and neutralize whatever they bind to -- against the glucagon receptor in mouse models of diabetes.

The article based on the information: Sciencedaily

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