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Alpha cell function and gene expression are compromised in type 1 diabetes according to Dr. Harlan, Dr. Greiner and a consortium of scientists

Date Posted: Monday, March 12, 2018

UMass Diabetes Center of Excellence co-directors, David Harlan, MD and Dale Greiner, PhD, in collaboration with established investigators from a consortium of institutions throughout the country lead by Drs. Marcela Brissova and Alvin C. Powers (Vanderbilt University), have been published in the latest issue of Cell Reports.   

Type 1 diabetes (T1D) development and progression in humans is poorly defined at the cellular level.  To better understand the functional and molecular properties of islets from donors with T1D, the team’s research used an approach that studied the pancreas and isolated islets from the same donor with T1D.  That allowed the scientists to better analyze the development, properties and behavior of T1D donor islets. 

Many patients with T1D still have residual beta cells long after disease onset, producing small amounts of insulin.  That said, individuals with T1D also develop an inadequate glucagon response to hypoglycemia.  By studying the pancreas and isolated islets from the same T1D individual, the research found that remnant beta cells appeared to maintain several aspects of regulated insulin secretion. However, the function of T1D alpha cells (which make glucagon) display impaired glucagon secretion and altered gene expression.  Further, the team found that unlike rodents, alpha to beta cell conversion in human T1D is a very rare event.  The T1D alpha cell functionality did show improvement when placed in an environment of normal blood glucose.

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