When blood sugar rises, beta cells in the pancreas release insulin, causing cells to take in more glucose and keeping blood sugar levels steady. Problems with this feedback mechanism can result in such metabolic disorders as diabetes and hypoglycemia.
Scientists already knew that ATP, cellular fuel produced through glucose breakdown, triggers insulin release, and since the oxidative phosphorylation step (OxPhos) in glucose metabolism produces significant ATP, OxPhos was thought to regulate insulin secretion.
However, research led by Richard G. Kibbey, MD, PhD, associate professor of medicine, indicates that another product of glucose metabolism, mitochondrial GTP (mtGTP), does the same thing—independent of OxPhos.
As reported July 16 in Cell Reports, when Kibbey’s team overexpressed the protein that makes mtGTP in beta cells, insulin levels increased in vitro. In mice overexpressing the mtGTP progenitor protein, insulin levels also rose, and blood sugar levels dropped. mtGTP also appeared to protect beta cells from metabolic stress. Kibbey says these results point to the mtGTP pathway as a promising new target for diabetes drugs.
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