by Dikshya Bastakoty
Glucose cycling, the dynamic equilibrium between glucose-6-phosphate (G6P) and glucose, is important for maintaining a constant concentration of glucose in the bloodstream.
There has been a debate about whether the activity of the enzyme G6PC2, which converts G6P to glucose in the beta cells of the pancreatic islets, is high enough to affect glucose cycling and hence glucose-stimulated insulin secretion. That, in turn, determines fasting blood glucose levels.
Using a novel stable isotope method, Jamey Young, Ph.D., Richard O’Brien, Ph.D., and colleagues show much higher levels of glucose cycling in islets than previously reported. This explains an earlier observation by the O’Brien group that deletion of the gene for G6pc2 in mice enhances glucose-stimulated insulin secretion.
It also explains why inter-individual variations (called single nucleotide polymorphisms or SNPs) in G6PC2 are the most important determinants of differences in fasting blood glucose among people.
The study, which was published online Dec. 31 in the journal Diabetes, highlights an important metabolic regulator that warrants further studies.
The study resulted from collaboration between Young and his colleagues in the Department of Chemical and Biomolecular Engineering in the School of Engineering, and O’Brien and his colleagues in the Department of Molecular Physiology and Biophysics in the School of Medicine.
First and second authors, Martha Wall and Lynley Pound, are graduate students in Chemical and Biomolecular Engineering, and Molecular Physiology and Biophysics, respectively. They were supported by a National Institutes of Health (NIH) grant (DK007563) to the Vanderbilt Molecular Endocrinology Training Program.
Other NIH grants supported the research: DK092589 and DK020593.
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