Glutamate dehydrogenase, insulin secretion, and type 2 diabetes: a new means to protect the pancreatic β-cell?
- Unit of Molecular Metabolism, Department of Clinical Sciences in Malmö, Lund University Diabetes Centre, Clinical Research Center 91:11, SE-205 02, Malmö, Sweden
- (Correspondence should be addressed to H Mulder; Email: hindrik.mulder{at}med.lu.se)
Abstract
In this issue of Journal of Endocrinology, Dr Han and colleagues report a protective effect of the glutamate dehydrogenase activator 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) under diabetes-like conditions that impair β-cell function in both a pancreatic β-cell line and db/db mice. Based on these observations, the authors suggest that BCH could serve as a novel treatment modality in type 2 diabetes. The present commentary discusses the importance of the findings. Some additional questions are raised, which may be addressed in future investigations, as there is some concern regarding the BCH treatment of β-cell failure.
- Received in final form 6 January 2012
- Accepted 9 January 2012
- Made available online as an Accepted Preprint 9 January 2012
- © 2012 Society for Endocrinology
