By deactivating a particular gene, scientists have been able to regulate the mass of insulin-producing beta cells in the pancreas of experimental mice1. The finding could have far reaching implications in the management of diabetes, which is directly linked to the amount of pancreatic beta cells in an individual.
The researchers (from left) Shalu Singh, D. Partha Sarathi, Vijay Pratap Singh with a transgenic mouse and Satish Kumar. Source: CCMB
The team knocked out the gene through 'gene targeting in mouse embryonic stem cells'. This gene encodes a protein which is a member of the WD-repeat protein family.
The CCMB scientists found that in the absence of Wdr13, the mice had higher pancreatic islet mass and blood serum insulin levels. As a result of the increased islet mass, the knockout mice had better glucose clearance as compared to their counterparts with the gene.
"Increase in islet mass in the knockout mice is a result of higher beta cell proliferation, which leads to more pancreatic islet mass suggesting the role of Wdr13 gene in cell proliferation," Kumar told Nature India .
Given higher insulin levels, better glucose clearance and better beta cell proliferation in Wdr13 gene-deficient mice, the protein may be explored as a potential drug target to treat poor glucose metabolism in diabetes, says Vijay Pratap Singh, the lead author of the research paper.
The researchers are presently working to find answers to certain limitations of this work. "These mutant mice also develop mild obesity in an age dependent manner. It is not yet clear whether this obesity is a consequence of high random insulin levels or a reflection of another additional biological function of this gene in fat metabolism," Kumar says.
The complete absence of Wdr13 gene may also result in tumors with advancing age. "Therefore, the challenge would be to discover suitable therapeutic molecules that may reduce the expression or function of Wdr13 gene without grossly deregulating cell proliferation," he adds.
