A potential drug target for the treatment of Type 2 Diabetes mellitus was discovered by a team of scientists led by Satish Kumar, Chief Scientist and Group Leader at Centre for Cellular and Molecular Biology (CCMB). The findings were published in the journal Diabetologia on 23 November 2014.
The team of scientists genetically deleted Wdr13 gene in a mouse afflicted severely with Type 2 diabetes and demonstrated that the absence of the gene corrects the pathology of the disease. It was found that the destruction of beta cells in severely diabetic model would be corrected with removal of the gene.
The deletion of the gene not only increased insulin production, but also showed better glucose clearance and reduced inflammation and triglycerides.
The significant reduction was noticed in the expression of genes involved in inflammation of pancreas, liver and adipose tissue.
In a previous study, the team had created a mutant mouse strain lacking Wdr13 gene and showed that the mutant mice had increased islet mass due to beta cells proliferation leading to enhanced insulin production.
Conclusion of the study
This study provides evidence that loss of WDR13 protein in the mouse model of diabetes is beneficial. Based on these findings, WDR13 may be a potential drug target for ameliorating hyperglycaemia and inflammation in diabetic conditions.
Type 2 Diabetes mellitus
Type 2 Diabetes mellitus is a metabolic disorder that is characterized by hyperglycemia (high blood sugar) in the context of insulin resistance and relative lack of insulin.
The classic symptoms are excess thirst, frequent urination, and constant hunger. Type 2 diabetes makes up about 90 percent of cases of diabetes. Obesity is thought to be the primary cause of type 2 diabetes in people who are genetically predisposed to the disease.
With diabetes emerging as a global epidemic and around 350 million suffering from the condition, the WHO has projected that deaths due to diabetes would double by 2030 and it would be the seventh leading cause of death by then.
When: 23 November 2014
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