Type-2 diabetes (T2D) is a complex metabolic disease associated with obesity and insulin resistance due to pancreatic beta-cell dysfunction.
‘Over expression of the gene RCAN1 is responsible for pancreatic beta-cell dysfunction, resulting in insulin resistance among people with type 2 diabetes and down syndrome.’
Many individuals with Down syndrome experience lower insulin secretion, mitochondrial dysfunction and increased oxidative stress in the insulin-producing beta cells of the pancreas.
These same conditions also appear in people with Type 2 diabetes.
In experiments with mice, the researchers found that the over expression of the gene RCAN1 can cause these problems common in both the disorders.
The findings, detailed in the journal PLOS Genetics
, suggest that this gene may be playing a lead role in development of Type-2 diabetes in the general population.
For the study, the team led by Damien Keating, professor at Flinders University in Australia, used four mouse models, two with high blood sugar and two without to identify genes duplicated in Down syndrome that contributed to problems with insulin secretion.
They narrowed down the list by comparing it to genes over expressed in beta cells from humans with Type-2 diabetes.