Are you a journalist? Please sign up here for our press releases
Subscribe to our monthly newsletter:
Share
Although diabetes is the Western world's most common metabolic disease, adult-onset diabetes, which affects 90% of diabetes sufferers, is still poorly understood. Unlike the rarer juvenile condition in which the body destroys its own insulin-producing cells, in adult-onset, or Type II diabetes, insulin production is mysteriously impaired.
A new study helps explain why adult-onset diabetics don't produce enough insulin. As reported in the September issue of Diabetes , the Weizmann Institute's Prof. Yoram Groner, Dr. Hilla Knobler of Kaplan Hospital and Weizmann doctoral students Yael Weiss and Mira Peled studied PFK, a key enzyme in glucose metabolism. When glucose levels rise, PFK is believed to serve as a messenger, directing the pancreas to produce insulin. However, as Knobler and Groner have discovered, imbalance in the composition of PFK may cause this directive to be garbled, interfering with insulin secretion and causing a condition similar to Type-II diabetes.
PFK consists of three different sub-units. The researchers engineered mice with abnormally high levels of the sub-unit known as PFK-L, and found that such mice develop symptoms of Type II diabetes. The results, which need to be confirmed in human studies, suggest that PFK imbalance may be responsible for impaired insulin production in adult-onset diabetics.
If the findings are confirmed, this may explain why Down syndrome patients have an increased incidence of diabetes. The gene for PFK-L is found on human chromosome 21 - the same chromosome that appears in three, rather than two copies in patients with Down syndrome. The presence of an additional gene for PFK-L may cause over-production of this enzyme sub-unit, causing an imbalance which is responsible for the disease.
This study comes four years after a team of French and American scientists uncovered a genetic mutation which contributes to the appearance of Type II diabetes in younger patients. However, this mutation explains the disease in less than 10 percent of cases. This new study indicates the possibility of another genetic defect which can cause Type II diabetes.
As scientists study the genetic underpinnings of adult-onset diabetes, it may one day be possible to parley this information into screening, which would detect a pre-disposition for the condition in patients who are not yet sick. Moreover, as new genetic technologies are developed, it may become possible to cure genetic defects which lead to diabetes, rather than simply treating its symptoms.
Prof. Groner holds the Barnet Berris Chair of Cancer Research. The research was supported by grants from the U.S. National Institutes of Health, the Fritz Thyssen Stiftung, Germany, the Weizmann Institute's Leo and Julie Forchheimer Center for Molecular Genetics, and the Shapell Family Biomedical Research Foundation, Los Angeles, California.
The Weizmann Institute of Science is a major center of scientific research and graduate study located in Rehovot, Israel.
A new study helps explain why adult-onset diabetics don't produce enough insulin. As reported in the September issue of Diabetes , the Weizmann Institute's Prof. Yoram Groner, Dr. Hilla Knobler of Kaplan Hospital and Weizmann doctoral students Yael Weiss and Mira Peled studied PFK, a key enzyme in glucose metabolism. When glucose levels rise, PFK is believed to serve as a messenger, directing the pancreas to produce insulin. However, as Knobler and Groner have discovered, imbalance in the composition of PFK may cause this directive to be garbled, interfering with insulin secretion and causing a condition similar to Type-II diabetes.
PFK consists of three different sub-units. The researchers engineered mice with abnormally high levels of the sub-unit known as PFK-L, and found that such mice develop symptoms of Type II diabetes. The results, which need to be confirmed in human studies, suggest that PFK imbalance may be responsible for impaired insulin production in adult-onset diabetics.
If the findings are confirmed, this may explain why Down syndrome patients have an increased incidence of diabetes. The gene for PFK-L is found on human chromosome 21 - the same chromosome that appears in three, rather than two copies in patients with Down syndrome. The presence of an additional gene for PFK-L may cause over-production of this enzyme sub-unit, causing an imbalance which is responsible for the disease.
This study comes four years after a team of French and American scientists uncovered a genetic mutation which contributes to the appearance of Type II diabetes in younger patients. However, this mutation explains the disease in less than 10 percent of cases. This new study indicates the possibility of another genetic defect which can cause Type II diabetes.
As scientists study the genetic underpinnings of adult-onset diabetes, it may one day be possible to parley this information into screening, which would detect a pre-disposition for the condition in patients who are not yet sick. Moreover, as new genetic technologies are developed, it may become possible to cure genetic defects which lead to diabetes, rather than simply treating its symptoms.
Prof. Groner holds the Barnet Berris Chair of Cancer Research. The research was supported by grants from the U.S. National Institutes of Health, the Fritz Thyssen Stiftung, Germany, the Weizmann Institute's Leo and Julie Forchheimer Center for Molecular Genetics, and the Shapell Family Biomedical Research Foundation, Los Angeles, California.
The Weizmann Institute of Science is a major center of scientific research and graduate study located in Rehovot, Israel.
Share
