Mount Sinai Hospital Scientist Wins World’s Largest Prize for Diabetes Research

Dr. Daniel Drucker, Senior Investigator at Mount Sinai Hospital’s Lunenfeld-Tanenbaum Research Institute, is the recipient of the world’s most valuable award for diabetes research, the 2014 Manpei Suzuki International Prize. The award, which was announced today by the Manpei Suzuki Diabetes Foundation in Tokyo, recognizes Dr. Drucker’s research in the area of gut hormones and how they control glucose and body weight, which have led to the development of two new classes of therapies for the treatment of type 2 diabetes.

“The 2014 Manpei Suzuki International Prize brings tremendous international recognition to the work that we have done for over 25 years, with my trainees and fellow scientists, both at the Lunenfeld-Tanenbaum Research Institute and at the University of Toronto,” says Dr. Drucker, who is also Professor of Medicine in the Division of Endocrinology at the University of Toronto.“We are honoured that our science has helped in the development of new medications for patients with diabetes, and delighted to have our research achievements recognized by our esteemed colleagues in Japan.”

Read more…

New Pathway for Type 2 Diabetes Research

Scientists at the Children’s Hospital of Eastern Ontario (CHEO) Research Institute have discovered a cellular pathway that is responsible for keeping blood sugar levels low in obese or pre-diabetic people, and may prevent the onset of Type 2 diabetes. The discovery published this month in a leading journal Nature Cell Biology.

Following a meal, beta cells found in islets of the pancreas secrete insulin that helps to store food energy for future use. The inability of islet beta cells to produce enough insulin leads to diabetes. Unlike other research that has focused on how to replicate beta cells, this study focused on how to make pre-existing beta cells more functional, or better at secreting insulin.

The research team, led by Canada Research Chair Dr. Robert Screaton, senior scientist at the CHEO Research Institute and associate professor at the University of Ottawa, started with a gene “knockout” strategy to remove a protein called SIK2 from all beta cells. They found that mice without SIK2 secrete less insulin during feeding because they fail to turn off a switch protein called p35, which prevents insulin secretion when blood sugar levels are low. The team also found that SIK2 works together with the protein PJA2 to turn off p35.

“We were very excited when we found obese animals had three times the amount of SIK2 in their beta cells, meaning they were working harder to compensate for high blood sugar by turning up SIK2,” said Dr. Screaton. “Diabetic mice have lost this ability to turn up SIK2 and compensation is lost. The SIK2-p35-PJA2 pathway provides us with new targets to try and improve beta cell functionality to prevent and treat Type 2 diabetes.”

Thanks to CHEO Research Institute for contributing this story.

Stem Cell Therapy Offers New Hope for Type 2 Diabetes Patients

For people at risk of the devastating ulcers and gangrene associated with type 2 diabetes, stem cell therapy could offer some hope for a new, effective therapy, according to research just published from Mount Sinai Hospital.

In the study, damaged muscle and blood vessels in mice with peripheral vascular disease showed “substantial” rapid healing after the injection of human umbilical cord blood stem cells. The research was lead by Associate Scientist Dr. Ian Rogers (photo) of the Lunenfeld-Tanenbaum Research Institute at Mount Sinai. It was published online (January 18, 2014) in Stem Cell Review and Report.

Read more…

New function for an old gene leads Mount Sinai researchers to possible therapy for kidney disease

A new finding by Mount Sinai Hospital researchers has the potential to slow the progression of kidney disease, one of the most serious complications for patients with diabetes. Researchers have found a protein associated with kidney disease which potentially can be targeted with drugs in early stages of the disease to prevent end-stage kidney failure.

Published August 13, 2013 in Diabetes, the journal of the American Diabetes Association, the study was led by Dr. George Fantus, an endocrinologist at Mount Sinai Hospital’s Leadership Sinai Centre for Diabetes and a scientist at the Lunenfeld-Tanenbaum Research Institute. The research team discovered that a previously known protein named SRC (pronounced “sark”) is abnormally active in kidney cells that show early signs of this disease. The inappropriately active protein can lead to the build up of scar tissue, which diminishes the kidneys’ filtering ability to eliminate waste and excess fluid from the body.

Read more …

Could turning on a gene prevent diabetes?

Type 2 diabetes accounts for 90 % of cases of diabetes around the world, afflicting 2.5 million Canadians and costing over 15 billion dollars a year in Canada. It is a severe health condition which makes body cells incapable of taking up and using sugar. Dr. Alexey Pshezhetsky of the Sainte-Justine University Hospital Research Center, affiliated with the University of Montreal, has discovered that the resistance to insulin seen in type 2 diabetics is caused partly by the lack of a protein that has not previously been associated with diabetes. This breakthrough could potentially help to prevent diabetes.

Read more…