There’s a term in diabetes research that most of us vaguely recognize: metabolic syndrome. “Metabolic syndrome” is the complex collection of conditions — things like excess body fat, high blood pressure, high cholesterol, and abnormal blood sugar levels — which are increasingly recognized as an indicator of a heightened risk of heart disease, stroke, diabetes, and other chronic diseases. Diabetes is the most commonly cited example of metabolic syndrome.
It turns out that there may be a possible compound in fact that triggers the metabolic syndrome. A certain protein, called the Insulin-like Growth Factor 1 receptor (ILGR1R), that is typically found in mammals is present in humans as well. In clinical trials, we have shown ILGR1R to be key in facilitating the release of insulin from the pancreas.
Of course, it’s not a new discovery. Like many drugs on the market, insulin is controlled by ILGR1R. It is also a target of the body’s immune system.
Interestingly, people with Type 1 diabetes have much less of ILGR1R than people without Type 1 diabetes. In the general population, half of men with Type 1 diabetes have more than 85 percent of the gene’s maximum expression. In the patients we treat, just 25 percent of them have that much ILGR1R.
Perhaps why the disease’s progression happens more slowly in people with Type 1 diabetes? Perhaps the key may be the antibody to ILGR1R, which is commonly used by doctors to target autoimmune disease.
In all of the clinical trials, it wasn’t the ILGR1R that was the treatment, but rather the immune system itself.
A lot of the data thus far has been about people with Type 1 diabetes who had a deficiency in ILGR1R, and not at all about people with it who had normal levels. The possibility of interfering with autoimmune disease should make people with Type 1 diabetes curious.
What, if anything, should be done about it? What else could we target? What is the future of insulin-producing cells? Is this really a panacea?
The road to new treatments may be long and difficult, but research into ILGR1R offers reasons to be hopeful. It’s easy to see how this will help some patients with Type 1 diabetes. In animal models of heart disease, pancreatic β cell transplantation has been shown to slow the course of diabetes in diabetic animals.
It’s not clear if ILGR1R will also work in people with Type 1 diabetes, but we can find out by testing it in another animal model, the type 1 mouse, whose host gene for insulin plays a key role in diabetics.
B. Joseph W. Kozlowski is the Dana Farber Program Director, immunology and metabolism at Brigham and Women’s Hospital and Harvard Medical School. Dr. Benjamin Leventhal is a member of the National Institutes of Health Scientific Advisory Committee on Diabetes. Mr. Kozlowski holds a National Science Foundation’s Investigator in Aging Award (SAR), and Mr. Leventhal holds a Memorial Sloan Kettering Investigator in Medicine Award.