Friday I went to a diabetes science day at the University of California, San Francisco. The speakers were hotshot researchers doing genetic studies on diabetes, mostly in mice. I really don’t know what results will come of their work, but they did have some interesting stories.
Michael German, MD, is working on therapies for revitalizing beta cells. He explained that beta cells have been regrown successfully in mice. Beta cells can grow in the intestines, not only in the pancreas. Unfortunately, the regrown cells have not worked well. They’re there, they can make insulin, but they don’t sense glucose, so they don’t help much.
The scientists are looking to find the genetic causes of diabetes as a pathway to either drug treatments or stem cell treatments. I advise not holding your breath while you wait. Immune system expert Christophe Benoist, MD, PhD, said that about 2,000 genes are suspected of playing roles in diabetes. That’s right, 2,000. He said probably no one gene will prove too important; it will be combinations of genes.
One way these guys explore the genes is with “knockout mice.” You take a mouse embryo and “knock out,” or inactivate, a particular gene. Then the mouse lives without the protein that gene would have produced. You can see what difference that particular protein makes. Many of these mice are so-called “non-obese diabetic” or NOD mice bred to have an illness like Type 1.
But there are so many genes, and their interactions with each other and with the environment are so complex, that I think it will be a long time before anything practical comes of this work. For now, I’m afraid they’re just bothering mice.
At one point, Dr. German categorically stated that “All Type 2s have beta cell damage.” He said that no matter how much insulin resistance there is, normal beta cells can overcome it. So Type 2 is a genetically-based illness, just like Type 1 is.
Suneil Kolliwad, MD, is studying the relationship between inflammation and insulin resistance. He reported research that visceral fat (fat around the abdominal organs) seems to promote inflammation and insulin resistance, but subcutaneous fat (the fat we can see) does not. There is no relationship between subcutaneous fat and the onset of metabolic illness such as diabetes, he said.
I came away from the day thinking that all types of diabetes are the result of unhealthy environments, genetic damage, or both. Fatness doesn’t play nearly as big a role as we think, and may play no role at all (although that is not certain).
Lots of drug companies and meter makers had tables at the event, promoting medicines and pumps. This was good, because drug company sponsorship usually comes with good food, in this case breakfast and lunch. Yummy, and presumably healthy, breakfast sandwiches!
I received literature from several of the pharmaceutical representatives. One medicine I came across had a one-year success rate of only 22%. People could potentially have to take the drug long-term, but that might not be so good, because it has been linked to suicide in some cases. Medicines are not always the answer.
