Results from what the New York Times calls “an explosion of new research,” indicated that the cause of diabetes and type 2 diabetes is more complex that previously thought.
With 73,000 deaths a year, diabetes is the fifth leading cause of death in United States. For decades, the medical profession has regarded diabetes – or the body’s inability to regulate glucose – as a failure in communication between the pancreas, the liver, muscle and fat.
Getting Down to the Bare Bones
However, working with mice, Dr. Gerard Karsenty of Columbia University has recently found that a hormone released from bone may help regulate blood glucose. In other studies, researchers have demonstrated that signals from the immune system, the brain and the gut play also critical roles in controlling glucose and lipid metabolism. (The findings are mainly relevant to type 2 diabetes.)
When Dr. Karsenty first dislosed the findings at a conference, the scientists in attendance “were overwhelmed by the potential implications,” said Dr. Saul Malozowski, senior adviser for endocrine physiology research at the National Institute of Diabetes and Digestive and Kidney Diseases. “It was coming from left field. People thought, ‘Oof, this is really new.’”
Elevated blood sugar is the hallmark of diabetes, but now it seems that the reasons underlying abnormal sugar levels “differ tremendously from person to person,” said Dr. Robert A. Rizza, a professor at the Mayo Clinic College of Medicine. “Rather than giving everyone the same drug,” Rizza adds, if doctors can ascertain which signals are involved in a particular case, treatment can be tailored to the individual.
(Except from the October 16th NY Times article)
In previous work, Dr. Karsenty had shown that leptin, a hormone produced by fat, is an important regulator of bone metabolism. In this work, he tested the idea that the conversation was a two-way street. “We hypothesized that if fat regulates bone, bone in essence must regulate fat,” he said.
Working with mice, [Karsenty] found that a previously known substance called osteocalcin, which is produced by bone, acted by signaling fat cells as well as the pancreas. Dr. Karsenty found that in mice prone to type 2 diabetes, an increase in osteocalcin addressed the twin problems of insulin resistance and low insulin production. That is, it made the mice more sensitive to insulin and it increased their insulin production, thus bringing their blood sugar down. As a bonus, it also made obese mice less fat. A deficiency in osteocalcin could also turn out to be a cause of type 2 diabetes, Dr. Karsenty said.
Another recent suspect in glucose regulation is the immune system. In 2003, researchers from two laboratories found that fat tissue from obese mice contained an abnormally large number of macrophages, immune cells that contribute to inflammation.
For a long time, inflammation has been suspected in some what to insulin resistance, which precedes nearly all cases of type 2 diabetes. In fact, around the turn of the century, aspirin was given to diabetes patients regularly. In recent years, the relationship of obesity, inflammation and insulin resistance has become a hot topic of reseach.
“Certain cellular anti-inflammatory proteins may now be important new targets for drug discovery for diabetes treatment,” said Dr. Jerrold M. Olefsky of the University of California, San Diego, School of Medicine.
With new understanding comes new hope for different and more effective treatments of one of America’s deadliest diseases.