Nov. 12, 99 -- A Brigham Young University study suggests one possible cause of type II diabetes, shows how exercise combats the disease and raises hope for eventually developing new drugs for diabetics unable to exercise.
Brigham Young University physiologist Will Winder said his research "helps us understand a little bit more about the mechanisms of the beneficial effects of exercise. It emphasizes the importance of exercising in individuals who have diabetes or a history of diabetes in their families."
The study by Winder and BYU zoology graduate students Burton Holmes and Emily Kurth-Kraczek was published today in the Journal of Applied Physiology.
A commentary by the journal's editors said the study gives new insight into how muscles normally absorb glucose in the blood, a process that goes awry in diabetes, allowing high blood-sugar levels to damage the heart, kidneys, eyes and other organs.
"We don't understand the causes of diabetes," said Dr. Don McClain, director of endocrinology and diabetes at the University of Utah. "A full understanding of how (muscle) cells control glucose uptake is clearly going to be important for understanding and treating this disease."
Type II diabetes, also known as adult-onset or non-insulin-dependent diabetes, afflicts 16 million Americans. It is treated by a combination of regular exercise, weight loss and a reduced-carbohydrate diet. Forty percent of the patients receive insulin injections.
Exercise helps because it stimulates the muscles to absorb glucose from blood. The research points the way for designing new drugs that mimic the effects of physical activity in diabetics unable to get adequate exercise because they are paralyzed or grossly obese, Winder said. He predicted development of such drugs will take at least five years.
Winder's study suggests, but does not prove, that for at least some type II diabetics, the muscles are unable to absorb enough glucose from blood because of a deficiency of the enzyme AMPK.
Previous studies showed AICAR, a drug that is similar to a natural substance produced when muscles contract during exercise, stimulates absorption of glucose by the rats' muscles. Those studies also suggested AICAR injections stimulate the burning of fat.
Other research showed exercise increases levels of the protein GLUT-4, which carries glucose into muscles. In type II diabetics, GLUT-4 fails to carry enough glucose into muscles.
Winder and his colleagues injected physically inactive rats for five days with AICAR and it increased levels of GLUT-4.
The new study suggests that prolonged use of AICAR triggers the AMPK enzyme to turn on a gene that produces more GLUT-4 so glucose is removed from blood and goes into muscles.
That is "a major finding because it gives us both an explanation for how exercise increases glucose uptake in muscle and a possible pharmacological treatment for diabetes," said Lynis Dohm of East Carolina University in Greenville, N.C.
AICAR itself cannot be used to treat humans because it is too toxic and would cause liver damage within days, Winder said. He said the eventual hope is to find a drug that acts like AICA.
The entire report will be posted at:
JAP Online
For more on Diabetes and how it is effecting Utahn's:
Diabetes Up In Utah
