(17-03-06) Insulin key to heart attack survival

WASHINGTON DC (myDNA News)

For people with Type 2 diabetes, the death rate from a first heart attack is two to three times the death rate for people without diabetes.
There's no question that diabetes and heart disease make a deadly combination. But doctors still aren't sure why.
New research from the Harvard Medical School-affiliated Joslin Diabetes Center in Boston may provide the answer.
Scientists have known for some time that one way heart disease patients live with their condition is by generating new blood vessel growth in the heart to bypass clogged coronary arteries. This blood vessel growth is stimulated by the release of a substance known as vascular endothelial growth factor (VEGF) from heart cells, and it aids in keeping the heart muscle supplied with oxygen-enriched blood.
"We have long recognized that in patients with diabetes, this blood vessel formation is not as robust as in people without diabetes," said George L. King, M.D., lead researcher of the Joslin center study, in a statement.
The researchers conducted experiments using two types of rats: Zucker rats, which are genetically obese and tend to develop Type 2 diabetes, and muscle-specific insulin receptor knockout (MIKRO) mice, which lack insulin receptors in their hearts and, therefore, can't respond to the insulin hormone.
Scientists found that diabetic rats exhibited relatively little cardiac blood vessel growth and less VEGF production compared to non-diabetic rats. This is due to a lack of response to insulin.
Insulin is the substance naturally produced by the body to aid in the uptake of sugar from the bloodstream. In Type 2 diabetics, the problem is not so much a lack of insulin as it is a lack of response to insulin.
Researchers found that this same insulin is responsible for triggering the production of VEGF and new blood vessel growth in heart cells. Since Type 2 diabetics aren't sensitive to the effects of insulin, the signal to produce VEGF is never heard. Consequently, blocked coronary arteries are not bypassed with new blood vessel formation, and premature death from a heart attack is more likely.
"We found that when insulin in the bloodstream binds with the insulin receptors on the outer membranes of heart cells, it activates the PI3K/AKT pathway, which is the pathway that produces VEFG," King said. "We also found that this response is blunted in patients with insulin resistance, a major cause of Type 2 diabetes that makes it harder for cells to use insulin. The heart produces less VEGF and forms fewer new blood vessels."
As predicted, the MIKRO mice, which lack insulin receptors in their hearts, showed lower levels of VEGF production and fewer new blood vessels, confirming that the insulin receptor is crucial in this process.
King and his colleagues hope their research will forge the way for new strategies to combat heart disease in diabetics.
"This study suggests that if we improve VEGF and insulin action in the heart, then the heart will be able to produce more new blood vessels," King said. "Scientists have already established several ways of improving insulin actions in general, so once we figure out which is best for the heart muscle, we should be able to decrease the mortality rate."

Source: www.mydna.com/health

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