Insulin, a hormone well known for its role in diabetes, may also lie at the root of another common but serious medical condition: age-related muscle loss, known as sarcopenia.
In fact, sarcopenia is in part due to muscle tissue not responding properly to insulin, according to a new study in the journal Diabetologia.
The researchers found that an increased dose of insulin restored the muscle-building processes that tend to deteriorate with old age. Unfortunately, insulin cannot be used as a treatment for sarcopenia due to its toxic effects in high concentrations. Still, the new results help clarify its role in muscle growth and could serve as a basis for future treatments. Sarcopenia affects 24 percent of adults between 45 and 70 years old, and half of people over 80.
“The new finding serves as a proof of concept,” said Elena Volpi, a researcher at the University of Texas Medical Branch at Galveston. “It confirms our belief that the age-related decline in muscle growth is a true case of insulin resistance, which is an important piece to the larger puzzle of treating sarcopenia.”
The Texas team’s results are “an exciting finding,” said Chhanda Dutta, chief of the Clinical Gerontology Branch at the National Institute on Aging. “It opens a new avenue towards a new therapeutic target in treating this condition.” Dutta noted, however, that there are other promising ways to treat sarcopenia as well.
“There are many different pathways that promote muscle growth and function,” Dutta said. “Insulin function is only one of them.”
In type 2 diabetes, insulin resistance — a condition in which normal amounts of insulin fail to produce a typical insulin response in the body — prevents the body from storing sugar molecules in cells, eventually leading to high blood sugar. Test subjects in the Texas study, however, had normal blood sugar levels. This suggests the insulin resistance seen in elderly people is not a matter of sugar control.
Instead, the researchers believe insulin resistance seen in old age results from changes in blood flow. In addition to helping store sugar, insulin acts as a signal for the dilation of blood vessels to increase blood flow and deliver nutrients to muscle tissue. When capillaries fail to respond to these signals, blood flow slows down and muscle growth decreases.
To assess insulin’s role in regenerating muscle, Volpi and her colleagues gave 14 non-diabetic elderly patients insulin injections and later took muscle biopsies. They could then measure protein levels to see how much muscle grew. Two injections were given to each patient — one equal to the amount of insulin normally released after eating a meal, and one double that quantity. Both injections were administered at specific rates to avoid reaching toxic levels of blood insulin.
The subjects that received a higher dose of insulin showed significantly greater muscle growth than those who received the lower one, indicating that the aging body has a type of resistance to normal amounts of insulin.
Better treatments for sarcopenia would not only help millions of people, but also save billions of dollars. In fact, a 2003 Tufts University study reported that a 10 percent decrease in sarcopenia prevalence could save the U.S. health care system $1.1 billion per year. Volpi explains that the cost is high because sarcopenia causes “crippling disabilities that affect everyday activities like climbing stairs or walking to a store. It is the number one reason people go to nursing homes.”
Volpi and her team are already exploring possible therapies that capitalize on her discoveries about insulin’s important role in sarcopenia. For example, they are currently investigating drugs that increase the dilation of blood vessels to help restore muscle growth.
“Though we can’t turn back the clock on aging, we can slow the downward trajectory of physical function,” said Volpi. “Our main goal is to help people age gracefully.”