- The Washington Times - Thursday, March 1, 2007

Insulin, a hormone known primarily for regulating blood-sugar levels, also seems to enhance significantly the healing of wounds, new research shows.

The finding by scientists at the University of California at Riverside could help explain why people with diabetes, a disease caused by inadequate production or utilization of insulin, are often frustrated by slow healing.

It also could lead to new treatments for people who suffer from poor healing — not only diabetics but also millions of patients with impaired mobility, said Manuela Martins-Green, a professor of cell biology at the university, who led the research.

So insulin or drugs that mimic the function of insulin “look promising for healing human wounds,” Ms. Martins-Green said.

She presented the results of her research at a December conference of the American Society for Cell Biology in San Diego. The society selected Ms. Martins-Green’s insulin study as among the 13 “most novel and newsworthy” research discoveries of the past year.

In the study, Ms. Martins-Green and her colleagues initially applied an insulin solution directly to skin wounds in rats and found that the wounds healed faster than those not treated with insulin.

When treated topically with insulin, surface cells in the rats’ epidermis covered the wound more quickly and cells in the dermis, the deeper part of the rats’ skin, were faster in rebuilding blood vessels.

The scientists also had encouraging results in follow-up studies of human skin cells in culture. They explored the molecular effect of topical insulin on keratinocytes, the cells that regenerate the epidermis after wounding, as well as on microvascular endothelial cells, which restore blood flow.

They found that insulin stimulates human keratinocytes in culture to proliferate and migrate.

“The epithelial cells not only move faster but also grow faster; therefore, covering the wound faster, which is important to protect it from infection,’ Ms. Martins-Green said.

She added that cultured human microvascular endothelial cells treated with insulin “move faster but do not divide faster, meaning they can presumably make microvessels more effectively.”

The investigators said the insulin works by “switching on cellular signaling proteins called kinases (specifically Src, PI3K and Akt) and a protein (SREBP) that binds elements in DNA that regulate production of cholesterol and its relatives.”

Asked why this is useful, Ms. Martins-Green said cells “need cholesterol and other lipids to make membranes, and this is very important during cell movement and growth.”

“When we know which cells respond to insulin and which molecules are involved, we may be able to develop ways in which we can make insulin work even better or find ways in which more affordable molecules that mimic these functions of insulin can be developed to treat people who suffer from poor healing.”

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