NEW YORK A peptide, along with its receptor, that is released when the body responds to stress and causes insulin secretion from the pancreas may influence diabetes, researchers found.
These findings, which will be published in this week's edition of the Proceedings of the National Academy of Sciences, may provide new insights into diabetes, particularly Type 1, as well as suggest novel targets for drug intervention. Researchers at the Salk Institute for Biological Studies found that corticotropin-releasing factor jump starts the stress process along the hypothalamus-pituitary-adrenal axis. The researchers also noted that CRF promotes the division of the insulin-producing beta cells in the pancreas. CRF, in line with its receptor, CRFR1, has long been known as key to the body's response to various forms of stress, but the pair is also involved in many more processes, including a number with direct ties to metabolism.
The pancreas is both an exocrine gland, producing enzymes that are secreted into the gut to help digest food, and an endocrine gland, secreting a cocktail of hormones, including insulin, which is manufactured by beta cells that reside in endocrine islets within the "sea" of exocrine tissue.
"We found that beta cells in the pancreas actually express the CRFR1 receptor," explained Mark O. Huising, Ph.D., a postdoctoral fellow in the Clayton Foundation Laboratories and lead author of the study. "And once we had established the presence of CRFR1 in the islet, we started filling in the blanks, trying to learn as much about pancreatic CRFR1 as we could.
"The thinking is that Type 1 diabetic patients usually have a few beta cells left in their pancreas, so those remaining beta cells, though not enough to control glucose levels, may seed a population of regenerating beta cells," Huising added.
"Anything we can find out that will drive proliferation or the division of beta cells is very interesting, and being able to stimulate beta cells to divide a little faster may be part of a solution that may ultimately, hopefully, allow management of Type 1 diabetes, " co-author Wylie Vale said. "But because it is an autoimmune condition, making the cells divide won't be enough. That is why researchers are working hard to solve the problem of destruction of beta cells."