JH Scientists Identify Critical Link In Type 2 Diabetes
Scientists from Johns Hopkins Medicine reported that they have identified an unlikely but critical link in the development of Type 2 diabetes.
Diabetes is a leading cause of heart disease and stroke. The disease affects almost 26 million people in the U.S. alone.
It is well known that the two hormones glucagon and insulin work together to maintain healthy blood sugar levels in the body. Glucagon stimulates sugar secretion while insulin stimulates absorption of the secreted sugar. The disease typically develops when glucagon and insulin hormones are off balance.
The Johns Hopkins scientists found that the hormone kisspeptitn-1 plays a crucial part by seemingly carrying out glucagon commands and interfering with insulin production.
“Our findings suggest that glucagon issues the command, but K1 carries out the orders, and in doing, so it appears to be the very cause of the declining insulin secretion seen in type 2 diabetes,” said Mehboob Hussain, endocrinologist and metabolism expert at the Johns Hopkins Children’s Center and lead investigator in the study. “Glucagon and insulin alone never really made complete sense. There was always something missing and, we feel, kisspeptitn-1 is a very good candidate to be that missing part. All our findings point in this direction.”
The discovery of the third hormone may prove to be a long missing link in understanding the origin of Type 2 diabetes. “Sugar provides critical fuel when an animal enters combat or is trying to run away from a predator. The high levels of insulin after a meal can cause dangerously low levels of blood sugar, which would render the animal weak and vulnerable. So our theory is that K1 is a defense mechanism that halts the sugar-reducing effects of insulin in such life-and-death situations,” said Hussain.
The researchers are now designing therapies to block kisspeptitn-1 from accessing insulin-producing cells in the pancreas. The results of the scientists’ research were published in the journal Cell Metabolism.