2023-04-30 13:02:30
Insulin is an essential hormone and not enough can be deadly, but too much can be just as harmful.
By: isbelia farias
A century of research has made it possible to understand how the insulin and what happens when it is missing, but how do you prevent hyperreactivity to the insulinwhich is potentially fatal, remains a lingering mystery.
The insulin is an essential treatment for type 1 diabetes and often type 2 diabetes as well. Approximately 8.4 million Americans use insulinaccording to the American Diabetes Association.
In a new study, published in the April 20, 2023, online issue of Cell Metabolism , a team of scientists at the University of California San Diego School of Medicine, along with colleagues elsewhere, describe a key player in the defense mechanism that protects us once morest excess insulin in the body.
“Although the insulin It is one of the most essential hormones, the insufficiency of which can cause death, too much insulin it can also be fatal,” said study lead author Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology at the UC San Diego School of Medicine.
“While our body finely tunes the production of insulinpatients who are treated with insulin or drugs that stimulate the secretion of insulin often experience hypoglycemia, a condition that if unrecognized and untreated can lead to seizures, coma, and even death, collectively defining a condition called insulin shock.”
Hypoglycemia (low blood sugar) is a major cause of death among people with diabetes.
Diabetic coma or insulin shock
In the new study, Karin, first author Li Gu, PhD, a postdoctoral fellow in Karin’s lab, and colleagues describe “the body’s natural defense or safety valve” that reduces the risk of shock from insulin.
That valve is a metabolic enzyme called fructose-1,6-bisphosphate phosphatase, or FBP1, which works to control gluconeogenesis, a process in which the liver synthesizes glucose (the main source of energy used by cells and tissues) during sleep. sleep and the secret to maintaining a constant supply of glucose in the bloodstream.
Gu and his colleagues found that FBP1 had multiple functions. Beyond playing a role in the conversion of fructose to glucose, FBP1 had a second non-enzymatic but critical function: it inhibited the AKT protein kinase, which is the main channel of fructose activity. insulin.
“Basically, FBP1 keeps AKT in check and protects once morest hyperreactivity to insulinhypoglycemic shock and acute fatty liver disease,” said first author Gu.
Working with Yahui Zhu, a visiting scientist at Chongqing University in China and second author of the study, Gu developed a peptide (a chain of amino acids) derived from FBP1 that disrupted the association of FBP1 with AKT and another protein that inactivates AKT.
“This peptide functions as a mimetic of the insulinactivating AKT,” Karin said. “When injected into mice that have become resistant to insulina very common pre-diabetic condition, due to prolonged consumption of a high-fat diet, the peptide (nicknamed E7) can reverse resistance to insulin and restore normal glycemic control.
Karin said that the researchers would like to further develop E7 as a clinically useful alternative to insulin “because we have every reason to believe that it is unlikely to cause insulin shock.”
Fuente: here
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