UNITED STATES (VOP TODAY NEWS) — We speak insulin, we mean diabetes . Diabetes mellitus is a chronic endocrine disease that affects millions of people worldwide; and insulin is a hormone that helps control this disease. But now a third party can join this duet: the hormone glucagon.
It used to be thought that the only goal of glucagon was to counteract insulin. But now researchers from the Montreal Institute of Clinical Research are ready to challenge this dogma.
Researchers describe the effects of these two hormones as follows. When the blood sugar level becomes too high, insulin sends a signal to the liver – to store excess glucose in the form of glycogen, and stop the release of glucose into the blood. Glucagon gives the opposite orders – it tells the liver to use the same glucose reserves accumulated under the command of insulin, and resume glucose production: this is necessary, for example, during fasting or when the body spends a lot of energy (training, hard work).
Because of the opposite effects, insulin and glucagon have long been considered rivals, fighting to send their signal to the liver. Many scientists even suspected that too much activity or a high level of glucagon is a risk factor for developing diabetes . But it turned out that these hormones do not compete, but rather protect each other.
When we fast for a certain period of time, or even when we just sleep all night (without night raids on the fridge!), Our glucagon level naturally increases. This is necessary to prevent a decrease in blood sugar levels, which can lead to hypoglycemia.
But it turns out that this is not all. When we start a meal after a long break, our insulin sensitivity increases . For example, when you get up and eat breakfast after a night’s sleep, your liver is much more susceptible to the insulin signal to stop producing your own sugar than usual. And this mechanism regulates glucagon.
Conducting experiments on the liver cells of mice, the researchers found that for better interaction with insulin, glucagon requires a protein called PGC1A. Activation of PGC1A did not lead to hyperglycemia at all, as previously thought, instead mice had the best response to insulin.
Scientists expect that this discovery will encourage other researchers to become more familiar with glucagon and PGC1A, which until now have been undeservedly considered pests due to perceived undesirable effects. This will help identify new therapeutic targets for diabetes, as well as other metabolic diseases.
This article is written and prepared by our foreign editors writing for VOP from different countries around the world – edited and published by VOP staff in our newsroom.
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