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New Findings could lead to improved or better blood sugar level control

Many polygenic disease patients don’t only have issues with their insulin, but also with the discharge of the hormone glucagon. Researchers at Uppsala University have now discovered a regulation mechanism that may provide a chance to boost blood sugar control in these patients. The research is published in the journal Diabetologia.

The hormone glucagon, that is discharged from alpha cells in the pancreas, plays an important role in blood sugar regulation. the release of hormone is usually pent-up once the blood sugar concentration increases after a meal, and when the glucose concentration eventually drops, the alpha cells resume the secretion of glucagon, that in turn stimulates the liver to release glucose into the blood. This mechanism prevents blood sugar from reaching perilously low levels between meals and during starvation.

In many ways, glucagon acts opposite to the known hormone insulin, which lowers blood sugar and which is released in low amounts in diabetes. However, several polygenic disease patients also show disturbed glucagon release. accordingly, glucagon is often stirred up after a meal, which aggravates the patients’ already high blood sugar levels. On the other hand, there’s a low release of glucagon when blood sugar drops to low levels, which can be dangerous in insulin-treated polygenic disease patients.

Despite the essential functions of glucagon very little is understood concerning how blood sugar controls the discharge of the hormone. By utilizing advanced microscopy techniques to measure completely different signalling molecules in alpha cells, researchers at Uppsala University have discovered a new regulatory mechanism.

The release of virtually all hormones is triggered when the concentration of calcium ions increases below the cell membrane. In alpha cells, however, the calcium levels are already increased regardless of whether or not the glucose concentration is low or high. so even if calcium is needed for glucagon to be released, it appears that another signal is controlling how much of the hormone is secreted.

When the researchers measured the signalling molecule cyclic AMP (cAMP), which inturn by itself cannot trigger secretion release however which amplifies the effects of calcium, it had been discovered that glucose influences the cAMP levels in an exceedingly manner that correspond to glucagon secretion.

By fixing cAMP levels perpetually high in the cells, the regulatory effect of glucose may be prevented. the discovery that blood sugar controls glucagon release by direct effects on alpha cell cAMP is very important as a result of it may lead to new potentialities to boost glucose control in polygenic disease patients.

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