07 November 2019

Cholesterol is the key to Insulin

Insulin, a hormone produced by beta cells of the pancreas, is the main regulator of blood glucose levels. Previous studies conducted by a group from Lund University in Sweden have identified 130 different receptors on the surface of beta cells that have different functional effects on them. 

In a new study conducted in collaboration with scientists from the University of Sharjah (United Arab Emirates), one of these receptors (GPR183) has been discovered that plays a key role in the release of insulin. The receptor is activated when it binds to a certain compound formed during the destruction of cholesterol in the liver – 7α-25-DHC. In rats, as well as in human pancreatic samples, the oxidized cholesterol metabolite showed the ability to significantly increase insulin secretion by activating the GPR183 receptor.

According to scientists, the cholesterol metabolite also protects beta cells from prolonged cellular stress caused by hyperglycemia, which is known to lead to impaired insulin secretion.

The authors write that this discovery may be important in another aspect: people with high cholesterol are often overweight or obese. With an excess of cholesterol, the specific metabolite 7α-25-DHC is produced in large quantities, and as a result, insulin secretion increases. This leads to the rapid absorption of glucose, the appearance of hunger and, as a result, the consumption of more food and weight gain. If it is possible to block the binding of the GPR183 receptor to the cholesterol metabolite and thus regulate the release of insulin, you can weaken the feeling of hunger.

Article by J. Taneera et al. Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced β-cell dysfunction published in the journal Molecular and Cellular Endocrinology.

Aminat Adzhieva, portal "Eternal Youth" http://vechnayamolodost.ru based on the materials of Lund University: Key mechanism in insulin release by cholesterol metabolite found.


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