As we know, storage of extra fats in our bodies predisposes them to diabetes-type2. Among the places the body stores fat in, are cell membranes. Normally, fats and their derivatives (phospholipids) surround cell receptors present in cell membranes in a certain programmed way to acquire a specific assembly. Changing the types of fat around the receptors which are proteins may change their configuration in a way that hinder their function.

If fat around insulin receptors is modified, then their response may be reduced and the cell response (e.g.muscle cell) is reduced, and this case is known as "Insulin Resistance". Normally, people cope with this case by producing more insulin, but people who develop diabetes cannot, probably by a fat-changed receptor in the pancreas cells that respond to glucose in blood by secreting insulin.

Recently, a team of Garvan's Diabetes Signaling Unit, led by Associate professor T.Biden and Dr C.Schmitz-Peiffer has identified an enzyme known as PKCepsilon (PKCe) that is active during diabetes and blocks the availability of insulin. They found that absence of this enzyme receptor can restore the capacity of the pancreas to produce insulin (Genetically modified mice- without PKCe enzyme- were fed high fat diet and became fat and insulin resistant but failed to develop diabetes, instead they excrete extra insulin.

Blocking PKCe would not stop people at high risk of developing diabetes from becoming insulin-resistant, but it will restore their capacity to compensate.

"In PKCe, we believe we have identified a very important biological target that will enable us to address one of the major underlying causes of diabetes". Said Biden. " The next step is to develop a targeted pharmaceutical that will inhibit PKCe and allow the insulin secreting cells of the pancreas beta cells to do their job."

Finally, diabetics will wait for the pharmaceutical to be produced, would they deal with fats the correct way while they are waiting?

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