Why type 2 diabetes happens

Everyone knows that diabetes is an insulin problem. Too little insulin means the body is unable to regulate sugar levels, high sugar levels damage blood vessels and then nerves etc.

But it is important to understand the root of the insulin problem.

Beta cells are insulin production centre

The insulin factory is located in a specialized area of the pancreas known as the Islet’s of Langerhans.

The cells tasked with pumping out the insulin hormone are the beta cells.

Diabetes happens because of production problems. But the cause of the production problems is different, depending on whether the person is suffering from type 1 or type 2 diabetes.

Factory burns down

In type 1 diabetics – the immune system attacks these beta cells, mistakenly believing that they do not belong.

The immune system treats the beta cells as if they were a bacteria. Firing all their weaponary at the poor defenceless cells. The effect of this attack is that the cells are completely decimated. The factory burns down – there is nothing left.

No factory means no insulin is produced.

To fix the problem, insulin must be pumped in form outside or a new factory constructed.

Factory cannot meet demand

But in type 2 diabetics the problem is a little different.

Before a person becomes diabetic, the beta cells are pumping insulin, lots of it. They are in fact having to produce excess quantities of the stuff to keep up with demand.

The reason why demand for the product has gone through the roof, is because the cells that normally respond to insulin have stopped reacting. The medical name for this condition is insulin resistance.

High sugar stimulates demand

Insulin production levels are determined by sugar levels.

Insulin resistance inevitably causes sugar levels to rise, since the body fails to remove the sugar from the blood steam timeously.

As sugar levels rise, a requisition is sent to the pancreas to ramp up production, fortunately production ramps up so sugar levels remain within normal ranges.

Wear and tear on factory causes production failures

Any factory that is pushing out product in high volumes, with no down time for maintenance, is vulnerable to equipment failures.

Researchers from University of Michigan Medical School have pieced together how this happens in beta cells.

CHOP protein gives beta cells the CHOP

CHOP is a protein that is produced when cells are very stressed because the cell is working too hard.

CHOP is part of a cell’s defence mechanism, as far as the body is concerned an overworked cell is probably defective – it could be infected with a virus or cancerous. Defective cells are potentially dangerous, so CHOP is tasked with killing the cell off (apoptosis).

The continuous excess production of insulin by the beta cells, activates the CHOP protein, resulting in beta cell death.

As the beta cells die – the body loses the battle to control the sugar levels and type 2 diabetes emerges.

Blocking CHOP restores beta cell function

The researchers were able to stop diabetic mice from producing the CHOP protein using some fancy genetic engineering technology.

When CHOP is stopped, beta cells stop dying in the mice. As the beta cell levels improve so does the ability to control sugar levels.

They can’t genetically engineer you – yet

Chopping out CHOP is not an option to treat type 2 diabetes yet. At this stage genetically engineering you, is a lot more complicated than genetically engineering mice.

But chopping down your body’s demand for insulin is something that is relatively easy to do – rein in insulin to fell the type 2 diabetes monster.

Chop deletion reduces oxidative stress, improves beta-cell function, and promotes cell survival in multiple mouse models of diabetes. Journal of Clinical Investigation (2008) 118(10):3378-3389. Benbo Song, Donalyn Scheuner, David Ron, Subramaniam Pennathur and Randal J. Kaufman

Control of Pancreatic ? Cell Regeneration by Glucose Metabolism. Cell Metabolism (2011) 13 (4): 440 Shay Porat, Noa Weinberg-Corem, Sharona Tornovsky-Babaey, Rachel Schyr-Ben-Haroush, Ayat Hija, Miri Stolovich-Rain, Daniela Dadon, Zvi Granot, Vered Ben-Hur, Peter White, Christophe A. Girard, Rotem Karni, Klaus H. Kaestner, Frances M. Ashcroft, Mark A. Magnuson, Ann Saada, Joseph Grimsby, Benjamin Glaser, Yuval Dor.

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