Molecular biologists are hoping that recent discoveries regarding the mechanisms that cause type-1 diabetes will help treat the more troublesome type-2.
Type-2 diabetes sucks and it’s a growing problem for the ever-expanding waistlines of the American population. As people eat more and more sugar and carbohydrates – which are converted directly to sugars in the digestion process – the cells that create insulin start to lose their sensitivity. Once this happens, the pancreatic beta cells work overtime and eventually wear out, leading to an insulin deficiency.
Though scientists know these are the steps involved in developing the disease, the exact biological mechanisms responsible remain a mystery. However, they’re hoping to uncover some clues from type-2 diabetes’ first cousin.
Type-1 diabetes debatably sucks even more for the unfortunate few that are born with the disease as there is no exercise or diet regime that can help stave off the disease. Instead, they are born with genetic mutations that prevent the beta cells from creating enough insulin.
I remember a girl in my elementary school that had the disease. I was always a little bit jealous that she got to eat animal crackers and drink apple juice every day. I obviously never saw the constant blood draws to check sugar levels, insulin shots and seizures.
I’m not sure exactly which type of diabetes she was afflicted with, but in a new study published in PLOS ONE, lead author Peter Arvan, director of the Michigan Comprehensive Diabetes Center, has made important strides in understanding Mutant INS-gene-induced Diabetes in Youth, or MIDY.
According to the study, MIDY is caused by a single distinct mutation to the INS-gene, which is responsible for controlling the production of insulin in the human pancreas. This particular mutation is especially nasty given that if someone has one mutated gene and one healthy gene, they still get diabetes.
For a quick course in insulin production, the substance is created by the endoplasmic reticulum; a network of transportation tubes, hard-working bubbles and discs of membranes in a cell responsible for the production of proteins. To do this, the network takes proinsulin protein – which can be seen as insulin raw material – and sends it through a series of folds and structures – or “refineries” – in order to convert it into fully functional insulin.
In MIDY, this insulin precursor is not folded correctly. Not only do these errors prohibit the proteins from becoming insulin, they cause errors in other, perfectly healthy copies of proinsulin, spreading the problem. This results in an insulin deficiency, which causes stress in the beta cells that produce insulin. It’s basically a giant snowball effect that eventually leads to full-fledged diabetes.
Though this misfolded protein is more common in MIDY, it can be seen in smaller numbers in type-2 diabetes as well. The researchers believe that these same errors –though fewer in numbers and not created by genetic mutations – play a significant role in the formation of type-2 diabetes as well. If this is found to be true, it may be possible to affect the protein folding process so that the proinsulin gets folded quickly, before they can be damaged by the existing errors.
If so, it may be possible in the coming years to stop type-2 diabetes before it starts.