The beta cells of the pancreas produce insulin in response to elevated blood glucose levels. They have enormous amounts of endoplasmic reticulum.

In diabetes, insulin production is deficient - often this is because the cells themselves are attacked by the immune system and destroyed. In some cases, defective insulin or other proteins accumulate in the ER and do not go on to the Golgi. The ER has a "quality control " pathway to stop unfolded proteins from being secreted. Recently it has been discovered that accumulation of unfolded proteins leads to a decrease in protein translation - to lessen the load on the ER (see here ) for a perspective by Sonenberg and Newgard about this pathway.

So, the answer to your question is that the number of proteins going into the ER is decreased when there is a heavy load of bad proteins that accumulate in the ER .

You have asked a very interesting question, and one that I am not very familiar with myself...so I had to do some searching around the web for the answer. Let me share what I have learned so far, and hopefully this will help answer your question.

As you probably know, scientists have found that diabetes is actually an auto-immune disease (i.e., the immune system sends out lymphocytes to attack cells in your body that it mistakes for invaders/foreign substances.) Other auto-immune diseases include AIDS, which, like diabetes, is thought to be triggered by a virus. In the case of AIDS, the HIV retrovirus is a known causative agent, but for Diabetes it hasn't been discovered yet. They are working hard on this though, as I gather from the medical websites I visited.

There are 2 types of diabetes: Type 1 diabetes mellitus and Type II diabetes mellitus. Type I is referred to an insulin-dependent diabetes (IDD) (your body has stopped making the hormone insulin), and Type II is called non insulin-dependent diabetes (NIDD) (your body still makes insulin but at a much reduced or sluggish rate compared to most people).

This next part I got from a the University of California Berkeley Molecular and Cellular Biology Class website taught by Dr. Paola Timiras: here

I have edited parts of it that might be of interest to you, but be sure to go to this website for more information (and to see what a college class is like!)

"The pancreas... is both an endocrine and an exocrine gland. The exocrine functions are concerned with digestion. The endocrine function consists primarily of the secretion of the two major hormones, insulin and glucagon. Four cell types have been identified in the islets (these are cells called the "islets of Langerhans" in the pancreas), each producing a different hormone with specific actions:

* A cells produce glucagon; * B cells produce insulin; * D cells produce somatostatin; and * F or D1 cells produce pancreatic polypeptide.

These hormones are all polypeptides. Insulin is secreted only by the B cells whereas the other hormones are also secreted by the gastrointestinal mucosa and somatostatin is also found in the brain.

"Question: what do all these hormones produced by A, B, C, and D cells in the islet of Langerhans in the pancreas do in your body?

Okay onward.... This next set of quotes came from another website by the Medical Library at the University of Utah Medical School.

Let see what happens to the islets of Langerhans once the autoimmune reaction is triggered in a person's body... "Type I: The islets of Langerhans are destroyed in type I diabetes mellitus. This occurs probably as a consequence of a genetic susceptibility, followed by the onset of autoimmune destruction triggered by some environmental factor such as a viral infection. Heavy lymphocytic infiltrates appear in and around islets. The number and size of islets are eventually reduced, leading to decreased insulin production and glucose intolerance.

Type II: The islets of Langerhans are normal in number or somewhat reduced with type II diabetes mellitus. Fibrosis and deposition of amylin polypeptide within islets are most characteristic of the chronic states of type II diabetes." From this information, I have to conclude that for Type 1 diabetes (IDD), the actual insulin -producing B cells are destroyed (along with all the other types of cells in the islets of Langerhans) when the lymphocytes mistakenly attack them. In this case, the rough endoplasmic reticulum (RER) would simply be broken down with the rest of the cells and recycled (much like white blood cells clean up damaged cells near a skin wound). However, it seems like with Type II diabetes (NIDD), the islets are not necessary destroyed all at once (as in Type I), but their functionality is hindered by "fibrosis and deposition of amylin polypeptide" (protein-like scar tissues that attaches to the cells) over time.

Something about these compounds causes the cells to die after a while (decreased exchange of gases? decreased energy for respiration? Scientists are still working on that part!). This is why some Type II diabetes patients require insulin injections after they have had the disease for many years, as opposed to Type I diabetes patients that have to have insulin injections immediately after developing the disease.

Question: Do you know how doctors help patients control Type 1 and Type II diabetes?