Endoplasmic Reticulum-Associated Degradation (ERAD) -
a physiological process, which our bodies already have, is the key to reversing Type 2 Diabetes
ERAD is an essential cellular survival mechanism that handles problematic proteins in our bodies. Well-known problematic proteins that cause diseases include β-amyloid, misfolded insulin (as proinsulin), alpha-synuclein and, etc.. Like that misfolded β-amyloid causes Alzheimer's Disease, accumulation of misfolded insulin in the Endoplasmic Reticulum (ER) results in ER Stress, which consequently kills pancreatic β cells by initiating apoptosis. In fact, ER stress has been recognized as the top leading cause of β cell death.
ERAD can specifically target misfolded or unfolded proteins such as insulin for degradation. As ERAD can eliminate the cause of ER Stress, it has been considered a therapeutic target for many diseases.
In this accompanying video, you have found information regarding how ER stress and ERAD affect the progression of type II diabetes in more detail. We hope you will find this video helpful.
ERAD Has a Critical Role in Supporting
Glucose-Stimulated Insulin Secretion
The pancreatic beta cells are the only tissue that can produce insulin. It has been scientifically proven that healthy ERAD function supports insulin secretion to cancel insulin resistance and help maintain healthy blood sugar and A1c.
Even better, the secretion is "Glucose-Stimulated," which means ERAD helps produce insulin only when our bodies need it. This kind of "made-to-order" stimulation will not result in hypoglycemia (too low blood sugar).
ERAD Has a Critical Role in Pancreatic Beta Cell Development
ERAD helps mature beta cells produce insulin and get immature (or newly born) beta cells ready to work.
With more mature beta cells, our bodies can produce more insulin without putting extra stress on the cells.
Don't worry. Unlike insulin injection, pancreatic beta cells will not produce "too much" insulin. They make insulin only when our bodies need it.
ERAD Helps Prevent Unwanted Beta Cell Death
